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By W. M. Manger, I. H. Page (auth.), Julian Rosenthal M.D. (eds.)

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Additional resources for Arterial Hypertension: Pathogenesis, Diagnosis, and Therapy

Example text

Removal of the transplant (isograft) was accompanied by a return of the pressure to prior hypertensive levels (Fig. 9). Similarly, renomedullary transplants prevented the development of malignant renovascular hypertension in rabbits. On the other hand, transplants of renal cortex, liver, or spleen had no influence on blood pressure. Crude extracts of fresh renal medulla given intravenously caused a prompt vasodepressor effect and prevented or delayed the development of renoprival hypertension. Muirhead also demonstrated that live renomedullary cells were required for the antihypertensive effect, since when these cells were lyophilized and transplanted into hypertensive animals there was no pressure change.

To ascertain whether renomedullary tissue could reverse established hypertension, inbred Wistar rats made hypertensive by renal artery clamping received either renocortical or medullary isografts. A blood pressure drop occurred only following medullary grafting; pressure stayed low until graft was removed and then returned to prior hypertensive level. Figure by Albert Miller, from Muirhead EE, ref 258, p 147. Reproduced with permission 24 W. M. Manger, I. H. Page content of renomedullary interstitial cells in experimental hypertension due to renovascular constriction or sodium 10ading.

He has concisely presented the evidence which supports or refutes various mechanisms which might explain low-renin essential hypertension. 318 However, Case and associates found no differences in renal cortical blood flow 20 W. M. Manger, I. H. Page Table 5. Clinical Conditions Affecting Renin Levels Decreased PRA Increased PRA Expanded fluid volume Salt loads, oral or i. v. ) Androgen therapy Decrease of renal tissue Hyporeninemic hypoaldosteronism Chronic renal disease (volume-dependent) Anephric Unknown Low-renin hypertension Shrunken fluid volume Salt deprivation Fluid losses Diuretic-induced Gastrointestinal losses Hemorrhage Salt-wasting renal disease Decreased effective plasma volume Upright posture Adrenal insufficiency Cirrhosis with ascites Nephrotic syndrome Decreased renal perfusion pressure Therapy with peripheral vasodilators Renovascular hypertension Accelerated -malignant hypertension Chronic renal disease (renin-dependent) Juxtaglomerular hyperplasia (Bartter's syndrome) Catecholamine excess Pheochromocytoma Stress: hypoglycemia, trauma Exercise Hyperthyroidism Hypokalemia Increased renin substrate Pregnancy Estrogen therapy Autonomous renin hypersecretion Renin-secreting tumors Acute damage to J-G cells Acute renal failure Acute glomerulonephritis From Kaplan NM, ref 167, p 191.

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