(Hypertension. 1997;29:58.)
© 1997 American Heart Association, Inc.
Research Articles (Issue 1, Part 1) |
Receptor Subtype for Vasopressin-Induced Release of Nitric Oxide From Rat Kidney
The Second Department of Internal Medicine (Y.H., H.H., M.K., A.T., E.S., D.N., K.K, A.G., M.O.) and Faculty of Pharmaceutical Sciences (K.K., T.N., M.H.), University of Tokyo (Japan).
Correspondence to Yasunobu Hirata, MD, The Second Department of Internal Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113, Japan. E-mail hirata-2im@h.u-tokyo.ac.jp
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
The vasopressin receptor subtype that causes nitric oxide (NO) release remains controversial. To elucidate this receptor-ligand interaction, we examined the effects of vasopressin receptor antagonists on vasopressin-induced release of NO from isolated perfused rat kidneys by using a sensitive chemiluminescence assay. Vasopressin increased renal perfusion pressure and NO signals in the perfusate in a dose-dependent manner. NG-Monomethyl-L-arginine abolished this increase in NO release; however, a similar increase in renal perfusion pressure induced by prostaglandin F2
was not associated with the increase in NO release. OPC-21268, a V1 receptor antagonist, significantly reduced the vasopressin-evoked renal vasoconstriction and NO release, whereas OPC-31260, a V2 receptor antagonist, had no effects. Moreover, desmopressin, a selective V2 receptor agonist, did not increase the NO signal. NO release by vasopressin was markedly attenuated in deoxycorticosterone acetate (DOCA)–salt hypertensive rat kidneys compared with control kidneys (10-10 mol/L vasopressin: +0.8±0.3 versus +6.9±1.4 fmol/min per gram kidney, DOCA versus control; P<.001). Histochemical analysis for renal NO synthase revealed a substantial attenuation of the staining of endothelial NO synthase in DOCA-salt rats. These results directly demonstrate that vasopressin stimulates NO release via the endothelial V1 receptor in the rat kidney.
Key Words: endothelium • hormone antagonists • desoxycorticosterone • nitric oxide
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Arginine vasopressin (AVP) exerts potent vasoconstrictive and antidiuretic effects. These actions are due to the stimulation of vasopressin V1 and V2 receptor subtypes, respectively. V1 receptors are mainly distributed on the vascular cells and are linked to intracellular Ca2+ mobilization. V2 receptors, however, are distributed mainly on the collecting ducts and are linked to an increase in cAMP.1 2 Intravenous AVP administration produces systemic vasoconstriction and elevates blood pressure. Conversely, AVP can exhibit a vasodilator rather than vasoconstrictor action in various arteries of humans and animals.3 4 5 6 7 8 9 10 11 12 It has been postulated that AVP-induced vasodilator effects include the release of NO,3 4 the production of prostanoid,13 and the inhibition of sympathetic nervous system activity.14 Despite these data, the precise mechanism for AVP action remains unclear. The central controversy surrounding this mechanism is which receptor subtype, V1,3 4 5 V2,6 7 8 9 10 11 or unclassified,12 is responsible for AVP-induced vasodilation. Furthermore, it is still unknown whether AVP increases NO release via stimulation of the V115 or V2 receptor subtype.8 10 11 We have recently developed a highly sensitive assay for NO measurement and have applied it to the isolated perfused kidney system.16 17 18 19 In the present study, to elucidate this receptor-ligand interaction, we examined the effects of AVP and its receptor antagonists on NO release from rat renal vessels by direct NO measurements. Furthermore, we compared the effects of AVP in DOCA-salt rats, in which vascular endothelium is known to be markedly damaged,20 and investigated renal NOS using immunohistochemical methods.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Animals
DOCA-salt and control rats were prepared as follows.21 The left kidneys of 6-week-old male Wistar rats were removed, and silicone pellets containing 200 mg/kg DOCA were implanted subcutaneously with rats under light ether anesthesia. Saline (0.9%) was given as drinking water for 8 weeks. Control rats were similarly uninephrectomized and given tap water. Blood pressure was determined by the tail-cuff method.
Isolated Perfused Rat Kidney
DOCA-salt and control rats were anesthetized with pentobarbital (30 mg/kg IP). Kidneys were isolated and perfused without ischemia as previously described.16 17 18 19 The right renal artery was punctured with an 18-gauge double lumen needle via the superior mesenteric artery. Perfusion was performed with a Krebs-Henseleit buffer, saturated with 95% O2/5% CO2, at a rate of 5 mL/min and 37°C. The perfusate contained 10-6 mol/L phenylephrine and 10-5 mol/L indomethacin. The renal vein was also cannulated with a silicone tube to drain the perfusate.
Measurements of NO Concentration in the Perfusate
The NO concentration in the perfusate was monitored continuously by the chemiluminescence method previously reported.16 17 18 19 Briefly, the venous effluent was drained at 2 mL/min with a double-head plunger pump and mixed with a chemiluminescence probe. The rest of the effluent overflowed through a three-way needle. The chemiluminescence probe, consisting of 18 µmol/L recrystallized luminol, 2 mmol/L H2O2, 2 mmol/L potassium carbonate, and 150 mmol/L desferrioxamine, was pumped at 0.5 mL/min. These solutions were passed through a reaction mixer before chemiluminescence detection. The renal perfusion pressure and chemiluminescence signal were monitored simultaneously with a polygraph recorder. The NO concentration in the perfusate was calibrated by use of an authentic NO solution of known concentration determined by the HbO2 method or a horseradish peroxidase solution that produced signals corresponding to the calibrated NO solution.
Study Protocol
After a 60-minute perfusion period for equilibration, we assayed for the effects of vehicle, AVP (Peptide Institute), and L-NMMA (Sigma Chemical Co) on RPP and NO chemiluminescence. Agents were administered by infusion pumps at a rate of 0.25 mL/min in this order: vehicle and 10-11, 10-10.5, 10-10, and 10-9.5 mol/L AVP at 10-minute intervals. Thereafter, 10-4 mol/L L-NMMA was added to 10-9.5 mol/L AVP. The effects of AVP on RPP and NO release were compared in 8 control and 14 DOCA-salt–treated rats. When the effects of AVP in control rats were compared with those in DOCA-salt rat kidneys, baseline RPP in DOCA-salt rats was adjusted to about 100 (n=8) or 150 (n=6) mm Hg by changing the phenylephrine concentrations according to the difference in blood pressure between control and DOCA-salt rats before renal isolation. The effects of the receptor antagonists on RPP and NO release were also examined.
To evaluate the role of V1 receptors in the action of AVP, we assayed the changes in RPP and NO chemiluminescence in six control rats by pretreatment and posttreatment with the V1 antagonist OPC-21268 (Otsuka Pharmaceutical Co).22 Similarly, we used OPC-31260 (Otsuka),23 a V2 antagonist, to delineate the role of V2 receptors in altered RPP and NO release (n=6). As a control for AVP, we examined the effects of PGF2, an endothelium-independent vasoactive substance, on RPP and NO release in control Wistar rats (n=5). To further define the responses to V2 receptor stimulation, we also studied the effects of DDAVP (Peptide Institute), a V2 agonist, on RPP and NO release.
Immunohistochemistry
NOS immunoreactivity was examined in renal tissues, as previously reported.24 In brief, the abdominal aorta of DOCA-salt and control rats was cannulated with rats under pentobarbital anesthesia, and the kidney was perfused and fixed with paraformaldehyde-lysine-periodate. The kidneys were sliced and the slices embedded in wax (polyethylene glycol 400 disterate, Polysciences Inc). Then, 3-µm wax sections were stained with primary antisera raised against endothelial NOS (EC-NOS), brain NOS (B-NOS), and macrophage-type inducible NOS (Transduction Laboratories) according to the avidin/biotin/horseradish peroxidase complex technique for light microscopic immunohistochemical observation. A section incubated with 1% bovine serum albumin served as the negative control. NADPH diaphorase activity was histochemically stained in the other kidney slices. Sections (50 µm thick) were incubated with 1 mmol/L reduced ß-NADPH, 0.2 mmol/L nitroblue tetrazolium, and 0.2% Triton X-100 for 45 minutes at 37°C and examined under a light microscope.
Statistical Analysis
Values are expressed as mean±SE. The effects of the test agents were analyzed by ANOVA for repeated measurements followed by Dunnett's test. Comparisons among groups were assessed by one-way ANOVA. A level of P<.05 was considered to be statistically significant.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Baseline parameters of the rats and isolated kidneys are summarized in the Table. Systolic pressure of both groups of DOCA-salt rats was much higher than that of control rats. Heart and kidney weights were also significantly greater in DOCA-salt rats than in control rats. However, no difference was observed between DOCA-salt rats at normal and elevated RPP regarding these three parameters. When the phenylephrine concentration of the perfusate was 1 µmol/L, baseline RPP was about 90 mm Hg in both control and DOCA-salt rats. About 5 µmol/L phenylephrine was required to maintain RPP at 150 mm Hg in DOCA-salt rats. The baseline rate of NO release was much lower in DOCA-salt rats than in control rats at either perfusion pressure, consistent with data from our previous reports.17 18
|
As shown in Fig 1, AVP elevated RPP in a dose-dependent manner in control and DOCA-salt rats. AVP did not significantly change RPP at any concentration between 10-12 and 10-8 mol/L in this preparation. The data for control rats indicate that renal vasoconstriction is associated with a parallel increase in NO concentration in the perfusate. Addition of L-NMMA further increased RPP. L-NMMA at 10-4 mol/L suppressed NO release in almost all the kidneys to zero. Consequently, the degree of the decrease in NO release by L-NMMA was similar among the three rat groups (control, -85±15%; DOCA-salt, -90±13%; and DOCA-salt at high RPP, -92±9%; P=NS among the groups).
|
To investigate which receptor subtype of AVP, V1 or V2, is responsible for NO release, we examined the effects of AVP receptor antagonists on AVP-evoked vasoconstriction and NO release. OPC-21268 or OPC-31260 given alone had no effect on RPP and NO release. Fig 2A shows that pretreatment with OPC-21268, a selective V1 antagonist, significantly suppressed both the AVP-induced vasoconstriction and NO release. Pretreatment with OPC-31260, the selective V2 antagonist, did not influence the RPP or NO signal changes caused by AVP (Fig 2B). When OPC-31260 was added to 10-10 mol/L AVP, neither RPP nor NO release changed. OPC-21268 again suppressed the AVP-induced increases in both RPP and NO release even when added after AVP administration (Fig 2C). Fig 3 illustrates the effects of AVP on RPP and NO release and the effects of AVP antagonists in normotensive control rats. The V1 antagonist (OPC-21268) but not the V2 antagonist (OPC-31260) significantly inhibited the effects of AVP on both RPP and NO release. The effects of AVP and V1 antagonists on RPP paralleled those on NO release. To delineate the nonspecific effect of the increase in RPP on NO signals, we examined the effects of PGF2, another vasoconstrictor. PGF2 caused a similar dose-dependent increase in RPP but did not increase NO release (Fig 4).
|
|
P<.01, 
P<.001 vs vehicle (AVP alone).
|
We then studied the effects of DDAVP, a V2 agonist, on the renal vasculature. DDAVP at concentrations of 10-8 and 10-7 mol/L did not change RPP or NO release. At 10-6 mol/L, DDAVP caused a slight elevation in RPP, and the increase in NO was negligible (Fig 5). Pretreatment with 10-7 mol/L OPC-31260 did not influence the DDAVP-induced increase of RPP. However, addition of 10-7 mol/L OPC-21268 diminished the vasoconstrictive effects of DDAVP.
|
Fig 6 compares the effects of AVP on RPP and NO release in DOCA-salt and control rats. Blood pressure was significantly higher in DOCA-salt rats than in control rats (Table). The AVP-induced NO release was markedly attenuated in the DOCA-salt hypertensive rats compared with control rats despite the fact that increases in RPP by AVP were comparable in both groups. The elevation of baseline RPP of DOCA-salt rats from 100 to 150 mm Hg slightly reduced the AVP-induced increase of RPP and increased the AVP-induced release of NO; however, the effects of changes in baseline RPP were not significant. AVP-induced vasoconstriction and NO release in DOCA-salt rats were also suppressed by treatment with OPC-21268.
|
P<.01, To examine the origin of NO released in the perfusate, we evaluated NOS immunoreactivity using immunohistochemical examination. The antibody for EC-NOS stained the endothelium in the renal vasculature and that for B-NOS stained macula densa cells (Fig 7). The negative control incubated with 1% bovine serum albumin did not show any staining. The localizations of EC-NOS and B-NOS were consistent with previous reports.24 25 The intensity of immunoreactivity for both NOS isoforms was weaker in DOCA-salt rats. The localization and intensity of NADPH diaphorase activity were also consistent with the results of the immunohistochemical examination. However, the immunoreactivity of inducible NOS was not detected in control or DOCA-salt rats.
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
In the present study, AVP significantly increased NO release in the isolated rat kidney and did not lower RPP. Although PGF2
elevated RPP to an extent similar to that of AVP, it did not increase NO release, suggesting that the effects of AVP are not a nonspecific phenomenon secondary to an increase in perfusion pressure. We demonstrated that this increase in NO release was mediated by the V1 receptor, as substantiated by the fact that only the V1 receptor antagonist (OPC-21268) blocked the enhancing effects of AVP on NO release. The lack of NO-releasing effects of the selective V2 agonist also supports this notion. AVP-induced vasodilation has been reported in animals and humans. In humans, Hirsch et al6 and Imaizumi et al7 showed that AVP at pharmacological doses caused vasodilation of vessels in the forearm. The AVP-evoked vasodilation was inhibited by a V2 receptor antagonist. Their subsequent work suggested that this vasodilator effect in the human forearm was due to NO because the NOS inhibitor L-NMMA abolished it.8 Similar vasodilator effects were observed with DDAVP, a specific V2 receptor agonist, in the rat aorta12 and dog systemic vasculature.10 However, the effects of DDAVP were not always inhibited by this V2 antagonist.12 Concerning the renal circulation, Naitoh et al9 showed that intrarenal infusion of AVP at physiological concentrations increased renal blood flow in conscious dogs. These authors also demonstrated the disappearance of AVP-induced vasodilation after treatment with a V2 receptor antagonist. Aki et al11 reported that intrarenal administration of AVP with a V1 receptor antagonist caused renal vasodilation in anesthetized dogs. The addition of a V2 receptor antagonist reduced the vasodilation. These authors also showed that an NOS inhibitor suppressed V2 receptor–mediated renal vasodilation.
On the other hand, the NO-releasing activity of AVP is also reportedly mediated by V1 receptor stimulation. Katusic et al3 4 showed that V1 receptor stimulation relaxed the dog brain stem artery. The relaxation was inhibited by L-NMMA, and arterial constriction was recovered by addition of L-arginine.4 In addition, AVP increased the production of cGMP, a second messenger of NO, in cultured porcine aortic endothelial cells through V1 receptor stimulation.15 Furthermore, Walker et al5 showed V1 receptor–mediated vasodilation in the isolated rat lung during hypoxia. Species differences and varying arterial character may contribute to these confounding reports.
NO release from vascular endothelial cells is primarily regulated by constitutive NOS. This regulation requires increases in intracellular Ca2+ concentration.26 27 For V2 receptor stimulation, cAMP acts as the second messenger. Direct effects of cAMP on constitutive NOS have not been shown, although cAMP activates inducible NOS in cultured vascular smooth muscle cells.28 There is no evidence for the presence of V2 receptors on the vessels.29 V2 receptor mRNA could not be detected in the renal vessels despite polymerase chain reaction amplification.30 Stimulation of V1 receptors increases the intracellular Ca2+ mobilization caused by phospholipase C hydrolysis.1 2 In fact, AVP increases intracellular Ca2+ in cultured endothelial cells31 as well as in vascular smooth muscle cells.32 Collectively, these findings strongly suggest that AVP releases NO via V1 receptors.
In the present study, AVP-induced NO release was always associated with renal vasoconstriction. The V1 antagonist suppressed not only NO release but also renal vasoconstriction. The V2 antagonist influenced neither AVP-induced NO release nor vasoconstriction. Furthermore, DDAVP did not induce NO release, and the renal vascular tone did not change. These results suggested that AVP-induced NO release may have been due to mechanical stress, ie, increases in vascular tone, rather than receptor-mediated mechanisms. To investigate this possibility, we examined the effect of PGF2, a potent vasoconstrictor, independent of 1 or V1 receptors. As the results showed, the increase in RPP induced by PGF2 was not accompanied by NO release, suggesting that AVP-induced NO release was not due to nonspecific effects of an elevated vascular tone.
We also examined whether differences in baseline perfusion pressure influence the renal response to AVP. A standard ex vivo perfusion pressure of 100 mm Hg is substantially low for kidneys of DOCA-salt hypertensive rats compared with their in vivo perfusion pressure. Such lower perfusion pressure may attenuate the renal responses of DOCA-salt rats to AVP. Therefore, we examined the effects of a perfusion pressure of 150 mm Hg, which was close to the mean arterial pressure of the hypertensive rats used here, on the response to AVP. We observed that at this perfusion pressure, the increase in NO release was slightly greater and that in RPP was less. However, the effects of changes in baseline RPP on NO release or vascular resistance were not statistically significant. These results suggested that the increase of the baseline perfusion pressure from 100 to 150 mm Hg did not influence the NO release in response to AVP. This may have been due to less shear stress because the perfusion flow rate was maintained constant in this study.
In this study, despite NO release, AVP did not produce renal vasodilation. The effects of V1 receptor stimulation on vascular smooth muscle cells most likely masked the endothelium-derived effects. Our previous data showed that acetylcholine produced a fivefold higher endothelium-derived release of NO than was seen here.17 18 The degree of AVP-evoked NO release may have been insufficient to reduce renal vascular resistance in rats. Similar phenomena were found when endothelin-1 was administered. We have reported that endothelin-1 does not decrease RPP despite a significant increase in NO release.19
AVP induced the release of a substantial amount of NO from the renal vasculature through stimulation of V1 receptors. However, no vasorelaxation was observed, regardless of the AVP dose administered to the kidney. Some previous in vivo studies showed that AVP actually dilated renal vessels. The reasons for such differences between the results of those previous studies and ours remain undetermined, although they may be partly explained by differences between in vivo and ex vivo experiments. In in vivo studies, renal vascular tone is mostly regulated by various neurohumoral mechanisms. AVP may interact with these mechanisms. In our ex vivo preparation, the effects of AVP could not have been influenced by any systemic or neural factors, suggesting that the direct effects of AVP on renal vascular tone are vasoconstrictive. Although AVP stimulated NO release, the effects of NO released by AVP did not seem to overcome the vasoconstrictive activity of AVP. However, in vivo, the renal vasculature is exposed to greater shear stress, a physiological regulator of NO release, than ex vivo because the kidney receives more blood flow with greater viscosity. Therefore, under some circumstances, the AVP-induced NO release in vivo may be augmented, resulting in renal vasodilation. Species-specific differences may also contribute to the controversy.
We also reported that endothelium-dependent vasodilation and NO release were markedly attenuated in DOCA-salt hypertensive rats.17 18 Therefore, attenuated responses of NO release from hypertensive rat kidneys to AVP suggest that AVP may release NO via stimulation of V1 receptors on the endothelium in rat kidneys. This is consistent with the results of histochemical analyses in the present study. In kidneys of DOCA-salt rats, the staining of EC-NOS was markedly attenuated. The immunoreactivity of B-NOS in the macula densa also decreased. However, the NO signal in the venous effluent began to increase immediately after AVP administration, suggesting that most of the signals in the perfusate may reflect the endothelium-derived NO. Despite attenuated release of NO, AVP-induced renal vasoconstriction was not augmented in DOCA-salt hypertensive rats. Since the plasma concentrations of AVP are elevated in animals with DOCA-salt hypertension,33 the lack of an augmented responsiveness to AVP may have been due to receptor downregulation in the vascular smooth muscle cells. Although both V1 and V2 receptors are involved in maintaining renal function, these data reveal that the V1 receptor is the principal player in AVP-mediated NO release.
|
Selected Abbreviations and Acronyms |
|---|
|
|
Acknowledgments |
|---|
This study was partly supported by a Grant-in-Aid for Scientific Research on Priority Areas ("Vascular Endothelium–Smooth Muscle Coupling") and by Grant-in-Aid Nos. 06274209 and 07557055 from the Japanese Ministry of Education, Culture and Science, Japan. The authors wish to thank Otsuka Pharmaceutical Co for supplying OPC-21268 and OPC-31260.
Received January 8, 1996;
first decision April 15, 1996; first decision July 23, 1996;
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Nabika T, Velletri PA, Lowenberg W, Beaven MA. Increase in cytosolic calcium and phosphoinositide metabolism induced by angiotensin II and [arg]vasopressin in vascular smooth muscle cells. J Biol Chem. 1985;260:4661-4670.
2. Thibonnier M. Vasopressin and blood pressure. Kidney Int. 1988;34(suppl 25):S52-S56.
3. Katusic ZS, Shepherd JT, Vanhoutte PM. Vasopressin causes endothelium dependent relaxations of the canine basilar artery. Circ Res. 1984;55:575-579.
4. Katusic ZS. Endothelial L-arginine pathway and regional cerebral arterial reactivity to vasopressin. Am J Physiol. 1992;262:H1557-H1562.[Medline] [Order article via Infotrieve]
5. Walker BR, Haynes J Jr, Wang HL, Voelkel NF. Vasopressin-induced pulmonary vasodilation in rats. Am J Physiol. 1989;257:H415-H422.[Medline] [Order article via Infotrieve]
6. Hirsch AT, Dzau VJ, Majzoub JA, Creager MA. Vasopressin-mediated forearm vasodilation in normal humans: evidence for a vascular V2 receptor. J Clin Invest. 1989;84:418-426.[Medline] [Order article via Infotrieve]
7. Imaizumi T, Harada S, Hirooka Y, Masaki H, Momohara M, Takeshita A. Effects of OPC-21268, an orally effective vasopressin V1 receptor antagonist in humans. Hypertension. 1992;20:54-58.
8. Tagawa T, Imaizumi T, Endo T, Shiramoto M, Hirooka Y, Ando S, Takeshita A. Vasodilatory effect of arginine vasopressin is mediated by nitric oxide in human forearm vessels. J Clin Invest. 1993;92:1483-1490.[Medline] [Order article via Infotrieve]
9. Naitoh M, Suzuki H, Murakami M, Matsumoto A, Ichihara A, Nakamoto H, Yamamura Y, Saruta T. Arginine vasopressin produces renal vasodilation via V2 receptors in conscious dogs. Am J Physiol. 1993;265:R934-R942.[Medline] [Order article via Infotrieve]
10. Liard JF. L-NAME antagonizes vasopressin V2-induced vasodilation in dogs. Am J Physiol. 1994;266:H99-H106.[Medline] [Order article via Infotrieve]
11. Aki Y, Tamaki T, Kiyomoto H, He H, Yoshida H, Iwao H, Abe Y. Nitric oxide may participate in V2 vasopressin-receptor-mediated renal vasodilation. J Cardiovasc Pharmacol. 1994;23:331-336.[Medline] [Order article via Infotrieve]
12. Yamada K, Nakayama M, Nakano H, Mimura N, Yoshida S. Endothelium-dependent vasorelaxation evoked by desmopressin and involvement of nitric oxide in rat aorta. Am J Physiol. 1993;264:E203-E207.[Medline] [Order article via Infotrieve]
13. Hassid A, Williams C. Vasoconstrictor-evoked prostaglandin synthesis in cultured vascular smooth muscle. Am J Physiol. 1987;245:C278-C282.
14. Floras JS, Aylward PE, Abboud FM, Mark AL. Inhibition of muscle sympathetic nerve activity in humans by arginine vasopressin. Hypertension. 1987;10:409-416.
15. Schini VB, Katusic ZS, Vanhoutte PM. Neurohypophyseal peptides and tachykinins stimulate the production of cyclic GMP in cultured porcine aortic endothelial cells. J Pharmacol Exp Ther. 1990;255:994-1000.
16. Kikuchi K, Nagano T, Hayakawa H, Hirata Y, Hirobe M. Detection of nitric oxide production from perfused organ by luminol-H2O2 system. Anal Chem. 1993;65:1794-1799.[Medline] [Order article via Infotrieve]
17. Kikuchi K, Nagano T, Hayakawa H, Hirata Y, Hirobe M. Real-time measurement of nitric oxide produced ex vivo by luminol-H2O2 chemiluminescence method. J Biol Chem. 1993;268:23106-23110.
18. Hayakawa H, Hirata Y, Suzuki E, Kimura K, Kikuchi K, Nagano T, Hirobe M, Omata M. Long-term administration of L-arginine improves nitric oxide release from kidney in DOCA-salt hypertensive rats. Hypertension. 1994;23:752-756.
19. Hirata Y, Hayakawa H, Suzuki E, Kimura K, Kikuchi K, Nagano T, Hirobe M, Omata M. Direct measurements of endothelium-derived nitric oxide release by stimulation of endothelin receptors in rat kidney and its alteration in salt-induced hypertension. Circulation. 1995;91:1229-1235.
20. Huttner I, Gabbiani G. Vascular endothelium in hypertension. In: Genest J, Kuchel O, Hamet P, Cantin M, eds. Hypertension. Physiopathology and Treatment. 2nd ed. New York, NY: McGraw-Hill Publishing Co; 1983:473-488.
21. Hirata Y, Matsuoka H, Suzuki E, Hayakawa H, Sugimoto T, Matsuda Y, Morishita Y, Kangawa K, Minamino N, Matsuo H, Sugimoto T. Role of endogenous ANP in DOCA-salt hypertensive rats: effects of a novel non-peptide antagonist for ANP receptor. Circulation. 1993;87:554-561.
22. Yamamura Y, Ogawa H, Chihara T, Kondo K, Onogawa T, Nakamura S, Mori T, Tominaga M, Yabuuchi Y. OPC-21268, an orally effective, nonpeptide vasopressin V1 receptor antagonist. Science. 1991;252:572-574.
23. Yamamura Y, Ogawa H, Yamashita H, Chihara T, Miyamoto H, Nakamura S, Onogawa T, Yamashita T, Hosokawa T, Mori T, Tominaga M, Tabuchi Y. Characterization of a novel aquaretric agent, OPC-31260, as an orally effective, nonpeptide vasopressin V2 receptor antagonist. Br J Pharmacol. 1992;105:787-791.[Medline] [Order article via Infotrieve]
24. Tojo A, Gross SS, Zhang L, Tisher CC, Schmidt HHHW, Wilcox CS, Madsen KM. Immunocytochemical localization of distinct isoforms of nitric oxide synthase in the juxtaglomerular apparatus of normal rat kidney. J Am Soc Nephrol. 1994;4:1438-1447.[Abstract]
25. Wilcox CS, Welch WJ, Murad F, Gross SS, Taylor G, Levi R, Schmidt HHHW. Nitric oxide synthase in macula densa regulates glomerular capillary pressure. Proc Natl Acad Sci U S A. 1992;89:11993-11997.
26. Lamas S, Marsden PA, Li GK, Tempst P, Michel T. Endothelial nitric oxide synthase: molecular cloning and characterization of a distinct constitutive enzyme isoform. Proc Natl Acad Sci U S A. 1992;89:6348-6352.
27. Nishida K, Harrison DG, Navas JP, Fisher AA, Dockery SP, Uematsu M, Nerem RM, Alexander RW, Murphy TJ. Molecular cloning and characterization of the constitutive bovine aortic endothelial cell nitric oxide synthase. J Clin Invest. 1992;90:2092-2096.[Medline] [Order article via Infotrieve]
28. Imai T, Hirata Y, Kanno K, Marumo F. Induction of nitric oxide synthase by cyclic AMP in rat vascular smooth muscle cells. J Clin Invest. 1994;93:543-549.[Medline] [Order article via Infotrieve]
29. Phillips PA, Abrahams JM, Kelly JM, Mooser V, Trinder D, Johnston CI. Localization of vasopressin binding sites in rat tissues using specific V1 and V2 selective ligands. Endocrinology. 1990;126:1478-1484.
30. Terada Y, Tomita K, Nonoguchi H, Yang T, Marumo F. Different localization and regulation of two types of vasopressin receptor messenger RNA in microdissected rat nephron segments using reverse transcription polymerase chain reaction. J Clin Invest. 1993;92:2339-2345.[Medline] [Order article via Infotrieve]
31. Emori T, Hirata Y, Ohta K, Kanno K, Eguchi S, Imai T, Shichiri M, Marumo F. Cellular mechanism of endothelin-1 release by angiotensin and vasopressin. Hypertension. 1991;18:165-170.
32. Matsui H, Kohmoto O, Hirata Y, Serizawa T. Effects of a non-peptide vasopressin antagonist (OPC-21268) in smooth muscle cells and ventricular myocytes. Hypertension. 1992;19:730-733.
33. Berecek KH, Murray RD, Gross F, Brody MJ. Vasopressin and vascular reactivity in the development of DOCA hypertension in rats with hereditary diabetes insipidus. Hypertension. 1982;4:3-12.
This article has been cited by other articles:
 |
|
 |
|
  N. Gassanov, M. Jankowski, B. Danalache, D. Wang, R. Grygorczyk, U. C. Hoppe, and J. Gutkowska Arginine Vasopressin-mediated Cardiac Differentiation: INSIGHTS INTO THE ROLE OF ITS RECEPTORS AND NITRIC OXIDE SIGNALING J. Biol. Chem., April 13, 2007; 282(15): 11255 - 11265. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. J. Scislo and D. S. O'Leary Vasopressin V1 receptors contribute to hemodynamic and sympathoinhibitory responses evoked by stimulation of adenosine A2a receptors in NTS Am J Physiol Heart Circ Physiol, May 1, 2006; 290(5): H1889 - H1898. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Yuan and A. W. Cowley Jr Evidence That Reduced Renal Medullary Nitric Oxide Synthase Activity of Dahl S Rats Enables Small Elevations of Arginine Vasopressin to Produce Sustained Hypertension Hypertension, February 1, 2001; 37(2): 524 - 528. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Loichot, C. Cazaubon, M. Grima, W. De Jong, D. Nisato, J.-L. Imbs, and M. Barthelmebs Vasopressin Does not Effect Hypertension Caused by Long-Term Nitric Oxide Inhibition Hypertension, February 1, 2000; 35(2): 602 - 608. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Kakoki, Y. Hirata, H. Hayakawa, A. Tojo, D. Nagata, E. Suzuki, K. Kimura, A. Goto, K. Kikuchi, T. Nagano, et al. Effects of Hypertension, Diabetes Mellitus, and Hypercholesterolemia on Endothelin Type B Receptor–Mediated Nitric Oxide Release From Rat Kidney Circulation, March 9, 1999; 99(9): 1242 - 1248. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Umino, E. Kusano, S. Muto, T. Akimoto, S. Yanagiba, S. Ono, M. Amemiya, Y. Ando, S. Homma, U. Ikeda, et al. AVP inhibits LPS- and IL-1beta -stimulated NO and cGMP via V1 receptor in cultured rat mesangial cells Am J Physiol Renal Physiol, March 1, 1999; 276(3): F433 - F441. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Park, A.-P. Zou, and A. W. Cowley Jr Arginine Vasopressin–Mediated Stimulation of Nitric Oxide Within the Rat Renal Medulla Hypertension, November 1, 1998; 32(5): 896 - 901. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||