Nitrendipine and the pressure-dependent vasodilation of vessels in the hydronephrotic kidney.
The influence of renal perfusion pressure on the vasodilation of the kidney caused by a calcium antagonist, nitrendipine, was studied. The diameter of several preglomerular and postglomerular vessels in the split hydronephrotic kidney of Inactin-anesthetized rats were measured by in vivo television microscopy. A reduction in the renal perfusion pressure to 80 mm Hg (femoral artery pressure) was achieved by clamping of the aorta above the renal arteries. The pressure reduction induced vasodilation of the arcuate arteries (proximal and distal), interlobular arteries (proximal and distal), and the afferent arterioles near the interlobular arteries. The afferent arterioles at sites near the glomerulus showed no pressure-dependent vasodilation. Topically applied nitrendipine led to a dose-dependent preglomerular vasodilation that did not further increase during perfusion pressure reduction. From these experiments, it is concluded that nitrendipine-induced renal vasodilation is independent of the renal perfusion pressure and primarily caused by its direct effect on preglomerular vessels.
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure; D004305:Dose-Response Relationship, Drug; D005260:Female; D006869:Hydronephrosis / Q000503:physiopathology*; D007668:Kidney / Q000503:physiopathology; D009568:Nitrendipine / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D012079:Renal Circulation / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects*
D009568:Nitrendipine; D000109:Acetylcholine