K+ deprivation potentiates the renal alkalosis-producing effect of mineralocorticoid

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Abstract
In the dog K+ deprivation alone does not result in metabolic alkalosis but potentiates the alkalosis-producing effect of superphysiologic amounts of mineralocorticoid hormone. To investigate the mechanism of this potentiating effect the renal response to chronic administration of superphysiologic amounts of deoxycorticosterone (DOC) was examined in dogs in which dietary K+ was either normal (NL K, group I) or reduced (LO K, group II). DOC administration resulted in a significantly greater cumulative increase in net acid excretion (NAE) and plasma [HCO3-] in the LO K group. The maximum difference between groups in daily NAE occurred on day 1 and the difference was due to a greater excretion of both titratable acid and NH4+. The exaggerated NH4+ excretory response appeared to be due in part to enhanced renal production of NH3 caused by LO K, which was evidenced by greater pre-DOC NH4+ excretion unaccounted for by lower values of urine pH. But LO K also appeared to enhance the stimulatory effect of DOC on H+ secretion independent of augmented renal NH3 production. Following DOC (day 1) a greater reduction in urine pH occurred in the LO K group despite the greater availability of NH3 for titration of secreted H+. The absolute value of urine pH following DOC was greater in the LO K group despite a greater urinary content of buffer (NH3). LO K apparently augments the NAE response to DOC in part by enhancing the urine pH-lowering effect of the hormone. The exaggerated NAE response was not associated with either an exaggerated Na+ reabsorptive response or an attenuated K+ excretory response. The Cl- reabsorptive response was attenuated and this attenuation conceivably contributes to the enhanced urine pH-lowering effect of DOC in LO K by limiting Cl- shunting of mineralocorticoid-dependent luminal negativity.