John C.H. Yun

Effect of bradykinin on renal function in dogs treated with indomethacin or propranolol.

The effect of bradykinin (BK) on renal function was examined in anesthetized dogs with or without treatment with either indomethacin or propranolol. Renal arterial infusion of BK (3 micrograms/min) in control dogs produced a sustained increase in urine flow rate (V), sodium excretion (UNaV), potassium excretion (UKV), and renal plasma flow (RPF) without a consistent change in glomerular filtration rate (GFR) or renin secretion rate (RSR). This increase in salt and water excretion and in RPF could not be blocked with indomethacin (5 mg/kg, followed by 2.1-3.2 mg/kg/h, i.v.). UNaV was 20.8 +/- 7.4 and 123.3 +/- 22.3 muEq/min (mean +/- SEM values) before and after 140 min of infusion of BK (p less than 0.005), respectively. Beta-receptor blockade with propranolol (5 mg/kg, followed by 2.8-3.4 mg/kg/h, i.v.) did not prevent the BK-induced rise in salt and water excretion, or in RPF. UNaV was 26.0 +/- 9.7 and 96.4 +/- 21.5 muEq/min before and after 140 min of infusion of BK (p less than 0.005), respectively. The data suggest that the effects of BK on renal handling of salt and water and on RPF are not mediated by either prostaglandins or beta receptors.

Structural Changes after Infusion of Mannitol in the Cat Kidney

Structural changes after the infusion of mannitol were examined in the kidney of the cat. Infusion of mannitol causes a decrease in the size of the glomerular vascular tuft and an increase in the lumi

Ca2+ Antagonists and db-cAMP Sustain a Rise in Renal Blood Flow Induced by Acetylcholine in Indomethacin-Treated Dogs

Renal arterial infusion of acetylcholine (ACh) in the dog normally produces a sustained rise in sodium excretion (UNaV) and in renal plasma flow (RPF). When prostaglandin (PG) synthesis is inhibited, ACh induces only a transient increase in UNaV and RPF followed by a progressive decline in UNaV and RPF, and a rise in renin secretory rate (RSR). Renal arterial infusion of PGE2 but not a vasodilator such as bradykinin restored the response to ACh to normal in indomethacin (Indo)-treated dogs. During renal arterial infusion of dibutyryl cyclic AMP (6 mg/min), ACh also produced a sustained increase in UNaV and RPF despite an inhibition of PG synthesis by Indo. Renal arterial infusion of verapamil (60 micrograms/min) or diltiazem (60 micrograms/min) also prevented the subsequent fall in RPF when ACh was infused; RSR, however, did not show a rise. The results suggest that synthesis of PGE2 with stimulation of cAMP is required for sustained ACh action. When PGE synthesis is inhibited, ACh may produce renal vasoconstriction by increasing intracellular Ca2+ concentration. The partial effect of calcium channel blockers suggests that release of calcium from intracellular stores as well as calcium entry may mediate the response.