T HE renal sympathetic nerve plays an important role in renal tubular electrolyte reabsorption and renovascular tone.'-2 Low frequency stimulation of the rat renal nerve causes an a,-adrenergic receptor-mediated increase in tubular sodium and water reabsorption.3 -3 Higher frequency renal nerve stimulation results in renovasoconstriction mediated by a,-adrenergic receptors. 5 -8 In light of the influence of the sympathetic nervous system on sodium and water reabsorption and renovascular tone, the potential importance of the renal nerve in the pathogenesis of experimental hypertension is well recognized.9 -10 Particularly compelling is evidence that efferent renal nerve activity is elevated andjunctional norepinephrine release is enhanced Received February 6, 1987; accepted March 29, 1988. in spontaneously hypertensive rats (SHR) when compared with Wistar-Kyoto rats (WKY) 13 and that renal denervation delays the onset of genetic hypertension. -16 Very recent evidence suggests that neuronal reflexes are impaired in SHR kidneys.17 Since a,-adrenergic receptors mediate important functions of the renal nerve, we hypothesize that this adrenergic receptor subtype plays an integral role in the pathogenesis of hypertension in SHR. Interestingly, it was recently reported 18 that renal membrane a,-adrenergic receptor density is increased in SHR compared with WKY.These findings suggest that a,-adrenergic receptor regulation is defective in SHR, since the receptors fail to down-regulate (and, in fact, are increased in density) under conditions of increased sympathetic nerve activity (and hence, increased junctional norepinephrine concentration or turnover, or both). It has thus been proposed 18 that this defect is responsible for enhanced sodium and water reabsorption and increased renovascular tone in SHR.

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