Hypothalamic #2-Adrenoceptor Control of Renal Sympathetic Nerve Activity and Urinary Sodium Excretion in Conscious, Spontaneously Hypertensive Rats

The contributions of /Si-, B -̂, and a2-adrenoceptors in the posterior hypothalamus to the increased renal sympathetic nerve activity and decreased urinary sodium excretion resulting from environmental stress (air jet) in conscious spontaneously hypertensive rats were examined. Air stress increased mean arterial pressure and renal sympathetic nerve activity (54% from 7.0 ± 0.7 integrator resets/min), and decreased urinary sodium excretion (44% from 2.7 ± 0.4 ̂ Eq/min per 100 g body weight). After bilateral injection of ICI 118,551 OS2-adrenoceptor antagonist) into the posterior hypothalamus of the same spontaneously hypertensive rats, air stress had no effect on renal sympathetic nerve activity (8% from 4.8 ± 0.7 integrator resets/min) or urinary sodium excretion (2% from 5.2 ± 0.8 /lEq/min per 100 g body weight), but still increased mean arterial pressure. Bilateral injection of isoproterenolol (/9-adrenoceptor agonist) into the posterior hypothalamus enhanced the renal sympathetic nerve activity and urinary sodium excretion (but not mean arterial pressure) responses to air stress. Air stress had no effect on renal sympathetic nerve activity or urinary sodium excretion when ICI 118,551 was given into the posterior hypothalamus before isoproterenol. Atenolol (/Ji-adrenoceptor antagonist) had no effect on the renal responses to air stress when given alone or before isoproterenol. Similarly, ICI 118,551 administered into the lateral hypothalamus or lateral cerebral ventricle, or guanabenz (a2-adrenoceptor agonist) given into the posterior hypothalamus, had no effects on the renal or mean arterial pressure responses to air stress. Thus, /32-adrenoceptors in the posterior hypothalamus mediate the increased renal sympathetic nerve activity and antinatriuresis resulting from environmental stress in conscious spontaneous hypertensive rats. (Circ Res 58: 241-248, 1986)