Abstract

The importance placed on dietary potassium on health and disease is underscored compared with dietary sodium, and less effort has been placed on studies on adequate dietary potassium. The benefits of potassium rich-food are known, however, the mechanisms of action are lacking. With the hypotheses that dietary potassium regulates renal sodium excretory hormonal system, we studied the effect of enriched potassium diet on kallikrein (Kall) and cyclooxygenase-2 (COX-2) SD male rats on normal potassium diet (0.9%, NK) or higher potassium diet (3%, HK) for 4 weeks, Kidney tissue was used for study protein (Western blot), mRNA (RT-qPCR), and cell features using immunohistochemistry (IHC). Kall was restricted to connecting tubule cells CNTc, HK increased the CNTc size and immunostaining with an hypertrophied pattern, increased Golgi and secretory-like vesicles. Kallikrein increased its enzyme activity (42±3 vs 27±3 mU, p<0.005), protein by Western blot (1.3 fold p<0.05), and mRNA by qRT-PCR (1.4 fold p<0.05). Kall activity correlated with UV potassium excretion (r=0.66, p<0.001). COX-2 containing cells were restricted thick ascending limb cells TAL, in response to HK was observed a decreased COX-2 cells number, a decreased protein level (0.4 fold p<0.05) and mRNA (0.5 fold p<0.05). There is a different cellular response of CNTc and TAL to higher potassium diet, Kallikrein CNTc respond with hypertrophy and increased synthesis, COX-2 TAL cells respond by decreasing the number of cells, a recruitment phenomenon. Upregulation of Kall is consistent with its vasodilatory, natriuretic effect. Downregulation of COX-2 requires further studies to elucidate its response to potassium.