%0 Journal Article
%T Science Review: Vasopressin and the cardiovascular system part 1 ¨C receptor physiology
%A Cheryl L Holmes
%A Donald W Landry
%A John T Granton
%J Critical Care
%D 2003
%I BioMed Central
%R 10.1186/cc2337
%X 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
%K adrenergic agents
%K antidiurectic hormone
%K cardiac inotropy
%K hypotension
%K nitric oxide
%K oxytocin
%K physiology
%K potassium channels
%K receptors
%K septic shock
%K smooth muscle
%K vasoconstriction
%K vascular
%K vasodilation
%K vasopressin
%U http://ccforum.com/content/7/6/427