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Na + dependence of K + ‐induced natriuresis, kaliuresis and Na + /Cl − cotransporter dephosphorylation
Author(s) -
Jensen I. S.,
Larsen C. K.,
Leipziger J.,
Sørensen M. V.
Publication year - 2016
Publication title -
acta physiologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.591
H-Index - 116
eISSN - 1748-1716
pISSN - 1748-1708
DOI - 10.1111/apha.12707
Subject(s) - kaliuresis , natriuresis , endocrinology , medicine , chemistry , dephosphorylation , excretion , cotransporter , biochemistry , sodium , phosphorylation , organic chemistry , phosphatase
Abstract Aim High dietary K + intake is associated with protection against hypertension. In mammals, acute K + intake induces natriuresis and kaliuresis, associated with a marked dephosphorylation of the renal Na + /Cl − cotransporter ( NCC ). It has been suggested that reduced activity of NCC increases the driving force for more distal tubular epithelial Na + channel ( EN aC)‐dependent K + secretion. This study investigated the EN aC dependence of urinary K + and Na + excretion following acute K + loading. Methods Mice were fed low (0.03%), control (0.2%) or high (2%) Na + diets for 25 days to preserve or promote Na + loss and thus EN aC activity. Once a week, the mice received either K + ‐containing gavage or a control gavage. Following the gavage treatment, the mice were placed in metabolic cages and urine was collected in real time. EN aC dependence of kaliuresis was assessed by benzamil injections prior to gavage. Results We confirmed that dietary Na + content is inversely related to plasma aldosterone, NCC phosphorylation and EN aC cleavage products. The novel findings were as follows: (i) acute K + feeding caused NCC dephosphorylation in all dietary groups; (ii) under all dietary conditions, K + loading induced natriuresis; (iii) high Na + diet markedly reduced the K + excretion following K + gavage; (iv) benzamil injection prior to K + loading increased natriuresis, decreased kaliuresis and eliminated the differences between the dietary groups. Conclusion These data indicate that acute K + ‐induced kaliuresis is EN aC dependent. Maximal K + excretion rates are attenuated when EN aC is physiologically down‐regulated or pharmacologically blocked. NCC is dephosphorylated following acute K + loading under all dietary Na + regimens. This leads to natriuresis, even in severely Na + ‐restricted animals.