Renal hemodynamics and excretory function of healthy young men during stimulation of their peripheral arterial chemoreceptors by almitrine bismesylate.

Renal hemodynamics and excretory function were studied using clearance-techniques in 13 healthy, normotensive, normoxic young men undergoing moderate osmotic diuresis. Each subject was measured in two experiments both lasting from 7:30 a.m. to 6:00 p.m. In one of them 50 mg almitrine bismesylate (Vectarion) was ingested at 12:00 o'clock, whereas the other test served as control. There were only negligible changes of the parameters measured in the control experiments. Immediately after ingestion of the drug a renal vasodilation occurred, but 2-3 h later renal hemodynamic resistance tended to increase. Urinary sodium excretion rose after administration of almitrine. Initially this increase seemed to be caused by the kidney vasodilation but between the 3rd and 6th hour after giving the agent a natriuresis occurred that resulted from inhibition of renal tubular sodium reabsorption. The maximum of this renal tubular response was apparently not reached at the end of the experiments, i.e. 6 h after oral administration of the drug. Almitrine did not increase the renal potassium excretion. The data indicate that pharmacological stimulation of the peripheral arterial chemoreceptors by almitrine bismesylate in normoxic healthy humans causes reflectorically a slight renal vasoconstriction and a long-lasting inhibition of renal tubular sodium reabsorption. These findings are in good agreement with previously published data obtained in animal experiments.