Abstract

Compelling literature shows that our diets, mostly derived from processed foods, contain a large excess of sodium in detriment of potassium. Diets in Western, industrialized countries, account for an intake of about 120 mmol/sodium and 70 mmol potassium/day. In contrast, non-processed foods such as provided by diets abundant in vegetables and fresh fruits have a positive ratio of potassium over sodium, with a daily potassium intake of aprox 200 and 70-80 mmol of potassium and sodium/day, respectively. The dietary changes from fresh crops to processed or elaborated food cause an unbalance in essential food salts, which among other reasons, favors, or is causally related to, a higher risk and incidence of vascular and heart diseases. Several investigations have observed favorable effects of potassium which reduces resting blood pressure and the risk of stroke and other cardiovascular disease in adults; the mechanism of this effect remains unknown. We hypothesize that the beneficial effects of dietary potassium supplements, is related to an enhanced endothelium-mediated vasodilatation, which includes NO production and its signaling pathway, rather than a reduction in vasopressor mechanism(s). Potassium supplements also include increased protective vascular effects. The increased signaling of vasodilators may be due to an overproduction of the molecules that lead to NO production such as ATP and related nucleotides, kinins, or eicosanoids or to an increased NO intracellular pathway signaling leading to blood vessel dilatation. In this proposal we plan to examine, using the isolated rat arterial mesenteric bed and also isolated endothelial cells from this vascular territory, the production of NO by several stimuli and its functional vascular responses in control or STZ-diabetics rats with and without potassium supplementation. Our proposal focuses on the auto/paracrine role of ATP and related nucleotides, bradykinin and eicosanoids in this vascular bed and on the putative dysfunction of the autocrine role of ATP due to vascular pathology including hypertension or diabetes, among others pathologies.