α 2-Adrenoceptors in amygdala control renal sympathetic nerve activity and renal function in conscious spontaneously hypertensive rats

Abstract

The contributions of α 2-andβ 2-adrenoceptors in the central amygdaloid nucleus to the increased renal sympathetic nerve activity and decreased urinary sodium excretion resulting from environmental stress (air jet) in conscious spontaneously hypertensive rats (SHR) were examined. Air stress increased mean arterial pressure and renal sympathetic nerve activity (47% from 9.3 ± 0.8 integrator resets/min), and decreased urinary sodium excretion (38% from 2.4 ± 0.3 μEq/min/100 g b. wt.). After bilateral administration of guanabenz (2 × 2.5 μg) (α 2-adrenoceptor agonist) into the central amygdaloid nucleus of the same SHR, air stress had no effect on renal sympathetic nerve activity (+7% from 7.5 ± 0.8integrator resets/min) or urinary sodium excretion (+5% from 3.5 ± 0.4 μEq-/min/100 g b. wt.), but still increased mean arterial pressure. These effects of guanabenz were prevented by the prior bilateral administration of the α 2-adrenoceptor antagonist, rauwolscine (2 × 15 μg), into the central amygdaloid nucleus; rauwolscine alone had no effect on the renal responses to air stress in SHR. Guanabenz in the lateral cerebral ventricle (2 μg), the basolateral amygdaloid nucleus (2 × 2.5 μg) or a site dorsal to the central amygdaloid nucleus in the area of globus pallidus (2 × 2.5 μg) had no effect on the renal sympathetic nerve activity or urinary sodium excretion responses to air stress. Similarly, ICI 118.551 (2 × 1 μg; β 2-adrenoceptor antagonist) in the central amygdaloid nucleus had no effect on the renal responses to air stress. In conclusion, stimulation of α 2-adrenoceptors in the central amygdaloid nucleus prevents the increased renal sympathetic nerve activity and antinatriuresis resulting from air stress in conscious SHR.