The specific aims of the research plan are: 1. To determine whether mild K depletion prevents the development of renovascular hypertension (RVH) and spontaneous hypertension (SHR) and reverses established RVH and SHR. 2. To describe the effect of K depletion on hemodynamics, pressor hormones, plasma volume and AII vascular reactivity in RVH and SHR. 3. To determine whether the protective effect of K depletion is mediated by a defect in angiotensin II (AII) binding to its vascular receptor or to post-receptor events. 4. To determine the effect of AII and K regulation of AII receptor binding constants. 5. To determine the role of AII receptor in the mechanism of the altered vascular reactivity of RVH and SHR. These investigations require the application of a variety of physiological and biochemical techniques including balance studies in intact rats, hemodynamic studies, hormone assays and radioreceptor assays. There are 25 million people in the United States with hypertension. Many patients are treated with diuretics and become mildly K depleted. The long term objective of the P.I. is to expand knowledge on the effect of this very common clinical problem and to determine whether diuretic induced K depletion is beneficial or detrimental for the control of blood pressure.
Nolan, C R; Linas, S L (1988) Mechanism of antihypertensive effect of potassium depletion in renovascular hypertension. Am J Physiol 255:H1181-7 |
Benedetti, R G; Linas, S L (1987) Mechanism of decreased vascular response to angiotensin II in renal vascular hypertension. Kidney Int 31:906-12 |
Linas, S L; Marzec-Calvert, R (1986) Potassium depletion ameliorates hypertension in spontaneously hypertensive rats. Hypertension 8:990-6 |
Benedetti, R G; Linas, S L (1985) Effect of potassium depletion on two-kidney, one-clip renovascular hypertension in the rat. Kidney Int 28:621-8 |