Hypertensive Vascular Disease and Humoral Factor(s) Originating from the Kidney

Abstract

Ligation or clipping of bilateral renal arteries caused angionecrosis, tissue edema and severe hypertension in the dogs and rats. The syndrome is identical to human malignant hypertension. These experiments lead a concept of a release of humoral agent(s) inducing vascular lesions from involved kidneys.
The possibility of the concept was studied in patients with malignant hypertension. Plasma renin activity (PRA), serum LDH, GOT and GPT on admission were compared between patients with malignant hypertension and hypertension accompanying chronic renal failure without papilledema. There was no difference of serum creatinine level between the two groups of the patients. Diastolic blood pressure, PRA, LDH and GOT were significantly higher in patients with malignant hypertension than in those without them. When one renal artery of rats was completely ligated, changes in blood pressure and an occurrence of angionecrosis were studied in comparison with those in unilaterally nephrectomized arts. On the 7th day after the ligation blood pressure was significantly elevated and reached the level of 150mmHg or more. Fibrinoid necrosis was observed in the mesenteric arteries in the experimental animals, but not in the controls. The ligated kidneys showed coaggulation necrosis.
Lysosomal fraction obtained from rat kidney cortex by subcellular centrifugation method of Shibko and Tappel showed high renin activity. The lysosomal fraction, when injected into bilaterally nephrectomized rats, caused increase in blood pressure, fibrinoid necrosis of the arterioles, tissue edema and increased vascular permeability in the experimental animals.