The reactions of renal hemodynamics, as well as of excretory and concentrating function (clearance-technique) in response to arterial chemoreceptor stimulation by almitrine bismesylate were studied in 3 groups of chloralosed, relaxed, and constantly ventilated cats. In 2 groups of chemoreceptor-intact animals an osmotic diuresis was induced by intravenous infusion of an isoionic solution containing equivalent amounts of either sorbitol or mannitol. Under similar conditions the 3rd series of experiments was carried out in cats under mannitol diuresis but with deafferented arterial chemoreceptors. The changes of mean arterial and central venous pressures as well as of the parameters of the arterial acid-base balance were similar in all groups of cats studied. The chemoreceptor-intact animals undergoing sorbitol diuresis did not show any natriuresis in response to the drug but reacted with a remarkable increase in their U/Posm and TCH2O/Cosm ratios. In contrast, the chemoreceptor-intact animals infused with mannitol in saline reacted to almitrine with a transient natriuresis but with only a weak increase in their U/Posm and TCH2O/Cosm ratios. The data suggest that arterial chemoreceptor stimulation inhibits proximal tubular sodium reabsorption. In the sorbitol-experiments during chemoreceptor stimulation the enhanced delivery of sodium by the proximal fluid was reabsorbed in the thick ascending limb of Henle's loop thus increasing medullary osmolality and renal concentrating ability. Mannitol apparently limited this additional sodium reabsorption in the thick ascending limb of Henle's loop; therefore in the mannitol-experiments during chemoreceptor stimulation a natriuresis but only relatively weak changes of renal concentrating function occurred. The data also suggest that a pharmacological chemoreceptor stimulation might support the recovery of renal excretory function post-anaesthetically, although the optimal solution infused to induce an osmotic diuresis remains to be determined.
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