Triphasic Response of Rat Intracerebral Arterioles to Increasing Concentrations of Vasopressin in vitro

Takayasu, Misako; Kajita, Yasukazu; Suzuki, Yoshio; Shibuya, Masabumi; Sugita, Kenichiro; Ishikawa, Tomohiko; Hidaka, Hiroyoshi

doi:10.1038/jcbfm.1993.38

Cited by 40 publications

(25 citation statements)

References 31 publications

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“…Data in the literature indicate that vasopressin may stimulate release of nitric oxide by activating VI (Katusic, 1992;Takayasu et al, 1993) or V2 (Aki et al, 1994) receptors. In our study we observed that neither vasopressin nor the V2 agonist desmopressin produced any relaxation in precontracted arteries, thus suggesting that, in the arteries examined in this study, activation of vasopressin receptors may not stimulate the release of enough nitric oxide to induce vasorelaxation.…”

Section: Discussionmentioning

confidence: 99%

“…In vitro and in vivo experiments indicate that a considerable regional heterogeneity exists in the reactivity of blood vessels to vasopressin, as this peptide produces marked constriction in cutaneous, splanchnic or muscular blood vessels (Schmid et al, 1974;Heydrickx et al, 1976;Liard et al, 1982), dilatation or weak constriction in renal vasculature (Schmid et al, 1974;Heydrickx et al, 1976;Naitoh et al, 1993), no effect or dilatation in pulmonary vasculature (Walker et al, 1989), dilatation in coronary arteries (Turlapaty & Altura, 1982), and both constriction or dilatation in cerebral vasculature (Lluch et al, 1984;Takayasu et al, 1993). The reasons for these differences are as yet unknown, and they may be related to the animal species and the experimental procedures used, as well as to the re-1 Author for correspondence.…”

Section: Introductionmentioning

confidence: 99%

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Regional differences in the arterial response to vasopressin: role of endothelial nitric oxide

Garcı́a-Villalón

García

Fernández

et al. 1996

British J Pharmacology

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1 The isometric response to arginine-vasopressin (10-1o 10-7 M) was studied in 2 mm long rabbit arterial segments isolated from several vascular beds (cutaneous, pial, renal, coronary, muscular, mesenteric and pulmonary). 2 Vasopressin induced contraction in central ear (cutaneous), basilar (pial), renal, coronary and saphenous (muscular) arteries, but had no effect in mesenteric and pulmonary arteries; the order of potency for the contraction was: ear > basilar > renal > coronary > saphenous arteries. 3 Treatment with the blocker of nitric oxide synthesis NG-nitro-L-arginine methyl ester (L-NAME; 106-I0-M) increased significantly (P< 0.05) the contraction to vasopressin in ear (148% of control), basilar (150% of control), renal (304% of control), coronary (437% of control) and saphenous (235% of control) arteries. Removal of the endothelium increased significantly (P<0.05) the contraction to vasopressin in basilar (138% of control), renal (253% of control), coronary (637% of control) and saphenous (662% of control) arteries, but not in ear artery. Mesenteric and pulmonary arteries in the presence of L-NAME or after endothelium removal did not respond to vasopressin, as occurred in control conditions. 4 The specific antagonist for V1 vasopressin receptors d(CH2)5Tyr(Me)AVP (3 x 10-9-10-7 M) was more potent (pA2=9.3-10.1) than the antagonist for both VI and V2 vasopressin receptors desGly-d(CH2)5-D-Tyr(Et)ValAVP (10-7-10-6 M) (pA2 =7.4-8.4) to block the contraction to vasopressin of ear, basilar, renal and coronary arteries. 5 The specific V2 vasopressin agonist [deamino-Cys1, D-Arg8]-vasopressin (desmopressin) (10-1o-10-7 M) did not produce any effect in any of the arteries studied, with or without endothelium. 6 In arteries precontracted with endothelin-1, vasopressin or desmopressin did not produce relaxation. 7 These results suggest: (a) most arterial beds studied (5 of 7) exhibit contraction to vasopressin with different intensity; (b) the vasoconstriction to this peptide is mediated mainly by stimulation of V1 vasopressin receptors, and (c) endothelial nitric oxide may inhibit the vasoconstriction to this peptide, especially in coronary and renal vasculatures.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Regional differences in the arterial response to vasopressin: role of endothelial nitric oxide

Garcı́a-Villalón

García

Fernández

et al. 1996

British J Pharmacology

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“…In animal studies, the administration of vasopressin, however, also increases CBF by dilating cerebral arteries. [15][16][17] Vasopressin also may regulate regional CBF by balancing the effects of increased flow mediated by nitric oxide released from the endothelium, with decreased flow in vessels contracted by direct stimulation of smooth muscle. 18 It has been postulated that the increase in CBF may be mediated through cerebral V2 receptors.…”

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confidence: 99%

Worsening of cerebral hyperemia by the administration of terlipressin in acute liver failure with severe encephalopathy

et al. 2004

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There is increasing evidence that terlipressin is useful in patients with cirrhosis and hepatorenal syndrome, but there are no data of its use in patients with acute liver failure (ALF) in whom hepatorenal syndrome is common. Although terlipressin produces systemic vasoconstriction, it produces cerebral vasodilatation and may increase cerebral blood flow (CBF). Increased CBF contributes to intracranial hypertension in patients with ALF. The aim of this study was to evaluate the safety of terlipressin in patients with ALF with respect to cerebral hemodynamics. Six successive patients with ALF were ventilated electively for grade IV hepatic encephalopathy. Patients were monitored invasively and CBF was measured (KetySchmidt technique). Measurements were made before and at 1, 3, and 5 hours after intravenous (single bolus) administration of terlipressin (0.005 mg/kg), median, 0.25 mg (range, 0.2-0.3 mg). There was no significant change in heart rate, mean arterial pressure, or cardiac output. CBF and jugular venous oxygen saturation both increased significantly at 1 hour (P ‫؍‬ 0.016). Intracranial pressure increased significantly at 1 hour (P ‫؍‬ 0.031), returning back to baseline values at 2 hours. In conclusion, administration of terlipressin, at a dose that did not alter systemic hemodynamics, resulted in worsening of cerebral hyperemia and intracranial hypertension in patients with ALF and severe hepatic encephalopathy. These data suggest the need to exercise extreme caution in the use of terlipressin in these patients in view of its potentially deleterious consequences on cerebral hemodynamics. (HEPATOLOGY 2004;39:471-475.)

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“…[15][16][17] The present investigation was designed to determine the in vitro vascular effects of desmopressin in human renal arteries. Observations were made in the presence and absence of endothelium as well as with peptide and nonpeptide V 1 and V 2 receptor antagonists.…”

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confidence: 99%

V2-receptor–mediated relaxation of human renal arteries in response to desmopressin

Medina

Segarra

Vila

et al. 1999

American Journal of Hypertension

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The effects of deamino-8-D-arginine vasopressin (desmopressin), a V 2 receptor antidiuretic agonist, were studied in isolated rings from branches of renal arteries obtained from 22 patients undergoing nephrectomy. The rings were suspended in organ bath chambers for isometric recording of tension. In precontracted rings with norepinephrine (10 ؊6 to 3 ؋ 10 ؊6 mol/L), desmopressin (10 ؊11 to 3 ؋ 10 ؊7 mol/L) caused endothelium-dependent relaxation (81% ؎ 4% reversal of the initial contraction in arteries with endothelium; 20% ؎ 4% in arteries without endothelium; P < . A rginine vasopressin promotes reabsorption of water in renal tubular cells through V 2 receptors coupled to adenylate cyclase activation and acts directly on human vascular smooth muscle to produce constriction through V 1 receptor stimulation.1-4 The specific V 2 receptor agonist deamino-8-d-arginine vasopressin (desmopressin) is a synthetic analogue of the natural hormone vasopressin with a strong V 2 antidiuretic effect and minimal V 1 pressor activity.5 Extrarenal actions of desmopressin include coagulation responses such as the release of factor VIIIc and von Willebrand factor, 6 -8 and cardiovascular effects such as increase in heart rate, decrease in mean arterial blood pressure, facial flushing, and increase in forearm blood flow. 9 -11 Whether these effects are mediated by receptors is not clearly established, but studies in humans demonstrate that an extrarenal V 2 receptor could be responsible for the coagulation and hemodynamic responses to desmopressin. 10 -12 Experiments in isolated arteries show that desmopressin induces concentration-dependent relaxation in human cerebral and mesenteric arteries that is prevented by the mixed V 1 -V 2 receptor antagonist desGly-d(CH 2 ) 5 -d-Tyr(Et)ValAVP but not

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Triphasic Response of Rat Intracerebral Arterioles to Increasing Concentrations of Vasopressin in vitro

Cited by 40 publications

References 31 publications

Regional differences in the arterial response to vasopressin: role of endothelial nitric oxide

Regional differences in the arterial response to vasopressin: role of endothelial nitric oxide

Worsening of cerebral hyperemia by the administration of terlipressin in acute liver failure with severe encephalopathy

V2-receptor–mediated relaxation of human renal arteries in response to desmopressin

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