Abstract

Background: The importance of dietary potassium in health and disease is underscored compared with that placed on dietary sodium. Much effort has been placed on reduction of sodium intake and less on the adequate dietary potassium, although natural food contains 10-15 times more potassium than sodium. The benets of a potassium-rich diet are known, and recent evidence showed that high potassium diet dephosphorylate NCC resulting in acute natriuresis. With the hypothesis that dietary potassium regulates renal sodium excretory hormonal systems at long-term, we studied the effect of high potassium diet on kallikrein (Kall), renin and cyclooxygenase-2 (COX-2).Methods: SD male rats on a normal sodium diet received normal potassium (0.9%, NK) or high potassium diet (3%, HK) for 4 weeks. Urine was collected in metabolic cages for measurement of electrolytes and enzyme activities. Renal tissue was used to analyze protein (Western blot) and mRNA (RT-qPCR) levels, and immunohistochemistry for morphometric analysis.Results: Kall was restricted to connecting tubule cells, HK increased the Kall positive cell size and immunostaining area; cells were hypertrophied with increased Golgi and secretory-like vesicles. Cell changes were associated with increased enzyme activity (p<0.005), increased protein (p<0.05) and mRNA levels (p<0.01). Renin staining was restricted to granular cells of the afferent arteriole; a HK diet decreased the number of renin positive cells and renin mRNA levels (p<0.01). COX-2 containing cells were restricted to a subset of thick ascending limb segment and in response to HK decreased number of COX-2 cells was observed with decreased protein (p<0.01) and mRNA levels (p<0.05). Conclusions: The increased renal kallikrein and decreased renin are consistent with the their contribution to the natriuretic and renoprotective effect of potassium. Downregulation of COX-2 could be compensatory and requires further study.Funding Fondecyt 1130741, CONICYT PIA/Basal PFB12, and CARE-SQM.