Preoptic recess noradrenergic receptors control modification of baroreflexsensitivity by hypertonicity

These studies examined the effects of alpha(1)- and alpha(2)-adrenoreceptor blockade in the anteroventral portion of the third cerebral ventricle (AV3 V) on modification of baroreflex-induced changes in heart rate and renal sy mpathetic nerve activity (RSNA) induced by hyperosmolality. Local administr ation of hypertonic artificial cerebrospinal fluid (aCSF) in the AV3V signi ficantly increased baroreflex-induced bradycardia during intravenous phenyl ephrine but did not alter changes in RSNA during the presser response or al ter tachycardia and neural responses evoked by decreased blood pressure. Th e enhanced cardiac response was not observed during simultaneous administra tion of phentolamine (alpha(1)- and alpha(2)-antagonist) or yohimbine (sele ctive alpha(2)-antagonist) in the AV3V region. However, treatment with praz osin (alpha(1)-antagonist) did not alter the exaggerated cardiac response e voked by hypertonic aCSF to increased blood pressure. These data demonstrat e that acute, local hypertonic stimulation in the AV3V region selectively e nhances baroreflex-induced bradycardia by stimulation of alpha(2)-adrenergi c receptors during acute plessor responses.