Abstract
Both the antidiuretic (volume) and vasoconstrictor (pressor) action of vasopressin can be considered as important biological properties in maintaining blood pressure [12]. These physiological effects are mediated by two different types of receptors; renal receptors coupled to adenylate cyclase mediating antidiuretic action, and vascular receptors coupled to a calcium dependent mechanism mediating vasoconstriction. The pressor action of vasopressin, previously thought to be a pharmacological effect, has recently been shown to be physiologically important in blood pressure homeostasis [20, 12]. Vasopressin was shown in vitro to be the most powerful vasoconstrictor agent known, more potent even than angiotensin [2]. Low infusion rates of vasopressin which produce plasma levels that are close to the physiologic range can elevate blood pressure [33, 27]. Several authors have recently provided evidence that vasopressin plays a crucial and quantitative role in maintaining blood pressure after haemorrhage [15, 10] or dehydration [1, 3]. Furthermore the vasoconstrictor properties of vasopressin have been considered to be important in the pathophysiology of various forms of experimental hypertension [12]. However, elevation of the blood pressure by vasopressin in vivo is limited by secondary compensatory mechanisms, including a direct negative chronotropic effect, modulation of the baroreceptor reflex, the modulation of autonomic nervous system and inhibition of renin release from the kidney by the vasopressin. Thus, vasopressin can influence blood pressure by several different mechanisms including an action on the central nervous system, modulation of the baroreceptor reflex or by potentiating the action of the sympathetic nervous system, catecholamines and other vasoactive hormones as well as direct vasoconstriction of the vasculature.
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Imai, Y., Nolan, P.L., Johnston, C.I. (1984). Role of Vasopressin in Blood Pressure Regulation Through its Modulatory Effect on Baroreceptor Reflex. In: Sambhi, M.P. (eds) Fundamental Fault in Hypertension. Developments in Cardiovascular Medicine, vol 36. Springer, Dordrecht. https://doi.org/10.1007/978-94-009-5678-0_19
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DOI: https://doi.org/10.1007/978-94-009-5678-0_19
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