Kidney function during arterial chemoreceptor stimulation. III. Long-lasting inhibition of renal tubular sodium reabsorption due to pharmacologic stimulation of the peripheral arterial chemoreceptors with almitrine bismesylate.
The reactions of the mean systemic arterial blood pressure, arterial acid-base balance kidney function (clearance-technique), and plasma aldosterone concentration (radio-immunoassay) elicited by stimulation of the peripheral arterial chemoreceptors with almitrine bismesylate were determined in chloralosed, non-vagotomized, spontaneously breathing cats in moderate mannitol-saline diuresis. The left renal nerves were cut; urine was collected separately from both the innervated and denervated kidneys. Intravenous injection of 0.2 mg/kg of the drug caused the expected long-lasting increase of the pO2 and pH and a decrease of pCO2 in the arterial blood, whereas the mean systemic arterial blood pressure slightly rose by an average of 2-4 mm Hg in the first hour of chemoreceptor stimulation but afterwards considerably decreased below the pre-injection values. The renal responses were characterized by a moderate vasoconstriction particularly in the innervated kidneys and a pronounced increase of sodium and urine excretion especially in the denervated kidneys. The inhibition of renal tubular sodium reabsorption underlying these natriuretic and diuretic reactions was fully demonstrable even at the end of the experiments, i. e. 4 h after the administration of the agent. Plasma aldosterone increased with the time of the experiments but did not show any clear relationships to the activity of the arterial chemoreceptors. The results show that the intravenous injection of almitrine bismesylate is connected with a renal response pattern which is typical for an excitation of the peripheral arterial chemoreceptors, i. e. moderate vasoconstriction (efferently mediated by the renal nerves) and an inhibition of renal tubular sodium reabsorption (efferently mediated by hormonal mechanisms). Furthermore, the data suggest that, on the one hand, under certain conditions these reactions of the kidney function could play the role of undesirable side effects but, on the other hand, the inhibition of renal tubular sodium reabsorption caused by almitrine bismesylate might possibly be used to treat diseases that are connected with a reduced ability of the kidneys to sufficiently excrete sodium.
Honig
A
A
Wedler
B
B
Zingler
C
C
Ledderhos
C
C
Schmidt
M
M
D000450:Aldosterone / Q000097:blood; D015765:Almitrine; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002415:Cats; D000697:Central Nervous System Stimulants / Q000494:pharmacology*; D002628:Chemoreceptor Cells / Q000187:drug effects / Q000502:physiology*; D003714:Denervation; D005260:Female; D005919:Glomerular Filtration Rate / Q000187:drug effects; D007668:Kidney / Q000502:physiology*; D007684:Kidney Tubules / Q000294:innervation / Q000502:physiology*; D007700:Kinetics; D008297:Male; D010879:Piperazines / Q000494:pharmacology*; D012079:Renal Circulation / Q000187:drug effects; D012964:Sodium / Q000378:metabolism*; D014655:Vascular Resistance / Q000187:drug effects
D000697:Central Nervous System Stimulants; D010879:Piperazines; D000450:Aldosterone; D015765:Almitrine; D012964:Sodium