title: Cardiorespiratory and renal responses to arterial chemoreceptor stimulation in early hypertension.
abstract: The peripheral arterial chemoreceptors (PAC) modify not only cardiorespiratory but also renal hemodynamic and excretory function. There is evidence that in hypertensive animals and humans the reflectoric actions of the PAC on ventilation and circulation differ from those of normotensive subjects. However, the influence of these receptors on kidney function of hypertensive subjects is poorly understood. Cardiorespiratory and renal responses to pharmacological stimulation of PAC by almitrine bismesylate during normoxia were measured in 16 normotensive (NT) and 13 age-matched borderline-hypertensive young men (BHT) undergoing water diuresis. Placebo experiments served as time controls in each subject. NT reacted to almitrine with significant rises in heart rate, minute ventilation, and filtration fraction. Renal vascular resistance tended to increase slightly. In BHT the drug caused a significant rise in heart rate and minute ventilation too, however, this reaction had a longer latency when compared to NT. In contrast to NT, filtration fraction, and renal vascular resistance decreased. Renal fractional sodium and lithium excretion did not show any clear response to almitrine in NT, but decreased in BHT. The results suggest that the weaker ventilatory response in BHT vs. NT might indicate a lower reactivity of their PAC to almitrine. The different reactions of the renal vascular bed to pharmacological chemoreceptor excitation in mild hypertensives might result from a different reactivity of the renal arterioles, whereas the enhanced proximal tubular sodium reabsorption could be due to an exaggerated increase in efferent renal nerve activity.
authors.affiliation: Institute of Physiology, Ernst-Moritz-Arndt University of Greifswald, Germany.
authors.forename: C
authors.initials: C
authors.lastname: Ledderhos
authors.forename: H
authors.initials: H
authors.lastname: Brauer
authors.forename: A
authors.initials: A
authors.lastname: Gens
authors.forename: R
authors.initials: R
authors.lastname: Sanchez
authors.forename: W
authors.initials: W
authors.lastname: Quies
authors.forename: R
authors.initials: R
authors.lastname: Schuster
authors.forename: A
authors.initials: A
authors.lastname: Honig
mesh_terms: D000328:Adult; D015765:Almitrine / Q000494:pharmacology; D001158:Arteries / Q000187:drug effects / Q000648:ultrastructure; D001794:Blood Pressure / Q000187:drug effects; D002319:Cardiovascular System / Q000187:drug effects / Q000503:physiopathology* / Q000648:ultrastructure; D002628:Chemoreceptor Cells / Q000187:drug effects* / Q000502:physiology; D004573:Electrolytes / Q000097:blood; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D007668:Kidney / Q000098:blood supply / Q000187:drug effects / Q000502:physiology*; D008297:Male; D012079:Renal Circulation / Q000187:drug effects* / Q000502:physiology; D012137:Respiratory System / Q000187:drug effects / Q000503:physiopathology* / Q000648:ultrastructure; D019141:Respiratory System Agents / Q000494:pharmacology; D013268:Stimulation, Chemical; D014556:Urine
chemical_list: D004573:Electrolytes; D019141:Respiratory System Agents; D015765:Almitrine