title: Function of the hypertensive kidney during calcium flux manipulation.
abstract: 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.
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002120:Calcium Channel Agonists / Q000494:pharmacology*; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D006973:Hypertension / Q000503:physiopathology*; D007668:Kidney / Q000503:physiopathology*; D051381:Rats; D013045:Species Specificity
chemical_list: D002120:Calcium Channel Agonists; D002121:Calcium Channel Blockers; D002118:Calcium