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Critical Care  2003 

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

DOI: 10.1186/cc2337

Keywords: adrenergic agents, antidiurectic hormone, cardiac inotropy, hypotension, nitric oxide, oxytocin, physiology, potassium channels, receptors, septic shock, smooth muscle, vasoconstriction, vascular, vasodilation, vasopressin

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Abstract:

Arginine vasopressin (hereafter referred to as vasopressin), also known as antidiuretic hormone, is essential for survival, as attested by its teleologic persistence. Oxytocin- and vasopressin-like peptides have been isolated from four invertebrate phyla and the seven major vertebrate families, representing more than 120 species [1]. Therefore, the ancestral gene encoding the precursor protein appears to antedate the divergence of the vertebrate and invertebrate families, about 700 million years ago [2]. Virtually all vertebrate species possess an oxytocin-like and a vasopressin-like peptide, and so two evolutionary lineages can be traced. The presence of a single peptide, vasotocin ([Ile3]-vasopressin or [Arg8]-oxytocin), in the most primitive cyclostomata supports the notion that primordial gene duplication with subsequent mutations gave rise to the two lineages [2].Vasopressin is essential for cardiovascular homeostasis. The vasopressor effect of pituitary extract, first observed in 1895, was attributed to the posterior lobe of this gland [3]. It was not until 18 years later that the antidiuretic effect of neurohypophyseal extract was demonstrated [4,5]. After isolation and synthesis of vasopressin in the 1950s, it was proven that the same hormone in the posterior pituitary possessed both antidiuretic and vasopressor effects [6,7]. The importance of vasopressin in osmotic defense is fundamental. Indeed, the antidiuretic effect of vasopressin has been exploited clinically for over half a century to treat diabetes insipidus. Only recently has vasopressin emerged as a therapy for shock states, renewing interest in the cardiovascular effects of vasopressin.Shock states induce an increase in vasopressin levels from 20- to 200-fold [8-12]. These supraphysiologic levels cause profound vasoconstriction and help to maintain end-organ perfusion [13,14]. Prolonged shock is associated with a fall in vasopressin levels [15-18], probably due to depletion of vasopressin stores

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