Effects of Vasopressin and Its Analogs on Rat Aortic Smooth Muscle and Renal Medullary Tubular Cells

Mb, Vallotton; Rp, Wüthrich; Pd, Lew; Am, Capponi

doi:10.1097/00005344-198600087-00003

Cited by 14 publications

(12 citation statements)

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“…This hormone exerts potent vasoconstrictor action through V1a receptors (V1aR) in vascular smooth muscles (23,27). It has been reported that a marked increase in plasma AVP following hemorrhage helps the recovery of blood pressure from hemorrhageinduced hypotension (11,19,26).…”

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confidence: 99%

Altered cardiovascular regulation in arginine vasopressin-overexpressing transgenic rat

Tachikawa¹,

Yokoi²,

Nagasaki³

et al. 2003

American Journal of Physiology-Endocrinology and Metabolism

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Although arginine vasopressin (AVP), an antidiuretic hormone, has been widely acknowledged to play an important role in cardiovascular regulation via V1a receptors (V1aR), its precise significance remains unclear. In this study, we investigated the effects of long-standing high plasma AVP status on cardiovascular regulation in the AVP-overexpressing transgenic (Tg) rat. Adult male homozygous Tg rats were compared with age-matched normal Sprague-Dawley rats as controls. There were no significant differences in mean arterial blood pressure (BP; MABP) or heart rate between Tg and control rats in the basal state. Subcutaneous injection of AVP significantly increased MABP in controls but did not cause any apparent increase in MABP in Tg rats. BP recovery from hemorrhage-induced hypotension was significantly delayed in Tg compared with control rats. Pretreatment with a selective V1aR antagonist, OPC-21268, which is thought to restore the downregulation of V1aR, markedly improved both of these impaired responses. Northern blot analysis confirmed that decreased expression of V1aR mRNA and pretreatment with V1aR antagonist significantly restored the downregulation of V1aR mRNA. These results suggest that the Tg rat has decreased sensitivity to the hypertensive effect of AVP due to downregulation of V1aR, which may function as an adaptive mechanism to maintain normal BP against chronic hypervasopressinemia. In addition, impaired restoration of BP after hemorrhage-induced hypotension in Tg rats supports a physiological role of AVP in cardiovascular regulation.

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confidence: 99%

Altered cardiovascular regulation in arginine vasopressin-overexpressing transgenic rat

Tachikawa¹,

Yokoi²,

Nagasaki³

et al. 2003

American Journal of Physiology-Endocrinology and Metabolism

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“…Activation of V, receptors is accompanied by an increase in the intracellular calcium concentration, which may mediate both prostanoid production and vascular smooth muscle contraction. 13 Although the level of tone in the pulmonary circulation has been previously shown to alter the nature of the response to adrenergic and cholinergic stimuli, the mechanism for the alteration is uncertain. 44 - 45 It is possible that changes in the physical state of cell membranes, which occur during vasoconstriction and dilation, 46 may play a role in the tone-dependent nature of vascular responses.…”

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Vascular responses to vasopressin are tone-dependent in the cerebral circulation of the newborn pig.

Armstead

Mirro

Busija

et al. 1989

Circulation Research

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“…As it is well known that phosphatidylcholine is also hydrolyzed to glycerophosphocholine by phospholipase A, and lysophospholipase, and to choline phosphate by phosphatidylcholine-specific phospholipase C, respectively, it is most likely that the increase of choline formation by AVP is mainly due to hydrolysis by phospholipase D. AVP is known to stimulate phosphoinositide hydrolysis in aortic smooth muscle cells (Nabika et al 1985;Vallotton et al 1986;Grillone et al 1988). In a previous study (Kondo et al 1989), we have shown that AVP-induced phosphoinositide hydrolysis is PTX insensitive in primary cultured rat aortic smooth muscle cells.…”

Section: Egtamentioning

confidence: 99%

“…AVP is well known for stimulating the proliferation of vascular smooth muscle cells (Campbell-Boswell andRobertson 1981, Scott-Burden et al 1992). AVP has been reported to induce phosphoinositide hydrolysis by phospholipase C through its binding to the V1 receptor in these cells (Nabika et al 1985, Vallotton et al 1986, Grillone et al 1988). Phosphoinositide hydrolysis leads to the formation of diacylglycerol and IPS .…”

Section: Introductionmentioning

confidence: 99%

Vasopressin activates phospholipase D through pertussis toxin-insensitive GTP-binding protein in aortic smooth muscle cells: function of Ca²⁺/calmodulin

Miwa

Kozawa

Suzuki

et al. 1995

Biochem. Cell Biol.

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In the present study, we examined the effect of vasopressin (AVP) on phosphatidylcholine-hydrolyzing phospholipase D activity in primary cultured rat aortic smooth muscle cells. AVP stimulation of choline formation was dose dependent. The time-course was quite different from those of inositol phosphates. The effect of AVP on the formation of inositol phosphates (EC50 was 3 nM) was more potent than that on the formation of choline (EC50 was 30 nM). 12-O-Tetradecanoylphorbol-13-acetate (TPA), an activator of protein kinase C (PKC), stimulated the formation of choline. However, 4 alpha-phorbol 12,13-didecanoate, which is inactive for PKC, had little effect. Staurosporine, an inhibitor of protein kinases, which inhibited the TPA-induced formation of choline, had little effect on the AVP-induced formation of choline. Neither calphostin C, a highly specific PKC inhibitor, nor PKC down-regulation with TPA affected AVP-induced formation of choline. A combination of AVP and TPA additively stimulated the formation of choline. The depletion of extracellular Ca2+ by (ethylenebis(oxyethylenenitrilo)tetraacetic acid significantly reduced the AVP-induced formation of choline. W-7, an antagonist of calmodulin, inhibited the AVP-induced formation of choline in a dose-dependent manner. NaF, an activator for GTP-binding protein (G-protein), stimulated the formation of choline. However, the formation of choline by a combination of AVP and NaF was not additive. Pertussis toxin had little effect on the AVP-induced formation of choline.(ABSTRACT TRUNCATED AT 250 WORDS)

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Effects of Vasopressin and Its Analogs on Rat Aortic Smooth Muscle and Renal Medullary Tubular Cells

Cited by 14 publications

References 0 publications

Altered cardiovascular regulation in arginine vasopressin-overexpressing transgenic rat

Altered cardiovascular regulation in arginine vasopressin-overexpressing transgenic rat

Vascular responses to vasopressin are tone-dependent in the cerebral circulation of the newborn pig.

Vasopressin activates phospholipase D through pertussis toxin-insensitive GTP-binding protein in aortic smooth muscle cells: function of Ca²⁺/calmodulin

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Effects of Vasopressin and Its Analogs on Rat Aortic Smooth Muscle and Renal Medullary Tubular Cells

Cited by 14 publications

References 0 publications

Altered cardiovascular regulation in arginine vasopressin-overexpressing transgenic rat

Altered cardiovascular regulation in arginine vasopressin-overexpressing transgenic rat

Vascular responses to vasopressin are tone-dependent in the cerebral circulation of the newborn pig.

Vasopressin activates phospholipase D through pertussis toxin-insensitive GTP-binding protein in aortic smooth muscle cells: function of Ca2+/calmodulin

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Vasopressin activates phospholipase D through pertussis toxin-insensitive GTP-binding protein in aortic smooth muscle cells: function of Ca²⁺/calmodulin