Pérez RA, Barber FMO, González NL, Barber GE, Victorio FM

Language: Spanish
References: 20
Page: 253-267
PDF size: 166.51 Kb.

ABSTRACT

Introduction: Hypertension is responsible for twelve million heart and vascular diseases diagnosed in the world every year. Searching for a single cause is still a challenge for researches. The physiopathology of hypertension involves diverse factors that point toward a polygenic origin, and new drugs arise for its treatment. Methods: Subtherapeutic doses of valsartan (a specific inhibitor of AT-1 receptors of the angiotensin II) were administered to 60 rats with normal blood pressure, and an experimental model of high blood pressure (HBP) was obtained. BP levels were determined in all the animals at the beginning of the experiment and at 20, 35 and 50 days of progress. Such moments corresponded with series A, B and C respectively. Plasmatic concentration, tubular load, reabsorbed and excreted quantity of sodium were determined in experimental and control animals on the 20, 35 and 50 days of the study. Results: BP figures started to rise in the experimental series B and C after the suppression of the drug, from 15 up to 50 days. In the experimental animals of the series B and C the fractional reabsorption of sodium increased and its excretion decreased, together with an increase of systolic pressure figures. This could be related to a hypertrophy of the proximal tubule. Conclusions: The modifications found in the renal exchange of sodium coincided with those expected according to the proposed mechanism of hydrosaline retention in the origin of hypertension in these animals.

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