[The role of the kidney in the pathogenesis of hypertension].

Neither a temporary increase in salt intake nor the activation of endogenous vasoconstrictor hormones alone will cause a rise in blood pressure in healthy subjects. High blood pressure rather results from an augmented product of cardiac output and peripheral vascular resistance, which also requires defective baroreceptor function. Experimental and clinical evidence from renal transplantation suggests that high blood pressure may be transmitted by the kidney. Morphological or functional inability of the kidney to adequately eliminate excessive salt, as in renoparenchymal hypertension, or with enhanced renal adrenergic activity in the presence of high salt intake, may induce initially salt- and volume-dependent hypertension with increased cardiac output and normal peripheral vascular resistance. In the case of reduced nephron population, this first stage was shown to be followed by a normalization of cardiac output, but a simultaneous rise in peripheral vascular resistance, including decreased compliance of the venous capacitance vessels. What are the underlying mechanisms which convert volume-dependent hypertension into high resistance hypertension without necessarily reducing central blood volume? Increased central blood volume, which may stimulate the secretion of an endogenous Na-K-ATPase inhibitor or other endogenous factors, may cause decreased transmembranous sodium transport, resulting in elevated intracellular concentrations of sodium and calcium with enhanced responsiveness of the vascular smooth muscle cell to vasoconstrictor hormones. Since increased central blood volume also decreases baroreceptor sensitivity, the disturbed interplay of cardiac output and peripheral vascular resistance will result in high blood pressure.