INTERACTIONS BETWEEN VASOPRESSIN AND BAROREFLEX CONTROL OF THE SYMPATHETIC NERVOUS-SYSTEM

1. In addition to its effects at the renal tubules to influence water retention and at vascular smooth muscle to cause vasoconstriction, the hormone arginine vasopressin also appears to modulate cardiovascular reflex control of the sympathetic nervous system. Infusion or endogeno us release of vasopressin results in enhanced baroreflex sympatho-inhi bitory responses compared with other pressor agents. In addition, when changes in arterial pressure are imposed on an elevated background le vel of circulating vasopressin, due either to infusion or endogenous r elease, the arterial baroreflex response is shifted to lower pressures , and the maximum sympatho-excitation to a decrease in pressure is red uced. 2. Evidence suggests that vasopressin may influence cardiovascul ar reflex function at multiple sites. Nevertheless, the primary site i nvolved in the effects of circulating vasopressin on baroreflex functi on appears to be in the central nervous system, specifically in the ar ea postrema. Lesion of the area postrema abolishes the ability of circ ulating vasopressin to modulate arterial baroreflex and cardiopulmonar y reflex function and electrical or chemical stimulation of this circu mventricular organ mimics the effects of vasopressin. In addition, vas opressin has been shown to influence the activity of area postrema neu rons in vivo and in vitro. Although not all studies agree, the effects of tile area postrema and vasopressin an cardiovascular reflex functi on appear to be dependent on afferent input from peripheral barorecept ors. 3. Most evidence suggests that vasopressin exerts its effects on baroreflex function through a V-1 vasopressin receptor mechanism. Syst emic administration or microinjection into the area postrema of a spec ific V-1 receptor antagonist abolishes the action of arginine vasopres sin on arterial baroreflex and cardiopulmonary reflex control of the s ympathetic nervous system. 4. The ability of vasopressin and the area postrema to influence baroreflex function appears to be dependent on a n alpha(2)-adrenoceptor mechanism at the level of the nucleus tractus solitarius (NTS). Blockade of alpha(2)-adrenoceptors in the NTS abolis hes the effects of vasopressin and the area postrema on the sympatheti c nervous system. Facilitation of NTS processing of baroreceptor affer ent inputs by the area postrema could contribute to the enhanced sympa tho-inhibition and shift of the baroreflex curve to lower pressures du ring elevations in circulating vasopressin.