ABSTRACT
We examined the factors regulating potassium excretion (UKV) in anesthetized, mechanically ventilated, mineralocorticoid-injected dogs undergoing acute unilateral nephrectomy (AUN). In control dogs, AUN caused both sodium excretion (UNaV) and UKV to increase in association with an increase in bicarbonate excretion (UHCO3V) but no change in chloride excretion (UClV). In dogs made acutely acidotic by intravenous infusion of dilute HCl, AUN led to comparable increase in UNaV and UKV, but with increased UClV and only a trivial change in UHCO3V. In dogs in which prostaglandin synthesis was inhibited by indomethacin or meclofenamate, AUN led to an increase in UKV but without any increase in UNaV or UHCO3V. The fractional excretion of potassium rose significantly and comparably in all groups. Our results indicate that the post-nephrectomy kaliuresis occurs without change in respiratory acid-base status or mineralocorticoid hormone activity, and can be dissociated from increased UHCO3V and, probably, increased delivery of fluid out of the proximal tubule. They therefore suggest a specific and potent effect of AUN to stimulate UKV through an increase in plasma potassium concentration or through some as yet undetermined mechanism.
