New concepts of the renin system and of vasoconstriction-volume mechanisms. Diagnosis and treatment of renovascular and renal hypertensions.
Information defining the renin-angiotensin-aldosterone axis as a control system concurrently regulating salt balance and blood pressure has been applied to examine the role of renin in the causation of experimental and clinical forms of renovascular and renal hypertension and thence to develop criteria for differentiating these entities. Experimantally there are two models of renovascular hypertension, one characterized by excess renin with reduced sodium (vasoconstrictor form) and the other by excess sodium with reduced renin (volume form). But with sodium depletion, the volume form switches to a vasoconstrictor form, illustrating how the two factors coordinate to maintain blood pressure. Human renovascular and renal hypertensions appear to be sustained by the same two mechanisms. Experimental and clinical studies both indicate that curable renal hypertension is in fact a renin-dependent vasoconstrictor hypertension. Three criteria, derived from four renin measurements, identify this situation: (1) Hypersecretion of renin is reflected by a high peripheral level when referenced against sodium excretion. (2) Lacteralization of renin secretion with contralateral suppression rules out occult bilateral disease. It is indicated by V-A = 0 from the uninvolved kidney. (3) A third criterion, (V-A)/A greater than 48 per cent from the ipsilat-eral kidney, identifies renal ischemia. These three criteria, when taken together in a combined scoring analysis, provide high precision in identifying the patient with the vasoconstrictor form of renal hypertension that is potentially reversible by appropriate surgery. Absence of these criteria identifies hypertension associated with either occult or overt bilateral renal disease. In these patients, the volume factor often predominates and is expressed by some suppression of plasma renin levels. Here, removal of renal tissue is contraindicated. Corroborative evidence to support these three criteria can be developed from the blood pressure response to angiotensin blocking drugs or to anti-renin therapy with propranolol. Thus in all of these renal hypertensions, the vasoconstrictor and volume factors can be identified using renin measurements and pharmacologic interventions.
D000450:Aldosterone / Q000097:blood; D000804:Angiotensin II / Q000037:antagonists & inhibitors / Q000097:blood; D000818:Animals; D000959:Antihypertensive Agents / Q000627:therapeutic use; D004195:Disease Models, Animal; D006801:Humans; D006977:Hypertension, Renal / Q000097:blood / Q000175:diagnosis* / Q000188:drug therapy / Q000503:physiopathology / Q000628:therapy; D011433:Propranolol / Q000627:therapeutic use; D012078:Renal Artery Obstruction / Q000097:blood; D012083:Renin / Q000097:blood* / Q000378:metabolism; D012964:Sodium / Q000172:deficiency / Q000378:metabolism / Q000502:physiology / Q000652:urine; D014666:Vasomotor System / Q000502:physiology*; D014882:Water-Electrolyte Balance; D000092502:Renin Inhibitors
D000450:Aldosterone; D000804:Angiotensin II; D000959:Antihypertensive Agents; D011433:Propranolol; D012083:Renin; D012964:Sodium; D000092502:Renin Inhibitors