(Hypertension. 1997;30:345.)
© 1997 American Heart Association, Inc.
Articles |
Regulation of Type 1 Angiotensin II Receptor in Adrenal Gland
Role of 
1-Adrenoreceptor
From the Department of Internal Medicine, Hypertension and Vascular Research Laboratories, University of Texas Medical Branch (Galveston).
Correspondence to Donna H. Wang, MD, Department of Internal Medicine, Hypertension and Vascular Research Laboratories, 8.104 Medical Research Bldg, University of Texas Medical Branch, Galveston, TX 77555-1065. E-mail dwang{at}utmb.edu
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Abstract |
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Abstract We have previously shown that sodium restriction upregulates the genes encoding angiotensin II receptor (AT1) subtypes, AT1A and AT1B, in the adrenal gland and that this upregulation is mediated by activation of the AT1 receptor. There are multiple interactions between the renin-angiotensin and the adrenergic nervous systems; thus, we conducted the present experiment to investigate whether low sodium-induced upregulation of adrenal AT1A and AT1B is modulated by the
1-adrenoreceptor. Seven-week-old male
Wistar rats were divided into four groups and given normal sodium diet
(0.5%, NS), NS+prazosin (3.5 µg · kg-1 ·
min- 1 by osmotic pump), low sodium diet (0.07%, LS), or
LS+prazosin. Body weight and mean arterial pressure were
not modified over the 2 weeks of treatment (P>.05). Pressor
responses to bolus injection of the 1-agonist
phenylephrine were inhibited in both prazosin groups,
compared with NS and LS rats (P<.05). Adrenal
AT1A mRNA, determined by Northern blot analysis,
was increased in LS (P<.05) but not in NS+prazosin
(P>.05), compared with NS. Prazosin enhanced the LS-induced
increase of AT1A mRNA (P<.05). Adrenal
AT1B mRNA was increased in both LS and NS+prasozin rats,
compared with NS rats (P<.05). Prazosin also enhanced the
LS-induced increase in AT1B mRNA (P<.05).
Therefore, blockade of 1-adrenoreceptor
results in an enhancement of LS-induced upregulation of adrenal mRNA
for AT1A and AT1B. These data suggest that the
sympathetic nervous system exerts an inhibitory action, via
activation of the 1-adrenoreceptor, on
AT1A and AT1B gene expression in the adrenal
gland during sodium depletion.
Key Words: receptors, angiotensin • receptors, adrenergic, alpha • adrenal glands • sodium, dietary
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Angiotensin II has direct and indirect actions on the adrenal gland to mediate its multiple physiological and pathophysiological functions. It has been shown that Ang II stimulates aldosterone secretion in humans and rodents,1 2 3 4 enhances cortisol secretion in cultured bovine adrenal fasciculata/reticularis cells,5 promotes bovine adrenocortical cell proliferation,6 and increases release of catecholamines from the adrenal medulla in rats.7 Although AT2 are abundantly expressed in both the adrenal cortex and medulla in rats,8 9 virtually all the known Ang II–induced effects on the adrenal gland are mediated by AT1 receptor. For example, Ang II–induced aldosterone secretion can be blocked by several AT1 selective receptor antagonists, including losartan,10 11 L158807,12 and SC51316.13 Also, AT1 receptor blockers inhibit Ang II–induced proliferation of bovine adrenocortical cells.14 Finally, losartan (but not the AT2 receptor antagonist PD123319) blocks Ang II–induced inhibition of cortisol secretion in response to corticotropin in bovine adrenal cells.15
Despite the important role of the AT1 receptor in adrenal function, the regulatory mechanisms for this receptor in this gland are poorly understood. They may involve alterations in transcription or degradation of receptor mRNA, internalization of receptor protein, and/or changes in its intracellular domain. Also, humoral factors may influence one or several of these processes in the whole animal in vivo. We recently demonstrated that sodium restriction significantly increases the gene expression for both AT1 receptor subtypes, AT1A and AT1B, in the adrenal gland and that these effects of sodium deprivation are prevented by losartan, ie, they are mediated by activation of the AT1 receptor by Ang II.16
Sodium restriction stimulates the renin-angiotensin system
and also the sympathetic nervous system.17 It is well
known that these two systems exhibit multiple interactions. Thus, Ang
II (1) augments sympathetic outflow to the periphery via effects on the
central nervous system, (2) facilitates release of
norepinephrine from sympathetic nerve terminals, and (3)
stimulates adrenomedullary and ganglionic transmission (for review, see
Reference 1818 ). On the other hand, stimulation of the sympathetic
nervous system leads to renin secretion and Ang II
generation.19 It is therefore conceivable that the
sympathetic nervous system participates in Ang II receptor–subtype
regulation in the adrenal gland, an organ with one of the highest
levels of gene expression for Ang II receptors. Understanding of
adrenal Ang II receptor regulation by the sympathetic nervous system
may provide insight into the overall mechanisms by which these two
pressor systems interact. Furthermore, the effects of the sympathetic
nervous system on adrenal Ang II receptors may be critical for the
involvement of this gland in the regulation of blood pressure,
electrolyte balance, and extracellular fluid volume. Therefore, we
designed a study to explore the role of the sympathetic nervous system,
specifically that of activation of the
1-adrenoreceptor, on the
upregulation of AT1 receptor–subtype gene expression
induced by sodium depletion in the adrenal gland.
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Methods |
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Animal Groups
Seven-week-old male Wistar rats weighing between 155 and 195 g (Charles River Laboratories, Inc, Wilmington, Mass) were divided into four groups (n=10 in each group) and treated for 2 weeks with a normal sodium diet (0.5%, NS, Harlan Teklad Diets), NS plus prazosin (NS+Pr), low sodium diet (0.07%, LS), or LS plus prazosin (LS+Pr). All the rats were anesthetized with a single intraperitoneal injection of ketamine hydrochloride (80 mg/kg) and xylazine (12 mg/kg). Alzet mini-osmotic pumps (model 2ML2, Alza) with a mean±SD capacity of 2.2±0.06 mL and infusion rate of 5.0±0.2 µL/h were filled with either 50% dimethyl sulfoxide (NS and LS rats) or prazosin (3.5 µg · kg-1 · min-1) in 50% dimethyl sulfoxide (NS + Pr and LS + Pr) as described previously.20 21 The pumps were implanted subcutaneously between the scapulae. Sterile technique was used, and the rats were given penicillin G (10 000 units) intramuscularly after the surgery. At the end of the 14-day treatment period, all rats were anesthetized with the dose of ketamine and xylazine described above, and the left carotid artery was catheterized for the measurement of MAP with a Statham 231D pressure transducer (Gould Inc) coupled to a Gould 2400s recorder (Gould Inc). MAP responses to bolus injection of
1-agonist phenylephrine
(3 and 6 µg/kg) were assessed in all four groups of rats to
evaluate the effectiveness of the treatment with
prazosin.22 All the animal procedures were in accordance
with the National Institutes of Health Guideline for the Care and
Use of Laboratory Animals.
Systolic Blood Pressure
Indirect tail-cuff systolic blood pressures were
routinely obtained in all rats by use of a Narco Bio-Systems
Electro-Sphygmomanometer. The pressures were measured in conscious rats
every 3 days for 14 days, beginning 1 day before surgery. The blood
pressure value for each rat was calculated as the average of three
separate measurements at each session.
Tissue Preparation
At the end of the treatment period and under
anesthesia, a midline incision in the abdomen was
performed. Adrenal glands were removed, frozen in liquid nitrogen, and
stored at -80°C. Adrenal glands from rats in each group were used
for RNA extraction for Northern blot analysis.
cDNA Probes for Northern Blot Analysis
cDNA probes were prepared as described
previously.16 23 24 Briefly, to make
AT1A-specific cDNA probes, the polymerase chain reaction
(PCR) method was used to amplify AT1A cDNA (for detailed
information, see our previous study16 ). A 235-bp PCR
product was inserted into the EcoRV site of pBluescript
KS(+) vector, and the fragment that was cleaved with EcoRI
and HindIII was used as a template for making
AT1A cDNA probes. A clone pBluescript KS(+) containing 2.3
kb of the rat AT1B receptor (kindly provided by Dr Tedashi
Inagami, Vanderbilt University School of Medicine, Nashville, Tenn) was
digested with HindIII and EcoRI to obtain a
noncoding region fragment (395 bp, +1246 through +1641).25
Both AT1A and AT1B cDNA probes were labeled
with 32P-dCTP using a Multiprime DNA labeling system
(Amersham Co) to a specific activity of 3x108 cpm/µg.
The labeled probes were separated from unincorporated
nucleotides using a Mini-Spin G-50 DNA purification spin
column (Worthington Biochemical Co). The specificities of the
AT1A and AT1B probes were confirmed by the lack
of a cross-hybridization to AT1B and AT1A cDNAs
in our previous study.16
RNA Extraction and Northern Blots
Total adrenal RNA was extracted using the guanidinium
thiocyanate-phenol-chloroform extraction protocol.26
Electrophoresis of 20 µg denatured RNA from each preparation was
carried out in a 1% agarose gel containing 2.2 mol/L
formaldehyde.16 RNA was transferred to a positively
charged nylon membrane. After prehybridization, the membrane was
hybridized with the 32P-labeled probes in the hybridization
buffer for 18 to 20 hours at 42°C and washed successively in 2x,
1x, and 0.5x SSC at 65°C. Blots were exposed to XAR-5 x-ray film
(Eastman Kodak Co). To control for the differences in RNA loading, cDNA
probes were stripped off from the Northern blots, and blots were
rehybridized with a 32P-labeled 18S rRNA probe.
Autoradiographic signals were scanned with a laser
densitometer (Ultrascan XL Laser densitometer). Relative gene
expression was expressed as the ratio of AT1A or
AT1B mRNA to 18S rRNA.
In Situ Hybridization
In situ hybridizations were carried out as previously
described.23 In brief, a 790 base pair from the coding
region of AT1A cDNA was used as a template to make
35S-UTP–labeled cRNA probes.23
35S-labeled cRNA probes were synthesized using Maxiscript
SP6/T7 kit (Ambion Inc). The adrenal gland was fixed in buffered 4%
paraformaldehyde, pH 7.4, at 4°C overnight and
paraffin embedded. Five micrometer tissue sections were
cut, mounted on superfrost-plus slides (Fisher Scientific), and baked
for 1 hour at 55°C. After deparaffinization, each section was
hybridized with 1x106 cpm/mL of 35S-labeled
AT1A cRNA probes at 55°C overnight. Sections were then
washed with decreasing concentrations of SSC, dehydrated in serial
graded ethanol, air-dried, coated with NTB2 emulsion
(Kodak), and exposed at 4°C for 4 weeks. To determine background
signal, slides were processed after hybridization with
35S-labeled sense cRNA probes.
Statistical Analysis
Results were expressed as mean±SEM. The data were
analyzed by two-way ANOVA followed by the Tukey-Kramer multiple
comparison test. Differences were considered statistically significant
at P<.05.
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Results |
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There was no significant difference in body weight among the four groups at the end of the experiment (NS, 283±4 g; NS+Pr, 288±8 g; LS, 286±5 g; LS+Pr, 290±3 g). MAP was not altered by prazosin treatment (97±5 mm Hg), low sodium intake (95±3 mm Hg), or the combination of the two (98±5 mm Hg), when compared with control animals (93±4 mm Hg). These data are in agreement with the results obtained from tail-cuff systolic blood pressure in conscious rats. At the end of the experiment, tail-cuff systolic blood pressure was 119±6 mm Hg in NS, 123±5 mm Hg in NS+Pr, 121±4 mm Hg in LS, and 117±4 mm Hg in LS+Pr.
MAP responses to bolus injection of the 1-agonist
phenylephrine were measured in all four groups of rats to
evaluate the efficacy of 1-adrenergic receptor blockade
by prazosin. In rats fed normal and low sodium diets, dose-dependent
increases in MAP induced by phenylephrine were observed,
but these increases did not reach statistical significance (see
Table). In contrast, the pressor
responses to phenylephrine in rats treated with prazosin
were completely abolished. In fact, decreases in MAP in response to
bolus injection of phenylephrine were observed in rats
treated with prazosin, which may be caused by activating
non–1-adrenergic receptors by
phenylephrine.
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AT1A mRNA content in rat adrenal glands was determined by
Northern blot analysis in all four experimental groups. Blots
were then stripped and rehybridized to 18S rRNA probes. Densitometric
analysis (Fig 1) indicated that
the ratio of AT1A mRNA to 18S rRNA was elevated by sodium
restriction (1.06±0.17, P<.05) compared with control
animals (0.69±0.06). Prazosin did not produce a statistically
significant change of AT1A mRNA levels in rats fed a normal
sodium diet (0.80±0.07). In contrast, this 1-adrenergic
receptor blocker significantly enhanced the low sodium–induced
increase in AT1A mRNA content (1.81±0.25,
P<.05).
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Similarly, AT1B mRNA content in rat adrenal glands was determined by Northern blot analysis in all four experimental groups. Blots were then stripped and rehybridized to 18S rRNA probes. Densitometric analysis (Fig 2) indicated that the ratio of AT1B mRNA to 18S rRNA was elevated by sodium restriction (1.01±0.11, P<.05) compared with control animals (0.60±0.08). In contrast to the observations with the AT1A receptor, prazosin increased AT1B mRNA in rats fed a normal sodium diet (0.90±0.10, P<.05) and enhanced the increased AT1B mRNA content of low sodium–fed rats (1.93±0.36, P<.05).
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Fig 3 shows the localization of changes of AT1A and AT1B mRNA in response to sodium restriction and prazosin treatment with in situ hybridization. Because cRNA probes used for in situ hybridization were generated from the coding region of AT1A cDNA where AT1A and AT1B cDNAs exhibit high nucleotide sequence identity,23 these probes hybridized to both AT1A and AT1B mRNA. The changes in AT1A and AT1B mRNA after sodium restriction and prazosin treatment were evident primarily for the zona glomerulosa.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The present study was designed to examine the role of the
1-adrenoreceptor in the regulation of
adrenal gene expression for AT1A and AT1B
receptors induced by low dietary sodium intake. With the use of
Northern blot analysis, we found that blockade of the
1-adrenoreceptor with prazosin enhances
low sodium–induced upregulation of both AT1A and
AT1B mRNA levels in the adrenal gland. We previously
described an inverse relationship between sodium intake and adrenal
gene expression for Ang II receptors, ie, low dietary sodium
significantly increased adrenal mRNA for both AT1A and
AT1B.16 In those experiments, upregulation of
AT1A and AT1B mRNA by low sodium was dependent
on activation of the AT1 receptor by Ang II, as confirmed
by blockade of the effect of low sodium by
losartan.16 In contrast, we now show that the
1-adrenoreceptor exerts an
inhibitory action on the upregulation of AT1A
and AT1B by dietary sodium deprivation. To the
best of our knowledge, ours is the first study to indicate that the
renin-angiotensin system and the sympathetic nervous system
interact in an opposing manner to regulate of expression of the
AT1A and AT1B receptors in the adrenal gland in
vivo. The adrenal gland is one of the few peripheral organs that express the genes encoding both AT1A and AT1B receptors throughout fetal and adult life.27 28 In the adult animal, adrenal AT1A/AT1B mRNA ratio is 1:1.29 While AT1A mRNA is widely distributed in different parts of the adrenal gland (with the highest intensity in the zona glomerulosa of the cortex), AT1B mRNA is present in the zona glomerulosa only.30 This differential distribution of the expression of AT1A and AT1B genes suggests that the two receptor subtypes may mediate different biological responses of Ang II in the adrenal gland. Despite this possibility, dietary sodium modified expression of the genes encoding AT1A and AT1B in the same direction, ie, sodium deprivation leading to upregulation of both receptor subtypes, confirming previous findings of our laboratory and laboratories of others.16 31 Because the increases of expression of AT1A and AT1B mRNA are primarily for the zona glomerulosa (Fig 3), these increases may be directly involved in increased aldosterone secretion during low sodium intake. Lehoux et al31 have shown that the increased aldosterone secretion induced by low sodium intake involves concomitant increases in AT1 receptor mRNA and receptor protein content in the adrenal gland. However, changes in zona glomerulosa Ang II receptors in monkey adrenal glands are opposite to those in the rat. Platia et al32 have shown that sodium restriction decreases Ang II receptor density in the zona glomerulosa of the monkey adrenal gland, indicating that there may be different regulatory mechanisms governing expression of the Ang II receptor in different species.
To explore the mechanism or mechanisms by which dietary sodium
regulates the expression of the genes encoding the AT1
receptor subtypes in the adrenal gland of the rat, we have previously
shown that low sodium– induced upregulation of AT1A and
AT1B gene expression in the adrenal gland of rats is
mediated by activation of the AT1 receptor because this
upregulation can be blocked by losartan.16
Therefore, it can be postulated that the elevated levels of circulating
and/or local tissue Ang II induced by dietary sodium
deprivation exert a positive feedback influence on gene
expression of the AT1 receptor subtypes in rats. Our
present results, enhanced upregulation of AT1A and
AT1B mRNA by prazosin during a low sodium diet, indicate
that (1) upregulation of AT1A and AT1B mRNA by
low sodium diet is not caused by activation of the
1-adrenergic receptor of the sympathetic nervous system
that accompanies sodium deprivation and (2) activation of
the 1-adrenergic receptor during sodium
deprivation exerts a negative feedback influence on gene
expression of the AT1 receptor subtypes. As a cautionary
note, the contribution of an activated
renin-angiotensin system to the enhancement of the
upregulation of AT1A and AT1B gene expression
by prazosin during low sodium intake cannot be ruled out. Because
blockade of the 1-adrenergic receptor did not lower
blood pressure, especially under low sodium conditions, compensatory
activation of the renin-angiotensin system may have an
effect on the enhanced adrenal AT1A and AT1B
mRNA levels.
From our data and those from others, we propose the sequence of events
shown in Fig 4. Sodium
deprivation activates the
renin-angiotensin system, leading to increased Ang II
levels. Ang II stimulation of adrenal AT1 receptors
enhances gene expression for the AT1 receptor subtypes and
stimulates the release of catecholamines.
Catecholamine binding to 1-adrenergic
receptors exerts counter-regulatory inhibition on the gene expression
for the AT1 receptor subtypes. The net effect of these
opposing influences of the AT1 receptors and
1-adrenoceptors on expression of adrenal AT1
receptor subtypes is low-sodium–induced upregulation. Therefore, it
follows that the stimulatory effect of AT1 receptor
activation is more powerful than the inhibitory effect of
1-adrenergic receptor activation. The exact cascade of
cellular events that leads to altered expression of AT1
receptor subtypes on activation of both AT1 and
1-adrenergic receptors in the adrenal gland remains to
be explored.
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An inhibitory effect of the sympathetic nervous system on
Ang II receptor expression in the adrenal gland is consistent
with observations reported in other tissues. For example, renal
denervation or sympathetic blockade with guanethidine increases
glomerular Ang II receptor density in normotensive and
hypertensive rats.33 Also, in brain neuronal cultures of
Wistar-Kyoto rats, norepinephrine decreases AT1
receptor density and its gene expression via activation of the
1A-adrenergic receptor.34 This effect of
norepinephrine was absent in brain neurons obtained from
spontaneously hypertensive rats,34 suggesting that
alterations in 1-adrenergic–mediated negative
feedback regulation of AT1 receptor expression may be
implicated in the pathogenesis of hypertension. Whether such an
alteration leads to overactivity of the effects of circulating or local
Ang II on the adrenal gland of hypertensive animal models remains to be
explored.
In conclusion, the present studies show that blockade of the
1-adrenergic receptor enhances low sodium– induced
elevation of both AT1A and AT1B receptor
subtypes in the adrenal gland, suggesting that the sympathetic
activation that accompanies low sodium intake may negatively regulate
adrenal AT1A and AT1B receptor subtypes. It
follows that elevation of AT1A and AT1B gene
expression by sodium deprivation in the adrenal gland is
independent of, and occurs despite, sympathetic activation. We
speculate that description of negative regulatory mechanisms will
broaden our understanding of the transcriptional regulation and
functional activity of AT1 receptor subtypes and will
enhance our ability to devise new methods to manipulate blood pressure,
ion homeostasis, and tissue growth.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This study was supported in part by National Institutes of Health grant HL-52279 and grants from Merck Research Laboratories and John Sealy Endowment Fund for Biomedical Research to Dr Donna H. Wang. We want to express our thanks to Drs Fernando Elijovich and Cheryl Laffer for their critical review and Wilma Frye for her expert secretarial skills.
Received September 17, 1996; first decision October 17, 1996; accepted January 31, 1997.
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References |
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1. Laragh JH, Angers M, Kelly WG. The effect of epinephrine, norepinephrine, angiotensin II and others on the secretory rate of aldosterone in man. JAMA. 1960;174:234-240.
2. Ganong WF, Mulrow PJ, Boryczka A. Evidence for a direct effect of angiotensin II on adrenal cortex of the dog. Proc Soc Exp Biol Med. 1962;109:381-384.
3. Kaplan NM, Bartter FC. The effect of ACTH, renin, angiotensin II and various precursors on biosynthesis of aldosterone by adrenal slices. J Clin Invest. 1962;41:715-724.[Medline] [Order article via Infotrieve]
4. Goodfriend TL, Peach MJ. Angiotensin III: (DES-aspartic acid)-angiotensin II: evidence and speculation for its role as an important agonist in the renin-angiotensin system. Circ Res. 1975;36(suppl 1):38-48.
5. Bird IM, Meikle L, Williams BC, Walker SW. Angiotensin II-stimulated cortisol secretion is mediated by a hormone-sensitive phospholipase C in bovine adrenal fasciculata/reticularis cells. Mol Cell Endocrinol. 1989;64:45-53.[Medline] [Order article via Infotrieve]
6. Gill GN, Ill CR, Simonian MH.
Angiotensin stimulation of bovine adrenocortical cell
growth. Proc Natl Acad Sci U S A. 1977;74:5569-5573.
7. Feldberg W, Lewis GP. The action of peptide on
the adrenal medulla: release of adrenaline by bradykinin and
angiotensin. J Physiol (Lond). 1964;171:98-108.
8. Shanmugam S, Lenkei Z, Gasc JM, Corvol P, Llorens-Cortes C. Ontogeny of angiotensin II type 2 (AT2) receptor mRNA in the rat. Kidney Int. 1995;47:1095-1100.[Medline] [Order article via Infotrieve]
9. Shanmugam S, Llorens-Cortes C, Clauser E, Corvol P, Gasc JM. Expression of angiotensin II AT2 receptor mRNA during development of the rat kidney and adrenal gland. Am J Physiol. 1995;268:F922-F930.[Medline] [Order article via Infotrieve]
10. Wong PC, Price WA, Chiu AT, Carini DJ, Duncia JV,
Johnson AL, Wexler RR, Timmermans PBMWM. Nonpeptide
angiotensin II receptor antagonists: studies
with EXP9270 and DuP 753. Hypertension. 1990;15:823-834.
11. Balla T, Baukal AJ, Eng S, Catt KJ. Angiotensin II receptor subtypes and biological responses in the adrenal cortex and medulla. Mol Pharmacol. 1991;40:401-406.[Abstract]
12. Chang RSL, Siegl PKS, Clineschmidt BV, Mantlo NB,
Chakravarty PK, Greenlee WJ, Patchett AA, Lotti VJ. In vitro
pharmacology of L-158,809, a new highly potent and selective
angiotensin II receptor antagonist.
J Pharmacol Exp Ther. 1992;262:133-138.
13. Olins GM, Corpus VM, McMahon EG, Palomo MA, Schuh JR,
Blehm DJ, Huang HC, Reitz DB, Manning RE, Blaine EH. In vitro
pharmacology of a nonpeptidic angiotensin II receptor
antagonist, SC-51316. J Pharmacol Exp
Ther. 1992;261:1037-1043.
14. Natarajan R, Gonzales N, Hornsby PJ, Nadler J.
Mechanism of angiotensin II-induced proliferation in bovine
adrenocortical cells. Endocrinology. 1992;131:1174-1180.
15. Bird IM, Magness RR, Mason JI, Rainey WE.
Angiotensin II acts via the type 1 receptor to inhibit 17
alpha-hydroxylase cytochrome P450 expression in bovine adrenocortical
cells. Endocrinology. 1992;130:3113-3121.
16. Du Y, Guo DF, Inagami T, Speth RC, Wang DH. Regulation of Ang II-receptor subtype and its gene expression in adrenal gland. Am J Physiol. 1996;271:H440-H446.[Medline] [Order article via Infotrieve]
17. Stein CM, Nelson R, Brown M, He H, Wood M, Wood AJ. Dietary sodium intake modulates systemic but not forearm norepinephrine release. Clin Pharmacol Ther. 1995;58:425-433.[Medline] [Order article via Infotrieve]
18. Brooks DP, Ruffolo RR. Functions mediated by peripheral angiotensin II receptors. In: Ruffolo RR, ed. Angiotensin II Receptors. Orlando, Florida: CRC Press Inc; 1994:71-102.
19. Garrison JC, Peach MJ. Renin and angiotensin. In: Gilman AG, Goodman LS, Gilman A, eds. Goodman and Gilman’s The Pharmacological Basis of Therapeutics. Vol 8. New York, NY: Macmillan Publishing Co Inc; 1990:749-763.
20. Wang DH, Prewitt RL, Beebe SJ. Regulation of PDGF-A: a possible mechanism for angiotensin II-induced vascular growth. Am J Physiol. 1995;269:H356-H364.[Medline] [Order article via Infotrieve]
21. King BD, Sack D, Kichuk MR, Hintze TH. Absence
of hypertension despite chronic marked elevation in plasma
norepinephrine in conscious dogs.
Hypertension. 1987;9:582-590.
22. Van Kleef EM, Smits JFM, De Mey JGR, Cleutjens JPM,
Lombardi DM, Schwartz SM, Daemen MJAP.
1-Adrenoreceptor blockade reduces the
angiotensin II–induced vascular smooth muscle cell DNA
synthesis in the rat thoracic aorta and carotid artery.
Circ Res. 1992;70:1122-1127.
23. Du Y, Yao A, Guo DF, Inagami T, Wang DH. Differential regulation of angiotensin II receptor subtypes in rat kidney by low dietary sodium. Hypertension. 1995;25[pt 2]:872-877.
24. Iwai N, Yamano S, Chaki S, Konishi F, Bardhan S, Tibbetts C, Sasaki K, Hasegawa M, Matsuda Y, Inagami T. Rat angiotensin II receptor: cDNA sequence and regulation of the gene regulation. Biochem Biophys Res Commun. 1991;177:299-304.[Medline] [Order article via Infotrieve]
25. Iwai N, Inagami T. Identification of two subtypes in the rat type I angiotensin II receptor. FEBS Lett. 1992;298:257-260.[Medline] [Order article via Infotrieve]
26. Chomczynski P, Sacchi N. Single-step method of RNA isolation by acid guanidinium thiocyanate-phenol-chloroform extraction. Ann Biochem. 1987;162:156-159.
27. Shanmugam S, Sandberg K. Ontogeny of angiotensin II receptors. Cell Biol Int. 1996;20:169-176.[Medline] [Order article via Infotrieve]
28. Shanmugam S, Corvol P, Gasc JM. Ontogeny of the two angiotensin II type 1 receptor subtypes in the rat. Am J Physiol. 1994;267:E828-E836.[Medline] [Order article via Infotrieve]
29. Llorens-Cortes C, Greenberg B, Huang H, Corvol
P. Tissue expression and regulation of type 1
angiotensin II receptor subtypes by quantitative reverse
transcriptase–polymerase chain reaction analysis.
Hypertension. 1994;24:538-548.
30. Gasc JM, Shanmugam S, Sibony M, Corvol P.
Tissue-specific expression of type 1 angiotensin II
receptor subtypes: an in situ hybridization study.
Hypertension. 1994;24:531-537.
31. Lehoux JG, Bird IM, Rainey WE, Tremblay A, Ducharme
L. Both low sodium and high potassium intake increase the level
of adrenal angiotensin II receptor type 1, but not that of
adrenocorticotropin receptor. Endocrinology. 1994;134:776-782.
32. Platia MP, Catt KJ, Hodgen GD, Aguilera G.
Regulation of primate angiotensin II receptors during
altered sodium intake. Hypertension. 1986;8:1121-1126.
33. Sahlgren B, Eklof AC, Aperia A. Regulation of glomerular angiotensin II receptor densities in renovascular hypertension: response to reduced sympathetic and vasopressin influence. Acta Physiol Scand. 1992;146:467-471.[Medline] [Order article via Infotrieve]
34. Yang H, Lu D, Raizada MK. Lack of cross
talk between 1-adrenergic and angiotensin
type 1 receptors in neurons of spontaneously hypertensive rat
brain. Hypertension. 1996;27:1277-1283.
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