Response of isolated Dahl rat kidney to calcium antagonists.
We studied the responses of isolated perfused kidneys from prehypertensive, salt-sensitive (DS) and salt-resistant (DR) Dahl rats to nitrendipine or verapamil, after norepinephrine vasoconstriction. The perfusion pressure was kept constant. Superimposition of these calcium antagonists upon norepinephrine increased DS GFR by 155% and DR GFR by 58% (P = 0.03), with verapamil increasing the GFR more than nitrendipine (P = 0.02). Nitrendipine and verapamil also partially reversed norepinephrine induced increases in renal vascular resistance, but did not decrease vascular resistance or increase GFR in the absence of norepinephrine. During the increase in GFR produced by calcium antagonists, DR sodium excretion increased, but DS sodium excretion did not. Therefore, calcium antagonists disproportionately increased DS kidney GFR but did not correct DS kidney sodium retention. These data raise the possibility that the DS rat kidney possesses an abnormality of cell calcium regulation affecting glomerular dynamics, and provide evidence that the renal perfusion pressure is more critical than the GFR in adjusting DS rat sodium-excretion.
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D004351:Drug Resistance; D005919:Glomerular Filtration Rate / Q000187:drug effects; D066298:In Vitro Techniques; D007668:Kidney / Q000187:drug effects* / Q000502:physiology; D008297:Male; D009568:Nitrendipine / Q000494:pharmacology*; D010477:Perfusion; D051381:Rats; D012964:Sodium / Q000378:metabolism; D012965:Sodium Chloride / Q000494:pharmacology; D014700:Verapamil / Q000494:pharmacology*
D012965:Sodium Chloride; D009568:Nitrendipine; D012964:Sodium; D014700:Verapamil; D002118:Calcium