Mechanisms underlying arginine vasopressin-induced relaxation in monkey isolated coronary arteries

Okamura, Tomio; Ayajiki, Kazuhide; Fujioka, Hideyuki; Toda, Noboru

doi:10.1097/00004872-199917050-00011

Cited by 69 publications

(37 citation statements)

References 24 publications

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“…Vasodilation also appears to be endothelium dependent and NO mediated. 63,91 There are significant differences in the ability of different arteries to vasodilate in response to vasopressin; for instance, arteries of the circle of Willis are more sensitive to the vasodilatory effects of vasopressin than are other intracranial and extracranial arteries. 92 The receptor subtype responsible for vasodilation is uncertain.…”

Section: Vasodilator Effectsmentioning

confidence: 99%

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Physiology of Vasopressin Relevant to Management of Septic Shock

Holmes

Patel

Russell

et al. 2001

Chest

538

395

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Section: Vasodilator Effectsmentioning

confidence: 99%

“…63 Thus, despite implicating different receptors, all of these studies suggest that vasopressin-induced vasodilation is mediated ultimately through NO release. 91 …”

Section: Vasodilator Effectsmentioning

confidence: 99%

Physiology of Vasopressin Relevant to Management of Septic Shock

Holmes

Patel

Russell

et al. 2001

Chest

538

395

View full text Add to dashboard Cite

“…It stimulates a phosphatidylinositol-calcium signal pathway leading to smooth muscle contraction [5]. But on the other side AVPR1a stimulation also causes production of nitric oxide, a potent vasodilator in pulmonary [8] and coronary vessels [9]. Also the stimulation of oxytocin receptors by low dose vasopressin can induce vasodilation [10].…”

Section: Introductionmentioning

confidence: 99%

Vasopressin Increases Cerebral Perfusion Pressure but not Cerebral Blood Flow in Neurosurgical Patients with Catecholamine-Refractory Hypotension: A Preliminary Evaluation Using the Non-Invasive Quantix ND in Comparison to the Literature

Bele¹

2014

JACCOA

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“…exogenous AVP mediate vasodilatation in coronary, cerebral, and pulmonary arterial circulation (20). The recognized effects of AVP on renal function are complex and include association of an antidiuretic effect through stimulation of V2 receptors, an increase of diuresis/natriuresis through V1 receptors by efferent arteriolar vasoconstriction, and oxytocin receptor-mediated stimulation (23).…”

mentioning

confidence: 99%

Comparative effects of vasopressin, norepinephrine, and l-canavanine, a selective inhibitor of inducible nitric oxide synthase, in endotoxic shock

Lévy

Vallée²,

Lauzier³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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. Comparative effects of vasopressin, norepinephrine, and L-canavanine, a selective inhibitor of inducible nitric oxide synthase, in endotoxic shock. Am J Physiol Heart Circ Physiol 287: H209 -H215, 2004. First published February 26, 2004 10.1152/ajpheart.00946.2003, a standard of care, AVP, an alternative candidate, and L-canavanine (LC), a selective inhibitor of inducible nitric oxide synthase, were compared for efficacy and innocuousness on global and regional hemodynamics, plasmatic and tissue lactate-to-pyruvate ratio (L/P), tissue high-energy phosphates, renal function, and tissue capillary permeability in a rat model of endotoxic normokinetic shock. Mean arterial pressure (MAP) decreased (ϳ35%) but aortic blood flow increased during endotoxin infusion (P Ͻ 0.05 vs. control). Additionally, there was a decrease in mesenteric (MBF) and renal (RBF) blood flows along with regional-to-systemic ratio (P Ͻ 0.05 vs. control). All tested drugs restored MAP to basal levels but slightly decreased abdominal aortic flow; however, RBF and MBF remained unchanged. Endotoxin significantly decreased diuresis and inulin clearance (ϳ3-to 4-fold), whereas AVP or LC attenuated this drop (P Ͻ 0.05 vs. control). In contrast, NE did not improve endotoxininduced renal dysfunction. Endotoxin induced gut and lung hyperpermeability (P Ͻ 0.05 vs. control). Endotoxin-induced gut hyperpermeability was inhibited by AVP, LC, and NE. Endotoxin-induced lung hyperpermeability was further worsened by NE (ϳ2-fold increase) but not AVP infusion (P Ͻ 0.05 vs. endotoxin). LC significantly improved endotoxin-induced pulmonary hyperpermeability. Endotoxin increased renal lactate and decreased renal ATP. NE did not change renal lactate or renal ATP. AVP and LC decreased renal lactate and normalized renal ATP. Finally, endotoxin was associated with increased lactate levels and L/P (ϳ2-and 1.5-fold increases vs. control, respectively), whereas AVP and LC, but not NE, normalized both parameters after endotoxin challenge. These results suggest that, in a short-term endotoxic shock model, AVP improves systemic hemodynamics without side effects and has particular beneficial effects on renal function. septic shock; vascular permeability; renal function THE HUMAN RESPONSE to septic challenge usually includes increased cardiac output, decreased peripheral resistance, low arterial pressure, and increased vascular permeability. AVP, also known as "the" antidiuretic hormone (ADH), is an emerging alternative candidate for management of redistributive shock (7). Indeed, AVP exhibits strong vasoconstrictor effects through stimulation of the V1 receptor leading to arterial pressure improvement (28). Moreover, low concentrations of exogenous AVP mediate vasodilatation in coronary, cerebral, and pulmonary arterial circulation (20). The recognized effects of AVP on renal function are complex and include association of an antidiuretic effect through stimulation of V2 receptors, an increase of diuresis/natriuresis through V1 receptors by efferent arteriolar vasoconstric...

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Mechanisms underlying arginine vasopressin-induced relaxation in monkey isolated coronary arteries

Abstract: It is concluded that AVP-induced monkey coronary arterial relaxation is mediated via nitric oxide synthesized from L-arginine in association with stimulation of V1 receptor subtypes in the endothelium.

Cited by 69 publications

References 24 publications

Physiology of Vasopressin Relevant to Management of Septic Shock

Physiology of Vasopressin Relevant to Management of Septic Shock

Vasopressin Increases Cerebral Perfusion Pressure but not Cerebral Blood Flow in Neurosurgical Patients with Catecholamine-Refractory Hypotension: A Preliminary Evaluation Using the Non-Invasive Quantix ND in Comparison to the Literature

Comparative effects of vasopressin, norepinephrine, and l-canavanine, a selective inhibitor of inducible nitric oxide synthase, in endotoxic shock

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