Experimental renal hypertension.
The study of hypertension resulting from procedures devised to modify renal function in diverse ways has been pursued intensively in the past forty years and has contributed greatly to the understanding of hypertensive processes in man. Such procedures have included partial or complete removal of renal tissue, interference with the renal circulation and the administration of sodium and hormones promoting the tubular reabsorption of sodium. From all these studies, certain basic conclusions can be drawn. The fundamental mechanism involved in all forms of renal hypertension appears to be an alternation in the relationship between renal perfusion pressure and sodium and water excretion. The probable way in which this fundamental mechanism operates is outlined. The kidney itself is susceptible to the effects of hypertension and changes take place within it which then contribute a renal element to the hypertension whatever its primary cause.
D000208:Acute Disease; D000804:Angiotensin II / Q000502:physiology; D000818:Animals; D001341:Autonomic Nervous System / Q000503:physiopathology; D001826:Body Fluids; D002908:Chronic Disease; D003250:Constriction; D006321:Heart / Q000503:physiopathology; D006439:Hemodynamics; D049673:History, 20th Century; D006801:Humans; D006977:Hypertension, Renal / Q000266:history / Q000503:physiopathology; D007668:Kidney / Q000503:physiopathology; D009206:Myocardium / Q000473:pathology; D009392:Nephrectomy; D009476:Neurons, Efferent / Q000502:physiology; D010953:Plasma Volume; D011311:Pressoreceptors / Q000502:physiology; D012077:Renal Artery / Q000502:physiology; D012083:Renin / Q000502:physiology; D012964:Sodium / Q000378:metabolism / Q000502:physiology; D014655:Vascular Resistance; D014666:Vasomotor System / Q000503:physiopathology
D000804:Angiotensin II; D012964:Sodium; D012083:Renin