[Calciuretic renal function in patients with essential hypertension].
Under the conditions of standard and customary calcium use, patients suffering from essential hypertension (EH) do not manifest any changes in calciuresis either at the expense of the glomerular or tubular mechanisms. After intravenous hypercalcemic injections EH patients demonstrate well-defined disorders in calciuretic renal function, caused by inadequate suppression of tubular reabsorption of calcium by parathyroid hormone (PTH). The hormonal-renal correlations in EH patients differ from those in normals. More pronounced alterations in the concentration of radioimmune PTH and calcitonin under acute hypercalcemia are not associated with an adequate increment of fractional excretion of calcium whereas the calciuretic effect of exogenous calcium-regulating hormones (CRH) realized at the tubular level is less remarkable. Therefore EH patients manifest changes not only in CRH secretion but also in the sensitivity to them of the renal tubules. White changing parathyroid regulation of calcium metabolism prolonged administration of calcium to EH patients enhances body capabilities of resisting acute alterations in calcemia because of normalization of calciuretic renal function, especially tubular calcium transport. In addition, it lowers arterial pressure and enables reduction of the dose of calcium antagonists used in the treatment of EH.
Kolomiets
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D000328:Adult; D002116:Calcitonin / Q000378:metabolism; D002118:Calcium / Q000652:urine*; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000503:physiopathology / Q000652:urine*; D007668:Kidney / Q000503:physiopathology*; D008875:Middle Aged; D010280:Parathyroid Glands / Q000502:physiology; D010281:Parathyroid Hormone / Q000378:metabolism; D011863:Radioimmunoassay
D010281:Parathyroid Hormone; D002116:Calcitonin; D002118:Calcium
Kal'tsiĭureticheskaia funktsiia pochek u bol'nykh gipertonicheskoĭ bolezn'iu.