Modulation of renal adrenergic effector mechanisms by calcium entry blockers.
Micropuncture studies in anesthetized Munich-Wistar rats were undertaken to investigate the effects of calcium channel blockade on the glomerular hemodynamic responses to 3-Hz renal nerve stimulation. Stimulation alone increased afferent and efferent arteriolar resistances by 85 and 35%, respectively. Because of these increases both single nephron plasma flow and glomerular capillary hydrostatic pressure difference fell to levels significantly below control, leading to a 26% reduction in single nephron filtration rate (P less than 0.005). These changes, however, were largely attenuated during calcium channel blockade (verapamil, nifedipine). Single nephron filtration rate was only decreased by 14% (P less than 0.05) due to a reduction in single nephron plasma flow. The role of angiotensin II on the residual vasoconstrictive effect of stimulation was also investigated. Pretreatment with an angiotensin-converting enzyme inhibitor (MK 421) of rats infused with verapamil abolished the residual vasoconstriction. The data suggest that calcium influx is an important step for the vasoconstrictive effects of the renal nerves. Additionally, angiotensin II contributes to increased vascular resistance during renal nerve stimulation via a separate, calcium channel mechanism.
D000320:Adrenergic Fibers / Q000502:physiology*; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000502:physiology*; D004558:Electric Stimulation; D005919:Glomerular Filtration Rate; D007668:Kidney / Q000294:innervation; D007678:Kidney Glomerulus / Q000098:blood supply / Q000187:drug effects / Q000502:physiology*; D008297:Male; D009543:Nifedipine / Q000494:pharmacology; D051381:Rats; D014655:Vascular Resistance; D014700:Verapamil / Q000494:pharmacology
D000804:Angiotensin II; D014700:Verapamil; D009543:Nifedipine; D002118:Calcium