AJP - Renal Physiology, Vol 258, Issue 4 1096-F1099, Copyright © 1990 by American Physiological Society
Role of prostaglandins in the renal response to calcium infusion
V. Lahera, M. J. Fiksen-Olsen and J. C. Romero
Department of Physiology and Biophysics, Mayo Clinic, Rochester, Minnesota 55905.
The effects of intrarenal infusions of calcium gluconate (10 and 100
micrograms Ca.kg-1.min-1) on renal hemodynamics and on renal excretory
function were studied in anesthetized mongrel dogs. In one group, the two
doses of calcium were infused for 30 min each (1 ml/min). In a second
group, the same doses were administered 30 min after the start of an
infusion of prostaglandin (PG) inhibitors (intrarenal indomethacin, 10
micrograms.kg-1.min-1, or intravenous bolus injection of meclofenamate, 5
mg/kg). No change with physiological significance was observed during the
infusion of 10 micrograms Ca.kg-1.min-1. However, the infusion of 100
micrograms Ca.kg-1.min-1 induced increases (P less than 0.05) in glomerular
filtration rate (50%), sodium excretion rate (180%), and fractional
excretion of sodium (160%), with respect to control precalcium values. All
these changes were prevented by the concurrent administration of PG
synthesis inhibitors. Urinary PGE2 and 6-keto-PGF1 alpha increased 220 and
85%, respectively, during the infusion of 100 micrograms Ca.kg-1.min-1, but
both decreased (P less than 0.05) below basal levels during the concurrent
administration of PG synthesis inhibitors. The infusion of 100 micrograms
Ca.kg-1.min-1 decreased (P less than 0.05) renal blood flow by 16% during
the administration of PG synthesis inhibitors. These results suggest that
PGs are mediating the increase in hemodynamic and excretory factors induced
by the intrarenal infusion of 100 micrograms Ca.kg-1.min-1.
