[Arg8]Vasopressin-induced responses of the human isolated coronary artery: effects of non-peptide receptor antagonists

Bax, Willem A.; Graaf, Pieter H. Van der; Stam, Wiro; Bos, Egbert; Nisato, Dino; Saxena, Pramod R.

doi:10.1016/0014-2999(95)00503-d

Cited by 27 publications

(13 citation statements)

References 10 publications

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“…On the other hand, OPC31260 at 3 x 10~8 M, which is almost equal to the IC50 value of the AVP binding assay on V2 receptors in rat preparations, was effective. Similar ineffectivenesses of OPC21268 to AVP actions were also reported in human internal mammary and coronary arteries [32,33]. In these studies, it has been concluded that OPC21268 does not act as a selective Vi antagonist in human arteries, but that OPC31260 seems to inhibit the V, receptor.…”

Section: Discussionsupporting

confidence: 57%

Receptor Subtypes Involved in Relaxation and Contraction by Arginine Vasopressin in Canine Isolated Short Posterior Ciliary Arteries

Okamura

Toda²,

Ayajiki³

et al. 1997

J Vasc Res

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Arginine vasopressin (AVP) produced relaxations at low concentrations (10^-11and 10^-10M)and contractions at higher concentrations in canine ciliary arterial strips with endothelium, partially contracted with prostglandin F_2α. The AVP-induced relaxation was abolished or reversed to a contraction by removal of the endothelium or treatment with N^G-nitro-L-arginine. The effect of this antagonist was reversed by L-arginine. The relaxant response was inhibited dose-dependently by SR49059 (10^–10–10^–9M), [Pmp¹Tyr(Me)²]^-Arg⁸-vasopressin (PMP-AVP) (10^–10–10^–9M), V₁ receptor antagonists, and OPC31260 (3 × 10^-8M), a reported V₂ receptor antagonist, but not by OPC21268 (10^–7–10^–6M), a reported V₁ antagonist. In the endothelium-denuded strips, the AVP-induced contraction was attenuated by SR49059, PMP-AVP and OPC31260, but not by OPC21268. It is concluded that AVP in low concentrations elicits intense relaxation of canine ciliary arteries, possibly due to nitric oxide synthesized in association with activation of the endothelial V₁ receptor subtype. AVP-induced contractions appear to be mediated also by the V₁ receptor in smooth muscle. Antagonistic selectivities of the OPC compounds to vasopressin receptor subtypes could not be seen in this particular material.

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Section: Discussionsupporting

confidence: 57%

Receptor Subtypes Involved in Relaxation and Contraction by Arginine Vasopressin in Canine Isolated Short Posterior Ciliary Arteries

Okamura

Toda²,

Ayajiki³

et al. 1997

J Vasc Res

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“…Furthermore, V1AR mRNA and protein were significantly lower in the mesencephalopontine region of infarcted rats compared to control rats [105]. Along with the cardiac and central effects, V1AR also alter blood pressure following MI via coronary artery constriction [106]. Additionally, V1AR expression in the renal medulla is increased after MI [105], and has been shown to contribute to hypertension [107].…”

Section: Exploration Of V1ar Effects On Cardiac Function and Survimentioning

confidence: 99%

Arginine vasopressin receptor signaling and functional outcomes in heart failure

Wasilewski

Myers

Recchia

et al. 2016

Cellular Signalling

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Heart failure (HF) continues to be a highly prevalent syndrome, affecting millions of patients and costing billions of dollars in treatment per year in the United States alone. Studies in failing human heart and in transgenic HF models led to the recognition that enhanced neurohormonal signaling plays a causative role in HF progression, and the use of neurohormone receptor antagonists have proven to decrease hospitalization rates. It has also been long recognized that patients with HF have abnormal water retention, hypo-osmolality, and hyponatremia secondary to elevations in the levels of the neurohormone arginine vasopressin (AVP). AVP is released from the hypothalamus in response to changes in plasma osmolality and pressure, acting at three distinct G protein-coupled receptors: V1AR, V1BR and V2R. Persistent AVP release causes hyponatremia via renal V2R activation, a risk factor for death and hospitalization, and there is a correlation between plasma AVP levels and HF severity/survival of chronic HF patients. Because of the adverse clinical consequences associated with the development of hyponatremia, V2R antagonists were developed for the treatment of HF patients with hyponatremia, however in contrast to other neurohormone blockers they do not relay a survival benefit and may exacerbate decompensated HF requiring inotropic support. Renewed interest in the cardiac V1AR system during HF has arisen due to several recent findings: 1) mice with myocyte-selective transgenic overexpression of cardiac V1AR developed cardiomyopathy in the absence of any pathological insult, 2) cardiac V1AR expression was shown to be increased late-stage human HF, and 3) V1AR antagonism prevented cardiomyopathy development in a mouse model of HF. While cardiac V1AR expression is increased in HF, the role of V1AR signaling in various forms of cardiac injury and in distinct cardiac cell types has been controversial. Therefore this review will primarily focus on V1AR signaling as a potential therapeutic target for HF treatment.

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“…Although our data suggest that cardiac β AR responsiveness is increased in the absence of V1AR, the use of global KO mice limits our ability to dissect this effect in vivo as V1AR is normally expressed in numerous tissues such as the CNS and vasculature that could affect cardiovascular function [13–16]. Thus, to determine whether enhanced cardiac β AR responsiveness in the absence of V1AR expression indeed occurs at the level of individual cardiomyocytes, we next evaluated contractility in isolated cardiomyocytes in response to ISO (0.1 μ M).…”

Section: Resultsmentioning

confidence: 99%

Vasopressin type 1A receptor deletion enhances cardiac contractility, β-adrenergic receptor sensitivity and acute cardiac injury-induced dysfunction

et al. 2016

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Vasopressin type 1A receptor (V1AR) expression is elevated in chronic human heart failure (HF) and contributes to cardiac dysfunction in animal models, in part via reduced β-adrenergic receptor (βAR) responsiveness. Although cardiac V1AR overexpression and V1AR stimulation are each sufficient to decrease βAR activity, it is unknown whether V1AR inhibition conversely augments βAR responsiveness. Further, although V1AR has been shown to contribute to chronic progression of HF, its impact on cardiac function following acute ischaemic injury has not been reported. Using V1AR knockout (V1AR KO) mice we assessed the impact of V1AR deletion on cardiac contractility at baseline and following ischaemic injury, βAR sensitivity and cardiomyocyte responsiveness to βAR stimulation. Strikingly, baseline cardiac contractility was enhanced in V1AR KO mice and they experienced a greater loss in contractile function than control mice following acute ischaemic injury, although the absolute levels of cardiac dysfunction and survival rates did not differ. Enhanced cardiac contractility in V1AR KO mice was associated with augmented β-blocker sensitivity, suggesting increased basal βAR activity, and indeed levels of left ventricular cAMP, as well as phospholamban (PLB) and cardiac troponin I (cTnI) phosphorylation were elevated compared with control mice. At the cellular level, myocytes isolated from V1AR KO mice demonstrated increased responsiveness to βAR stimulation consistent with the finding that acute pharmacological V1AR inhibition enhanced βAR-mediated contractility in control myocytes. Therefore, although V1AR deletion does not protect the heart from the rapid development of cardiac dysfunction following acute ischaemic injury, its effects on βAR activity suggest that acute V1AR inhibition could be utilized to promote myocyte contractile performance.

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[Arg8]Vasopressin-induced responses of the human isolated coronary artery: effects of non-peptide receptor antagonists

Cited by 27 publications

References 10 publications

Receptor Subtypes Involved in Relaxation and Contraction by Arginine Vasopressin in Canine Isolated Short Posterior Ciliary Arteries

Receptor Subtypes Involved in Relaxation and Contraction by Arginine Vasopressin in Canine Isolated Short Posterior Ciliary Arteries

Arginine vasopressin receptor signaling and functional outcomes in heart failure

Vasopressin type 1A receptor deletion enhances cardiac contractility, β-adrenergic receptor sensitivity and acute cardiac injury-induced dysfunction

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