Function of the hypertensive kidney during calcium flux manipulation

Dihydropyridine calcium channel agonists and antagonists elicit exaggerated glomerular and circulatory responses from kidneys isolated from Dahl rats genetically programmed to develop NaCl-induced hypertension (Dahl S rats). These differential responses are further magnified by NaCl loading. In contrast, "chemical sympathectomy" with 6-hydroxydopamine enhances renal vascular responses to calcium channel agonists in a manner that depends on the antecedent dietary NaCl intake, and is independent of genetic predilection to develop NaCl-induced hypertension. These findings are consistent with the hypothesis that aberrations of vascular and perhaps glomerular calcium entry modulation may be determinants of altered renal hemodynamics in NaCl-sensitive hypertension. The latter may be responsible for the enhanced responsiveness to calcium channel antagonists observed in NaCl-sensitive hypertension in humans.