Abstract

A possible link between chemoreceptor activity and kidney function has been demonstrated by several groups (Bardsley and Suggett 1987, Bardsley et al. 1991, Behm et al. 1992, Karim et al. 1987, Honig et al. 1985, Honig 1989, Schmidt et al. 1985). Most of these studies were performed in anaesthetized animals and led to conflicting results with marked differences between hypoxic and pharmacological chemoreceptor stimulation. Hypoxic stimulation of the vascularly isolated carotid bodies resulted in an increase in renal nerve activity (Linden et al. 1981), and in decreases in glomerular filtration rate (GFR), renal blood flow (RBF) and increase in tubular sodium reabsorption (Karim et al. 1987). After sectioning of the renal nerves the same type of chemoreceptor stimulation caused an increase in urinary water and sodium excretion. This shows that the chemoreceptors in the carotid bodies mediate reflex effects on renal function in two ways, one dependent on renal nerves and the other one on the release of one or more hormones. In intact conscious animals it is likely that hypoxic chemoreceptor stimulation activates the neuronal sympathetic pathway thereby masking the humoral axis. As a net result there is antidiuresis and antinatriuresis (Behm 1991).KeywordsSham OperateMean Arterial Blood PressureCarotid BodyRenal NerveTubular Sodium ReabsorptionThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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