α₁-adrenergic receptor binding in the spontaneously hypertensive rat

Increased sympathetic outflow from the central nervous system to the periphery may contribute to the initiation of hypertension in spontaneously hypertensive rats (SHR). As this alteration in sympathetic activity may be mediated in part by α₁-adrenergic receptors in the central nervous system, the current study examined aradrenergic receptors in various brain areas of SHR and normotensive Wistar-Kyoto control rats (WKY). The α₁-adrenergic receptor number and apparent affinity constants of brain sections of both young prehypertensive animals (4 weeks old) and mature hypertensive animals (12 weeks old) were studied with the α₁-adrenergic receptor antagonist [³H]WB-4101 to label the α -adrenergic receptor. Five brain regions were studied: rostral hypothalamus, caudal hypothalamus, locus ceruleus, nucleus tractus solitarius, and frontal cortical poles. In comparison to normotensive controls, mature hypertensive rats had a significantly greater density (p < 0.05) of the α₁-radrenergic receptors in the rostral hypothalamus (+ 11%), caudal hypothalamus (+ 25%), and frontal cortical poles (+ 20%). Significantly greater (p < 0.05) α₁- aradrenergic receptor density was found in the rostral hypothalamus (+ 27%), caudal hypothalamus (+ 60%), and locus ceruleus (+ 39%) of the young prehypertensive SHR compared with age-matched WKY, These results indicate the presence of altered adrenergic receptor systems in the brains of genetically hypertensive animals and suggest that changes in the receptor systems take place during establishment of the hypertension.