AJP - Renal Physiology, Vol 252, Issue 4 613-F620, Copyright © 1987 by American Physiological Society
Modulation of renal adrenergic effector mechanisms by calcium entry blockers
J. C. Pelayo
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.
