Preoptic recess noradrenergic receptors control modification of baroreflex sensitivity by hypertonicity

These studies examined the effects of alpha(1)- and alpha(2)-adrenoreceptor blockade in the anteroventral portion of the third cerebral ventricle (AV3V) on modification of baroreflex-induced changes in heart rate and renal sympathetic nerve activity (RSNA) induced by hyperosmolality. Local administration of hypertonic artificial cerebrospinal fluid (aCSF) in the AV3V significantly increased baroreflex-induced bradycardia during intravenous phenylephrine but did not alter changes in RSNA during the presser response or alter tachycardia and neural responses evoked by decreased blood pressure. The enhanced cardiac response was not observed during simultaneous administration of phentolamine (alpha(1)- and alpha(2)-antagonist) or yohimbine (selective alpha(2)-antagonist) in the AV3V region. However, treatment with prazosin (alpha(1)-antagonist) did not alter the exaggerated cardiac response evoked by hypertonic aCSF to increased blood pressure. These data demonstrate that acute, local hypertonic stimulation in the AV3V region selectively enhances baroreflex-induced bradycardia by stimulation of alpha(2)-adrenergic receptors during acute plessor responses.