We examined the effect of ␣2-adrenoreceptor blockade in the nucleus of the solitary tract (NTS) on baroreflex responses elicited by electrical stimulation of the left aortic depressor nerve (ADN) in urethane-anesthetized spontaneously hypertensive rats (SHR, n ϭ 11) and normotensive Wistar-Kyoto rats (WKY, n ϭ 11). ADN stimulation produced a frequencydependent decrease in mean arterial pressure (MAP), renal sympathetic nerve activity (RSNA), and heart rate (HR). In SHR, unilateral microinjection of idazoxan into the NTS markedly reduced baroreflex control of MAP, RSNA, and HR and had a disproportionately greater influence on baroreflex control of MAP than of RSNA. In WKY, idazoxan microinjections did not significantly alter baroreflex function relative to control vehicle injections. These results suggest that baroreflex regulation of arterial pressure in SHR is highly dependent on NTS adrenergic mechanisms. The reflex regulation of sympathetic outflow to the kidney is less influenced by the altered ␣ 2-adrenoreceptor mechanisms in SHR.hypertension; medulla; norepinephrine IN HYPERTENSION, the arterial baroreflex is often characterized by a decrease in reflex sensitivity and/or a resetting of reflex function to higher than normal pressures (9,10,15,31,34). In the spontaneously hypertensive rat (SHR), for example, resting blood pressure may be 40-60 mmHg higher than in normotensive rats, and the sigmoid curve describing baroreflex control of mean arterial pressure (MAP) and sympathetic nerve activity is shifted upward but remains parallel to the normal baroreflex curve (9,12,38). In contrast, baroreflex control of heart rate (HR) is markedly attenuated in the SHR (2, 15, 21, 34), despite a resting HR that is comparable to that of its normotensive control, the Wistar-Kyoto rat (WKY). Because baroreflex impairment is present in many forms of hypertension and may contribute to the development and maintenance of the disease (9,10,15,31,34), an understanding of the neurochemical mechanisms involved is of great importance. Neurochemical derangements in hypertension might alter afferent and efferent signaling or integration of baroreceptor information within the central nervous system.In the brain, the medial nucleus of the solitary tract (NTS) in the caudal medulla is the primary central termination site for baroreceptor afferents (16). The integrity of this region is necessary for normal baroreflex control of blood pressure (29). In the SHR and other rat models of hypertension with altered baroreflex function, declines in norepinephrine content and ␣ 2 -adrenoreceptor density within the NTS have been documented (27,33,36,37). Because selective blockade of ␣ 2 -adrenoreceptors in the medial NTS of normotensive subjects can increase resting blood pressure and attenuate baroreflex function (19,30,35), this decline in ␣ 2 -adrenoreceptor density in the NTS of hypertensive animals has been hypothesized to contribute to autonomic dysfunction in these animals. However, the physiological impact of these neurochemical changes o...