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Biomedical subjects

J R Gill

Publications and source records attributed to J R Gill.

114 records · Page 7Linked to original sources
PubMedDate not supplied

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.

Acetylcholine↗
PubMedDate not supplied

Role of prostacyclin in the renal response to acetylcholine.

Renal arterial infusion of acetylcholine (ACh; 40 micrograms/min) in control dogs produced a sustained rise in urinary sodium excretion (UNa V) and in renal plasma flow (RPF). When prostaglandin (PG) synthesis was inhibited with indomethacin (5 mg/kg), ACh produced only a transient rise in UNa V and RPF followed by a progressive decline in UNa V and RPF. Renal arterial infusion of PGI2 (0.2 microgram/min) restored the response to ACh to normal in indomethacin-treated dogs. The RPF was 84 +/- 9 ml/min during control and increased to 132 +/- 19 ml/min with the infusion of PGI2 (p < 0.01). RPF increased further to 188 +/- 18 ml/min at 20-min infusion of ACh and was maintained at 189 +/- 14 ml/min at 100-min infusion of ACh (p < 0.01). Our data suggest that the initial rise in RPF by ACh is independent of the PG system, whereas maintenance of the rise in RPF by ACh requires an intact synthesis of PGs, presumably PGI2 synthesized in the vascular tissues.

Acetylcholine↗