Key result
Experimental compression of the renal parenchyma or main renal arteries induced lasting hypertension, highlighting the relationship between the kidneys and increased arterial pressure.
A historical overview of the pathogenesis of arterial hypertension, focusing on the renal origins of essential and malignant hypertension.
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Underpins renal hypertension models; confirms classic experiments but leaves open targeted therapies in essential hypertension.
Increased arterial pressure of known or suspected causation occurs in at least forty-seven syndromes, which, according to pathogenesis, are grouped as neurogenic, endocrine, cardiovascular and renal. 1 However, as a problem in clinical practice, hypertension is largely limited to those syndromes called essential and malignant hypertension. The genesis of these states, which had been regarded as renal since the time of Bright, has remained obscure since their separation from glomerulonephritis in the works of Allbutt, Janeway, Volhard, Keith and others. The demonstration by Goldblatt 2 that lasting hypertension occurs after partial compression of one or both main renal arteries by a metal clamp revived interest in the relationship of the kidneys to increased arterial pressure. Experimental hypertension of similar nature was subsequently induced by one of us, 3 who produced fibrocollagenous perinephritis by application of silk or cellophane to the kidneys. Compression of the renal parenchyma in the scar resulted
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Corcoran et al. (1941) conducted a review in Arterial hypertension. Renal artery compression or perinephritis was evaluated. Experimental compression of the renal parenchyma or main renal arteries induced lasting hypertension, highlighting the relationship between the kidneys and increased arterial pressure.
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