Chumpol PholpramoolSamisukh SophasanPawinee PiyachaturawatPhunpen Napradit2024-09-062024-09-06199319932024Thesis (M.Sc. (Physiology))--Mahidol University, 1993https://repository.li.mahidol.ac.th/handle/20.500.14594/101021Physiology (Mahidol University 1993)In order to study the effect of chronic potassium deficiency and subsequent to potassium repletion on extrarenal potassium homeostasis, adult male and female Sprauge-Dawley rats were divided into 2 groups. Potassium depletion was induced in one group by feeding with a potassium-deficient diet for up to 120 days. The other group was paired-fed with normal rat chow at the same amount consumed by the first group serving as controls. During potassium depletion, the rats had low food intake and their growths were retarded compared to the control period. The males appeared to gain less but lost more weight than the female counterparts, however, these differences were statistically insignificant. Polyuria, polydipsia, an impairment of urinary concentrating ability and a reduction in urinary K+ excretion were also observed. The potassium-depleted males developed more severe polyuria and polydipsia than the females in the late phase of potassium deficiency. Dietary potassium deprivation for 16-17 weeks resulted in a significant decreased in plasma K+ concentration to 1.5-2 mEq/l, total blood K+ concentration, red cell K+ content and plasma Cl- concentration whereas plasma Na+ concentration was virtually not changed. In addition, potassium deficiency caused a metabolic alkalosis, a reduction in K + but an accumulation in Na+ contents in muscle. The K+ contents in SOL and EDL were decreased by 46 and 39 % in the males and by 38 and 33 % in the females, respectively. The reduction in muscle K+ content was not fully compensated for by an increase in Na+ content. More reduction in growth rate and muscle K+ content as well as severe polyuria and polydipsia were observed in potassium-depleted males indicate indirectly that prolonged and severe potassium deficiency may affect the males more than the females. However, 2 weeks repletion of potassium by feeding normal rat chow resulted in marked increases in body weight, rapid restoration to control levels in water intake and urine output. Furthermore, electrolyte changes in plasma, total blood, red cell and skeletal muscles as well as the change in acid base status were also reversible. To investigate the extrarenal potassium homeostasis, functional nephrectomy and adrenalectomy were performed in the potassium-depleted, potassium-supplemented (in which normal rat chow was fed for 14 days to the previously potassium-depleted rats), diet-restricted and normal-untreated rats. Acute K-loading was challenged by intravenous infusion with KC1 at a dose of 2 mEq/kg/hr for I hr. This resulted in elevations of plasma K+ concentration and muscle K+ content in all groups. The increment in plasma K+ concentration was significantly lower in the potassium-depleted rats versus the normal rats (max ΔpK 1.9 ± 0.3 vs. 3.9 ± 0.1 mEq/l, P<0.001) whereas the increases in muscle K+ content was higher than those in the other groups. Furthermore, following KC1 infusion blood pH was significantly decreased (P<0.05) and plasma Na+ concentration was increased (P<0.05) in the potassium-depleted rats but those in the other groups were virtually not changed. These results were related to a greater K+ uptake in the potassium-depleted group indicating an alteration in the extrarenal potassium disposal after chronic potassium deficiency. It is concluded that following KCI infusion the K+ ion may be an appropriate stimulus that leads to a marked activation of the residual Na(+)-K(+)pump in the potassium-depleted rats sufficient to lower plasma K+ concentration than in the normal rats. This effect may be mediated by insulin as well as an accumulation of Na(+) in the muscle, an increase in extracellular HCO(,3)- and metabolic alkalosis developed after chronic potassium deficiency. However, the alteration in extrarenal potassium disposal is completely reversed after potassium repletion.xiii, 120 leaves : ill.application/pdfengผลงานนี้เป็นลิขสิทธิ์ของมหาวิทยาลัยมหิดล ขอสงวนไว้สำหรับเพื่อการศึกษาเท่านั้น ต้องอ้างอิงแหล่งที่มา ห้ามดัดแปลงเนื้อหา และห้ามนำไปใช้เพื่อการค้าHomeostasisPotassium DeficiencyMaster ThesisMahidol University