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(Hypertension. 1999;34:943-949.)
© 1999 American Heart Association, Inc.
Scientific Contributions |
Role of Angiotensin and Oxidative Stress in Essential Hypertension
From the Department of Physiology and Biophysics, Mayo School of Medicine and Division of Hypertension, Mayo Clinic (J.C.R.) Rochester, Minn; and the Department of Physiology and Biophysics and the Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center (J.F.R.), Jackson, Miss.
Correspondence to J. Carlos Romero, MD, Department of Physiology, Mayo Clinic, Rochester, MN 55905.
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Abstract |
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Abstract—In this review, we examine the possibility that small increments in angiotensin II are responsible for an increase in blood pressure and maintenance of hypertension through the stimulation of oxidative stress. A low dose of angiotensin II (2 to 10 ng · kg-1 · min-1, which does not elicit an immediate pressor response), when given for 7 to 30 days by continuous intravenous infusion, can increase mean arterial pressure by 30 to 40 mm Hg. This slow pressor response to angiotensin is accompanied by the stimulation of oxidative stress, as measured by a significant increase in levels of 8-iso-prostaglandin F2
(F2-isoprostane). Superoxide radicals and nitric oxide can
combine chemically to form peroxynitrite, which can then oxidize
arachidonic acid to form
F2-isoprostanes. F2-isoprostanes exert
potent vasoconstrictor and antinatriuretic effects.
Furthermore, angiotensin II can stimulate endothelin
production, which also has been shown to stimulate oxidative
stress. In this way, a reduction in the concentration of nitric oxide
(which is quenched by superoxide) along with the formation of
F2-isoprostanes and endothelin could potentiate the
vasoconstrictor effects of angiotensin II. We hypothesize
that these mechanisms, which underlie the development of the slow
pressor response to angiotensin II, also participate in the
production of hypertension when circulating
angiotensin II levels appear normal, as occurs in many
cases of essential and renovascular hypertension.
Key Words: isoprostane • endothelin • oxidative stress • hypertension, essential • angiotensin II
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Introduction |
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Despite the fact that essential hypertension is one of the most prevalent diseases of developed Western societies and is an unequivocal risk factor for cardiovascular morbidity and mortality, the underlying pathophysiological abnormalities that lead to the development of the elevated arterial pressure in this disorder remain elusive.1 However, in the past decade, many clinicians have suggested that essential hypertension must be related to the renin-angiotensin system and to an undefined renal dysfunction.2 These assumptions are motivated first by the efficacy of converting-enzyme inhibitors or angiotensin receptor antagonists to reduce blood pressure in essential hypertension, even when plasma levels of angiotensin II (Ang II) are normal or slightly elevated.3 4 5 Second, hypertension can be induced in a normotensive human or animal by transplantation of a kidney from a hypertensive subject,2 or, alternatively, hypertension can be cured by transplanting a kidney from a normotensive donor into a previously hypertensive individual.3 Third, studies recently have shown that Ang II can stimulate oxidative stress,6 which could activate several vasopressor mechanisms that may potentiate the vasoconstrictor effect of Ang II. Any hypothesis concerning the basic elements involved in the pathogenesis of essential hypertension should consider these characteristics. Such is the objective of this review.
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Can Normal Concentrations of Angiotensin in Plasma Induce and Sustain Hypertension? |
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 TopAbstractIntroduction Can Normal Concentrations of... Activation of Fast and...Role of Ang II,...Oxidative StressEndothelinIsoprostanesVascular Effects of...The Relationship Among Sodium...References |
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The functional mechanisms that are responsible for long-term maintenance of hypertension in the presence of so-called "normal" levels of plasma renin activity remain unexplained.3 4 5 Note that plasma renin activity is defined by the amount of Ang I generated in plasma7 during a given period of incubation and under predefined laboratory conditions (pH, peptidase inhibitors, etc). Therefore, the amount of Ang II generated in the plasma in most essential hypertensive patients is not different from that seen in normotensive individuals (50% to 60%).3 4 5 Furthermore, a subset of the population of hypertensives exists in whom the level of circulating Ang II is significantly less than that detected in normotensives (25% to 35%).3 However, these levels of Ang II may contribute to the maintenance of hypertension, because blood pressure is markedly reduced by the administration of either converting enzyme inhibitors4 or angiotensin antagonists.5 These seemingly paradoxical observations can be reconciled by the original observation of Dickinson et al,8 who demonstrated in 1963 in rabbits that the infusion of very small amounts of Ang II that were not sufficient to elicit an immediate elevation of blood pressure nonetheless produced chronic hypertension. Two years later, McCubbin et al9 reported similar findings in dogs. These studies were critical to the determination of the difference between the so-called fast and slow pressor effects of Ang II.10 The fast pressor responses are produced by relatively high concentrations of Ang II, which induce a rapid contraction of the smooth muscle when administered as a bolus.11 The response reaches the maximal pressor response in seconds and returns to normal levels in 2 to 3 minutes. The intracellular signaling involved in mediating such a rapid angiotensin-induced vasoconstriction has been investigated extensively.12 However, the mechanisms that could account for the slow pressor responses remain unknown.8 9 10 Slow pressor responses need 5 to 10 hours to develop and reach a maximal peak 3 to 5 days after the onset of the infusion.10 The important characteristics of slow pressor responses are as follows: (1) these responses are not specific for any particular animal species and have been demonstrated in man,13 rats,14 rabbits,8 and dogs.9 In our laboratory, we have demonstrated similar responses in a swine model.15 (2) Slow pressor responses appear to evolve at doses of Ang II that are insufficient not only to produce an immediate elevation of blood pressure, but also to stimulate steroidogenic and dipsogenic actions typical of blood-borne angiotensin.14 16 (3) Slow pressor responses also have been produced by the continuous infusion of norepinephrine.17 18 However, the rise in blood pressure is much lower than that observed with Ang II (
12 mm Hg), but significantly higher plasma concentrations of
norepinephrine (18-fold higher) are required to produce a similar
pressor response as Ang II.14 These latter findings are
confounded by the fact that norepinephrine can stimulate
the release of renin because of its intrinsic ß-adrenergic agonist
effect. The consistent delay of small subpressor doses of Ang
II to produce an increase in blood pressure suggests a time requirement
for the activation of additional vasoconstrictor processes, which can
then trigger an autocatalytic reaction that accelerates or potentiates
the vasoconstrictor effect of Ang II. For example, Brown et
al14 demonstrated in rats that the administration of 20
ng · kg-1 ·
min-1 of Ang II did not alter blood pressure
during the first hour of infusion (see
Table), but on the morning of the
following day, blood pressure was significantly increased, by 15
mm Hg. Thereafter, blood pressure rose progressively and peaked on the
seventh day, at which time mean arterial pressure was
153±6 mm Hg. The basal levels of blood pressure before infusion
were 103±4 mm Hg. In studies conducted in a separate group of
animals, these investigators also showed that the amount of
angiotensin needed for a 1-hour infusion to achieve a
comparable level of blood pressure (155±1.1 mm Hg) was 810
ng · kg-1 ·
min-1 Ang II (Figure 1), whereas an infusion of 270 ng
· kg-1 · min-1
of Ang II produced an elevation of blood pressure of 146±3
mm Hg. Furthermore, the circulating level of Ang II on day 7 of
the infusion of 20 ng · kg-1 ·
min-1 Ang II was determined to be 
230 pg/mL,
which did not differ considerably from the 150 pg/mL found in animals
during the infusion of 20 ng · kg-1
· min-1 of Ang II for 1 hour when blood
pressure was still normal (Figure 1). In contrast, the level of
Ang II found in acutely hypertensive animals (146±3 mm Hg)
infused with 270 ng · kg-1 ·
min-1 Ang II for 1 hour was 2500 pg/mL. These
observations unequivocally prove that small subpressor doses of Ang II,
continuously infused, are capable of raising blood pressure without a
concomitant increase in plasma levels of Ang II. This phenomenon has
been best explained as an autopotentiation of the vasoconstrictor
effects of Ang II.8 In an extensive review on this
subject, Lever10 ruled out the participation of other
mechanisms such as the central nervous system, vascular
hypertrophy, etc. In this survey, we examine the
possibility that the slow responses to Ang II may be due to the
vasoconstrictor effects of oxidative stress.
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Activation of Fast and Slow Intracellular Signaling Modalities by Ang II |
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Like fast pressor responses, slow pressor responses are triggered by the binding of Ang II to AT1 receptors.19 After binding AT1 receptors, angiotensin activates a G-protein, which subsequently may stimulate different signaling pathways, depending on the length of the stimulation of the AT1 receptors. Ang II can trigger rapid smooth-muscle contraction through the phosphoinositide-Ca2+–protein kinase C effector system.20 21 22 23 24 The binding of a vasoconstrictor substance such as Ang II to its receptor activates phospholipase C. This enzyme induces the hydrolysis of phosphatidylinositol bisphosphate and thus liberates inositol triphosphate (IP3), which releases Ca2+ from intracellular stores, and diacylglycerol, which activates protein kinase C.20 21 22 Protein kinase C regulates Ca2+ transmembrane flux. An important concept concerning the interrelationship of Ang II with the phosphoinositide-Ca2+ system was proposed by Rasmussen and Barrett.25 They suggested that the stimulation of the IP3-Ca2+ system accounts for the initial effect of Ang II, namely rapid development of smooth-muscle contraction. In contrast, the sustained actions of Ang II (chronic smooth-muscle contraction) could be primarily maintained through protein kinase C, which stimulates calcium channels and thus perpetuates contractile response (1) by facilitation of the entrance of extracellular Ca2+, (2) by stimulation of lipoxygenase production, or (3) by the release of other autocoids that may potentiate the vasoconstrictor response to Ang II. A difficult but critical task will be to determine whether the activation of this intracellular pathway differs from the stimulation of other mechanisms that are also affected by the chronic administration of Ang II, such as the synthesis of proto-oncogenes, tissue hypertrophy, and inflammatory processes.26 Among the several mechanisms stimulated by Ang II, the effects on oxidative stress appear to be the most likely to potentiate Ang II, because these involve a reduction in nitric oxide (NO) along with the release of potent vasoconstrictors.
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Role of Ang II, Oxidative Stress, NO, and Isoprostanes in the Slow Responses to Ang II |
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Ang II has been shown to stimulate the production of superoxide, which quenches NO.6 27 On the other hand, the chemical combination of superoxide with NO is known to yield peroxynitrite, which is a potent oxidant that could oxidize arachidonic acid and thus release a potent renal vasoconstrictor, antinatriuretic substance 8-iso-prostaglandin F2
(isoprostane). This sequence of events is illustrated in Figure 2.27 Additionally,
Ang II may also stimulate endothelin (ET) synthesis,28 29 30
which can be further increased by the oxidative stress cascade
mentioned above.31 32 33 34 Therefore, the reduced NO,
increased isoprostane, and increased ET represent potent
vasoconstrictor effects that can enhance the vasopressor action of Ang
II and may explain how hypertension is maintained in pathological
situations (such as 2-kidney, 1 clip Goldblatt hypertension or
essential hypertension) in which the levels of angiotensin
are frequently found to be normal.35 The occurrence of
this sequence of events, which is further examined below, deserves to
be investigated, because it could be used to assess stages in the
development of hypertension more accurately than measurement of the
levels of plasma renin activity or angiotensin itself. In
fact, the metabolites of oxidative stress have been proposed to play a
critical role in the pathophysiology of renovascular hypertension and
renal damage.36 37
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Oxidative Stress |
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Pryor and Squadrito27 have shown that oxygen free radicals (superoxide) are constantly being combined with NO to form peroxynitrite, which is in equilibrium with peroxynitrous acid (superoxide+NO
peroxynitrite OONO).27 Peroxynitrite has
a greater oxidative capacity than any other compound27
(Figure 2). An important observation that links superoxide
production to an increased level of Ang II was obtained by
Rajagopalan et al.6 This study showed that arteries
isolated from rats rendered hypertensive by the administration of a
large amount of Ang II (0.7 mg/kg/dayx5 days) exhibited an impaired
relaxation to acetylcholine associated with an increased level of
superoxidation. These alterations were corrected by pretreating the
rats with losartan (an Ang II antagonist) or by
treatment of vessels with liposome-encapsulated superoxide dismutase.
In this study, hypertension was not thought to be responsible for
stimulating superoxide production because
norepinephrine infusion, which raised blood pressure to
levels similar to those of Ang II, was not accompanied by activation of
superoxide. Additional studies6 showed that the
stimulation of superoxide production in intact vascular
segments was not related to the participation of xanthine oxidase,
mitochondrial electron transport, cyclooxygenases,
NO synthase, or lipoxygenases, because the response was
unaffected by the administration of oxypurinol, rotenone,
indomethacin, nitro-L-arginine-methyl ester (L-NAME),
or nordihydroguayaretic acid, respectively. We have recently shown that
oxidative stress can be stimulated by very low doses of Ang II in swine
because it increases plasma unbound isoprostanes (Figure 3). This effect was not seen in
age-matched control animals that were not treated with Ang II.
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Endothelin |
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Whether ET plays a role in mediating oxidative stress or is affected by oxidative stress is not clear. Both ET production and NO synthesis can be stimulated by Ang II.28 29 30 38 In cultured endothelial cells, inhibition of NO synthesis can stimulate the release of ET, whose effects can be inhibited by bosantan, a nonspecific ET antagonist.39 40 NO can also regulate the vasoconstrictor effects of ET in vascular smooth muscle.41 42 In support of the hypothesis that both NO reduction and ET stimulation play a role in mediating the oxidative stress induced as a consequence of slow pressor responses to Ang II are the data in which the acute hypertension induced by NO synthase inhibition can be attenuated by acute nonselective ETA/ETB antagonism,43 44 whereas chronic NO synthesis inhibition (4 weeks) cannot be attenuated by acute ETA specific receptor antagonism.45 The role that ET plays in 2-kidney, 1 clip Goldblatt hypertension is not clear, because oxidative stress, measured by production of isoprostanes, can induce the release of ET from smooth muscle cells.31 32 33 More directly we have recently observed that stimulation of oxidative stress by hypercholesterolemia in pigs evolves with a reduction in circulating NO and a significant increase in isoprostanes and that these changes can be obliterated by ET antagonism.46 This indicates the need to evaluate whether ET stimulates oxidative stress or whether oxidative stress stimulates production of ET. Caution should be taken in ascribing to ET a definitive role in the hypertension experimental models, because it has been shown to have a potent diuretic and natriuretic effect at doses that do not lower glomerular filtration rate; this would antagonize any hypertensive effect.47 48
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Isoprostanes |
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Isoprostanes are prostaglandin-like compounds produced by free radical–catalyzed peroxidation of arachidonic acid.49 Although 64 compounds can be theoretically formed by peroxidation of polyunsaturated fatty acids, 4 classes of regioisomers are currently found in mammals, of which the most abundant is F2
isoprostane50 51 (Figure 2).
This compound is detected in plasma from healthy volunteers at levels
of 35±6 pg/mL, whereas urine contained 1.6±0.6 ng/mg of
creatinine.52 53 54 The levels of isoprostanes
in plasma exceed by 10 to 20 times the levels of circulating
prostaglandins.52 Isoprostane is increased
200 times after oxidant injury inflicted by carbon tetrachloride
(CCl4) or the herbicide
diquat.52 53 Evidence exists that shows that,
unlike prostaglandins, isoprostanes can be formed while the
molecule of arachidonic acid is still esterified to
phospholipids, from which it subsequently can be released by
phospholipases.55 This effect is clearly shown during the
administration of CCl4, which increases the
amount of isoprostane bound to liver phospholipids (by 40 times at 2
hours), which are then released into circulation. Unbound isoprostane
peaks in the circulation 8 hours after the administration of
CCl4.56 Arachidonic acid oxidation can also form iso-D2/E2, isothromboxane, and isoleukotrienes. Although some of these compounds can be detected in tissue, they are not detected in circulation under normal conditions.51 Another important issue is that isoprostane, the most abundant compound form in vivo, has been shown to be the most reliable index of lipid peroxidation.57 This provides an important tool to evaluate oxidative stress in vivo. A good review on this issue has been recently published by Morrow and Roberts.51
Isoprostane can be produced locally in the kidney.31 52 Administration of isoprostanes into the rat (low nanomolar range) produces a potent renal vasoconstriction that reduces glomerular filtration rate and renal blood flow by 40% to 45%.31 52 These effects appear to be predominantly exerted on the afferent arteriole.31 32 Reckelhoff et al58 have shown that aging rats (22 months old) exhibit 50% reduction in glomerular filtration rate and 3-fold increases in renal isoprostane versus young rats (3 to 4 months old). Chronic treatment (for 9 months) with the antioxidant vitamin E normalizes renal isoprostane levels and improves glomerular filtration rate significantly.58 In rabbits and rats, isoprostane is a potent pulmonary artery vasoconstrictor, and it causes bronchoconstriction in the rat lung.59 60 In addition, isoprostane has been shown to induce a significant release of ET from bovine aortic endothelial cells.34
An important characteristic concerning the biological activity of isoprostane is that the vasoconstrictor effects are blocked by thromboxane receptor antagonist SQ29548.31 However, much indirect evidence61 has shown that isoprostane interacts with a receptor in vascular smooth muscle that is distinct from the thromboxane receptor. Studies using molecular cloning strategies will be required to provide unequivocal proof for the existence of a unique isoprostane receptor.
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Vascular Effects of Peroxynitrite |
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The postulation that peroxynitrite leads to a vasoconstrictor effect through the synthesis of isoprostane should be tempered by the discovery of parallel biochemical effects, the role of which remains undefined in the regulation of vascular tone. Some evidence indicates that peroxynitrite may not follow the oxidative pathway through arachidonic acid with the production of isoprostane but could combine with thiol groups of glutathione to produce S-nitroglutathione.62 This compound could subsequently degenerate to produce NO and vasodilatation.62 This effect has been postulated to explain the prolonged vasodepressor effect elicited by peroxynitrite in pulmonary arteries.63
The extent to which peroxynitrite produces vasodilatation through S-nitroglutathione or by acting directly on the vasculature constitutes an important area of research. Some of the effects directly attributed to peroxynitrites are those induced by coronary ischemia-reperfusion.64 Furthermore, a study conducted by Wei and colleagues65 showed that the vasodilatation produced by peroxynitrite or hydrogen peroxide in cerebral arteries (topical application through cranial windows) is mediated by an ATP-sensitive potassium channel. Interestingly, superoxide generated by xanthine oxidase acting on xanthine also induced a cerebral vasodilatation, but that effect was mediated by stimulation of calcium-activated potassium channels.65 No other studies have been conducted to determine whether this potassium channel–mediated effect is restricted to cerebral circulation. The notion that the vasodilator effects of peroxynitrite exerted through degeneration of S-nitroglutathione or through a specific potassium channel is further supported by the study of Benkusky et al,66 which shows that the systemic administration of peroxynitrite significantly inhibited the vascular pressor responses elicited in hindquarters and renal, and mesenteric vasculature by the administration of different catecholamines (epinephrine, norepinephrine, and phenylephrine). These investigators thought that such an opposing effect was selective for catecholamines because peroxynitrite failed to protect against the vasoconstrictor effect of arginine vasopressin.66
The difficulty in determining the physiological relevance of the previous studies is that they were conducted in in vitro preparations or using pharmacological doses of peroxynitrite. This does not allow for a great deal of speculation on the physiological effects of compounds whose formation depends on oxidative stress. Most importantly, one of the major characteristics of the administration of peroxynitrite in hindquarter, renal, and mesenteric vasculature is the development of rapid tachyphylaxis, which alters subsequent vascular responses to other dilators. In fact, a study conducted by Benkusky et al67 showed that after the development of tachyphylaxis to peroxynitrite, the hemodynamic effect produced by the systemic administration of acetylcholine and prostacyclin was significantly attenuated. Interestingly, Villa et al68 also observed that the peroxynitrite-dependent tachyphylaxis in coronary circulation was critically dependent on its concentration. The tachyphylaxis occurred at 3 µmol/L, which was subthreshold as a dilator, and at 1000 µmol/L, which was supermaximal. No tachyphylaxis developed during the administration of peroxynitrite at 30 and 100 µmol/L. This investigator interpreted these data as representing an important manifestation of vascular dysfunction produced by peroxynitrite because of tachyphylaxis to its own vasodilator actions and the long-lasting impairment of the response to other vasodilators.68 Furthermore, the deleterious effect of peroxynitrite has also been suggested by Zou et al,69 who provided evidence showing that peroxynitrite not only eliminated the vasodilatory, growth-inhibiting, antithrombotic, and antiadhesive effects of prostaglandin I2 but also allowed and promoted action of the potent vasoconstrictor, prothrombotic agent, growth promoter, and leukocyte adherent prostaglandin H2.69
The case under discussion is that the prolonged administration of subpressor doses of Ang II produces a progressive vasoconstriction, which we think can be largely due to the concomitant reduction of NO and accumulation of isoprostane. The vasodilator effects of peroxynitrite should not be manifested if the concentration of this compound does not exceed 3 mmol/L, because these levels are below the physiological threshold and because they develop tachyphylaxis. At >3 µmol/L, the vasodilator effects of peroxynitrite may significantly decrease the level of hypertension produced by small doses of Ang II.
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The Relationship Among Sodium Intake, Plasma Renin Activity, Extracellular Fluid Volume, and the Development of Oxidative Stress |
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TopAbstractIntroductionCan Normal Concentrations of...Activation of Fast and...Role of Ang II,...Oxidative StressEndothelinIsoprostanesVascular Effects of...The Relationship Among Sodium...References |
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The proposition that small increments in plasma concentrations of Ang II are ultimately responsible for hypertension through the development of oxidative stress appears to be difficult to reconcile with the fact that during dietary sodium restriction the levels of plasma Ang II are
10-fold higher than during a normal sodium
diet.3 These conditions are illustrated in Figure 4, which also shows that a progressive
increase in sodium intake produces a proportional volume expansion that
exhibits a tight inverse correlation with the circulating levels of
plasma renin activity. As shown Figure 4, when the levels of
extracellular fluid volume have achieved a maximal expansion with high
sodium intake, plasma renin activity has virtually disappeared from
circulation. Guyton et al70 have suggested that this
inverse relationship between fluid volume and plasma renin is extremely
critical to maintaining blood pressure within the normal limits. If
this relationship is altered, for example, if the levels of plasma Ang
II are driven above those that correspond to a given level of either
sodium intake or extracellular fluid volume, then the organism becomes
susceptible to develop hypertension through slow responses to Ang II.
This is shown in the figure where the levels of Ang II have been
"inappropriately" increased in animal models to levels A, B, C, and
D, which induce proportional increments in mean arterial
pressure (Figure 4, bottom). This assumption has led us to
suggest that the circulating levels of angiotensin are
inappropriate or in excess considering the level of extracellular fluid
volume. This hypothesis is largely supported by the studies of DeClue
et al,71 who showed that when sodium intake is increased
without allowing the circulating levels of angiotensin to
be decreased, because of a continuous intravenous infusion,
the level of blood pressure is strictly determined by the level of
sodium intake. The observations of DeClue et al have many
physiological and clinical implications. From the
physiological standpoint, they demonstrate that
hypertension, through slow pressor responses, can be induced by small
elevations of circulating angiotensin that are
inappropriate for the existing levels of extracellular fluid volume,
and, reciprocally, they show that hypertension can also be produced if
the intake of sodium is inappropriate with respect to the existing
levels of circulating Ang II. The corollary of this conclusion is that
the disruption of the reciprocal interaction between extracellular
fluid volume and plasma renin activity (which serves to maintain blood
pressure) appears to activate a permissive mechanism that
renders oxidative stress susceptible to be stimulated by Ang II.
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An alternative interpretation, suggested by Wilcox and colleagues,72 is that long-term effects of Ang II are characterized by stimulation of aldosterone and sympathetic activity and produce a simultaneous uncoupling of NO release and shear stress.73 These investigators also have found that the administration of a superoxide dismutase mimetic to spontaneously hypertensive rats normalizes mean arterial pressure.74 As is apparent, more studies are needed to unravel the specific pathways of oxidative stress that could affect blood pressure regulation.
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Acknowledgments |
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This work was supported by National Institutes of Health grant HL-16496 and program grant HL-51971, Mayo Foundation, the American Heart Association grant 9740007N, and a grant from Fundacion Barcelo Argentina.
Received May 8, 1999; first decision June 17, 1999; accepted July 15, 1999.
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N. Kawada, E. Imai, A. Karber, W. J. Welch, and C. S. Wilcox A Mouse Model of Angiotensin II Slow Pressor Response: Role of Oxidative Stress J. Am. Soc. Nephrol., December 1, 2002; 13(12): 2860 - 2868. [Abstract] [Full Text] [PDF]
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T. Ogihara, T. Asano, K. Ando, Y. Chiba, H. Sakoda, M. Anai, N. Shojima, H. Ono, Y. Onishi, M. Fujishiro, et al. Angiotensin II-Induced Insulin Resistance Is Associated With Enhanced Insulin Signaling Hypertension, December 1, 2002; 40(6): 872 - 879. [Abstract] [Full Text] [PDF]
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 R. J Woodman, T. A Mori, V. Burke, I. B Puddey, G. F Watts, and L. J Beilin Effects of purified eicosapentaenoic and docosahexaenoic acids on glycemic control, blood pressure, and serum lipids in type 2 diabetic patients with treated hypertension Am. J. Clinical Nutrition, November 1, 2002; 76(5): 1007 - 1015. [Abstract] [Full Text] [PDF]
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V. Alvarez, Y. Quiroz, M. Nava, H. Pons, and B. Rodriguez-Iturbe Overload proteinuria is followed by salt-sensitive hypertension caused by renal infiltration of immune cells Am J Physiol Renal Physiol, November 1, 2002; 283(5): F1132 - F1141. [Abstract] [Full Text] [PDF]
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P. H. Lane Diabetic kidney disease: impact of puberty Am J Physiol Renal Physiol, October 1, 2002; 283(4): F589 - F600. [Abstract] [Full Text] [PDF]
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S. P. Didion, M. J. Ryan, G. L. Baumbach, C. D. Sigmund, and F. M. Faraci Superoxide contributes to vascular dysfunction in mice that express human renin and angiotensinogen Am J Physiol Heart Circ Physiol, October 1, 2002; 283(4): H1569 - H1576. [Abstract] [Full Text] [PDF]
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 Y. Higashi, S. Sasaki, K. Nakagawa, H. Matsuura, T. Oshima, and K. Chayama Endothelial Function and Oxidative Stress in Renovascular Hypertension N. Engl. J. Med., June 20, 2002; 346(25): 1954 - 1962. [Abstract] [Full Text] [PDF]
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 G. R. Ellis, A. K. Nightingale, D. J. Blackman, R. A. Anderson, C. Mumford, G. Timmins, D. Lang, S. K. Jackson, M. D. Penney, M. J. Lewis, et al. Addition of candesartan to angiotensin converting enzyme inhibitor therapy in patients with chronic heart failure does not reduce levels of oxidative stress Eur J Heart Fail, March 1, 2002; 4(2): 193 - 199. [Abstract] [Full Text] [PDF]
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M.-G. Feng, S. A. W. Dukacz, and R. L. Kline Selective effect of tempol on renal medullary hemodynamics in spontaneously hypertensive rats Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2001; 281(5): R1420 - R1425. [Abstract] [Full Text] [PDF]
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J. P. Bell, S. I. Mosfer, D. Lang, F. Donaldson, and M. J. Lewis Vitamin C and quinapril abrogate LVH and endothelial dysfunction in aortic-banded guinea pigs Am J Physiol Heart Circ Physiol, October 1, 2001; 281(4): H1704 - H1710. [Abstract] [Full Text] [PDF]
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M. C. Ortiz, M. C. Manriquez, J. C. Romero, and L. A. Juncos Antioxidants Block Angiotensin II-Induced Increases in Blood Pressure and Endothelin Hypertension, September 1, 2001; 38(3): 655 - 659. [Abstract] [Full Text] [PDF]
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 J. Chanda and C. C. Canver Reversal of preexisting vasospasm in coronary artery conduits Ann. Thorac. Surg., August 1, 2001; 72(2): 476 - 480. [Abstract] [Full Text] [PDF]
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J. F. Reckelhoff Gender Differences in the Regulation of Blood Pressure Hypertension, May 1, 2001; 37(5): 1199 - 1208. [Abstract] [Full Text] [PDF]
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E. M. A. Mervaala, Z. J. Cheng, I. Tikkanen, R. Lapatto, K. Nurminen, H. Vapaatalo, D. N. Muller, A. Fiebeler, U. Ganten, D. Ganten, et al. Endothelial Dysfunction and Xanthine Oxidoreductase Activity in Rats With Human Renin and Angiotensinogen Genes Hypertension, February 1, 2001; 37(2): 414 - 418. [Abstract] [Full Text] [PDF]
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Z. J. Cheng, T. Vaskonen, I. Tikkanen, K. Nurminen, H. Ruskoaho, H. Vapaatalo, D. Muller, J.-K. Park, F. C. Luft, and E. M. A. Mervaala Endothelial Dysfunction and Salt-Sensitive Hypertension in Spontaneously Diabetic Goto-Kakizaki Rats Hypertension, February 1, 2001; 37(2): 433 - 439. [Abstract] [Full Text] [PDF]
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L. O. Lerman, K. A. Nath, M. Rodriguez-Porcel, J. D. Krier, R. S. Schwartz, C. Napoli, and J. C. Romero Increased Oxidative Stress in Experimental Renovascular Hypertension Hypertension, February 1, 2001; 37(2): 541 - 546. [Abstract] [Full Text] [PDF]
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A. Nishiyama, T. Fukui, Y. Fujisawa, M. Rahman, R.-X. Tian, S. Kimura, and Y. Abe Systemic and Regional Hemodynamic Responses to Tempol in Angiotensin II-Infused Hypertensive Rats Hypertension, January 1, 2001; 37(1): 77 - 83. [Abstract] [Full Text] [PDF]
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J. D. Imig Eicosanoid regulation of the renal vasculature Am J Physiol Renal Physiol, December 1, 2000; 279(6): F965 - F981. [Abstract] [Full Text] [PDF]
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J. M. Roberts Angiotensin-1 Receptor Autoantibodies : A Role in the Pathogenesis of Preeclampsia? Circulation, May 23, 2000; 101(20): 2335 - 2337. [Full Text] [PDF]
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A. Nishiyama, S. Kimura, T. Fukui, M. Rahman, H. Yoneyama, H. Kosaka, and Y. Abe Blood flow-dependent changes in renal interstitial guanosine 3',5'-cyclic monophosphate in rabbits Am J Physiol Renal Physiol, February 1, 2002; 282(2): F238 - F244. [Abstract] [Full Text] [PDF]
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