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      Science Review: Vasopressin and the cardiovascular system part 1 – receptor physiology

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          Abstract

          Vasopressin is emerging as a rational therapy for vasodilatory shock states. Unlike other vasoconstrictor agents, vasopressin also has vasodilatory properties. The goal of the present review is to explore the vascular actions of vasopressin. In part 1 of the review we discuss structure, signaling pathways, and tissue distributions of the classic vasopressin receptors, namely V 1 vascular, V 2 renal, V 3 pituitary and oxytocin receptors, and the P 2 class of purinoreceptors. Knowledge of the function and distribution of vasopressin receptors is key to understanding the seemingly contradictory actions of vasopressin on the vascular system. In part 2 of the review we discuss the effects of vasopressin on vascular smooth muscle and the heart, and we summarize clinical studies of vasopressin in shock states.

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          G protein pathways.

          Susana Neves, Prahlad Ram, Ravi Iyengar (2002)
          The heterotrimeric guanine nucleotide-binding proteins (G proteins) are signal transducers that communicate signals from many hormones, neurotransmitters, chemokines, and autocrine and paracrine factors. The extracellular signals are received by members of a large superfamily of receptors with seven membrane-spanning regions that activate the G proteins, which route the signals to several distinct intracellular signaling pathways. These pathways interact with one another to form a network that regulates metabolic enzymes, ion channels, transporters, and other components of the cellular machinery controlling a broad range of cellular processes, including transcription, motility, contractility, and secretion. These cellular processes in turn regulate systemic functions such as embryonic development, gonadal development, learning and memory, and organismal homeostasis.
          Article 0 comments Cited 287 times – based on 0 reviews     Review now
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            The pathogenesis of vasodilatory shock.

            D W Landry, J A Oliver (2001)
            Article 0 comments Cited 181 times – based on 0 reviews     Review now
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              Physiology of vasopressin relevant to management of septic shock.

              Cheryl L Holmes, Bhavesh Patel, James A. Russell … (2001)
              Vasopressin is emerging as a rational therapy for the hemodynamic support of septic shock and vasodilatory shock due to systemic inflammatory response syndrome. The goal of this review is to understand the physiology of vasopressin relevant to septic shock in order to maximize its safety and efficacy in clinical trials and in subsequent therapeutic use. Vasopressin is both a vasopressor and an antidiuretic hormone. It also has hemostatic, GI, and thermoregulatory effects, and is an adrenocorticotropic hormone secretagogue. Vasopressin is released from the axonal terminals of magnocellular neurons in the hypothalamus. Vasopressin mediates vasoconstriction via V1-receptor activation on vascular smooth muscle and mediates its antidiuretic effect via V2-receptor activation in the renal collecting duct system. In addition, vasopressin, at low plasma concentrations, mediates vasodilation in coronary, cerebral, and pulmonary arterial circulations. Septic shock causes first a transient early increase in blood vasopressin concentrations that decrease later in septic shock to very low levels compared to other causes of hypotension. Vasopressin infusion of 0.01 to 0.04 U/min in patients with septic shock increases plasma vasopressin levels to those observed in patients with hypotension from other causes, such as cardiogenic shock. Increased vasopressin levels are associated with a lesser need for other vasopressors. Urinary output may increase, and pulmonary vascular resistance may decrease. Infusions of > 0.04 U/min may lead to adverse, likely vasoconstriction-mediated events. Because clinical studies have been relatively small, focused on physiologic end points, and because of potential adverse effects of vasopressin, clinical use of vasopressin should await a randomized controlled trial of its effects on clinical outcomes such as organ failure and mortality.
              Article 0 comments Cited 95 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Crit Care
                Title: Critical Care
                Publisher: BioMed Central (London )
                ISSN (Print): 1364-8535
                ISSN (Electronic): 1466-609X
                Publication date (Print): 2003
                Publication date (Electronic): 26 June 2003
                Volume: 7
                Issue: 6
                Pages: 427-434
                Affiliations
                [1 ]Staff intensivist, Department of Medicine, Division of Critical Care, Kelowna General Hospital, Kelowna BC, Canada
                [2 ]Associate Professor, Department of Medicine, Columbia University, New York, New York, USA
                [3 ]Assistant Professor of Medicine, Faculty of Medicine, and Program Director, Critical Care Medicine, University of Toronto, and Consultant in Pulmonary and Critical Care Medicine, Director Pulmonary Hypertension Program, University Health Network, Toronto, Ontario, Canada
                Article
                Publisher ID: cc2337
                DOI: 10.1186/cc2337
                PMC ID: 374366
                PubMed ID: 14624682
                SO-VID: c89e6871-4857-469c-82a6-6d7997a9042c
                Copyright © Copyright © 2003 BioMed Central Ltd
                History
                Categories
                Subject: Review

                ScienceOpen disciplines: Emergency medicine & Trauma
                Keywords: potassium channels,cardiac inotropy,oxytocin,vasoconstriction,hypotension,antidiurectic hormone,nitric oxide,physiology,receptors,vasopressin,septic shock,smooth muscle,vascular,vasodilation,adrenergic agents
                Data availability:
                ScienceOpen disciplines: Emergency medicine & Trauma
                Keywords: potassium channels, cardiac inotropy, oxytocin, vasoconstriction, hypotension, antidiurectic hormone, nitric oxide, physiology, receptors, vasopressin, septic shock, smooth muscle, vascular, vasodilation, adrenergic agents

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