Role of Central and Peripheral Adrenergic Mechanisms in Neurogenic Hypertension Produced by Brainstem Lesions in Rat

Abstract

Bilateral lesions of the nucleus tractus solitarius (NTS) in rats result in acute fulminating hypertension (NTS hypertension) as a consequence of central deafferentation of baroreceptors. The hypertension is due to increased peripheral resistance and decreased cardiac output. The hypertension is blocked and cardiac output is increased by phentolamine, trimethaphan (Arfonad), and reserpine but not by propranolol. In the present experiment, systemically administered 6-hydroxydopamine (6-OH-DA) did not alter NTS hypertension if the adrenal glands were intact. Adrenalectomy, however, blocked the lesion-induced rise in blood pressure in 6-OH-DA-treated rats. Intracisternally administered 6-OH-DA (600 µg) lowered the concentration of norepinephrine only in the spinal cord and blocked the development of NTS hypertension. Local injection of 6-OH-DA into the lateral hypothalamus did not affect the hypertension. Injection of 6-OH-DA into the NTS resulted in a mild, transient elevation in blood pressure. The results of these experiments demonstrate that (1) NTS hypertension is due to increased sympathetic neural discharge, (2) during NTS hypertension sufficient adrenomedullary catecholamines are released to produce hypertension when sympathetic terminals are destroyed, (3) central noradrenergic neurons participate in the expression of NTS hypertension, and (4) baroreceptors can inhibit the release of adrenal catecholamines.