Critical Degree of Renal Arterial Stenosis That Causes Hypertension in Dogs

• Published in: Angiology 1992-10, Vol.43 (10), p.833-842
• Main Authors: Imanishi, Masahito, Akabane, Satoshi, Takamiya, Makoto, Kawamura, Minoru, Matsushima, Yohkazu, Kuramochi, Morio, Omae, Teruo
• Format: Article
• Language: English
• Subjects: Animals; Arterial hypertension. Arterial hypotension; Biological and medical sciences; Blood and lymphatic vessels; Cardiology. Vascular system; Dinoprostone - secretion; Dogs; Experimental diseases; Hypertension, Renovascular - etiology; Hypertension, Renovascular - metabolism; Hypertension, Renovascular - pathology; Hypertension, Renovascular - physiopathology; Kidney - secretion; Medical sciences; Radiography; Renal Artery - diagnostic imaging; Renal Artery - pathology; Renal Artery Obstruction - complications; Renal Artery Obstruction - diagnostic imaging; Renal Artery Obstruction - pathology; Renal Artery Obstruction - physiopathology; Renal Circulation; Renin - secretion
• ISSN: 0003-3197; 1940-1574
• DOI: 10.1177/000331979204301006

The minimum degree of renal arterial stenosis needed to cause hypertension was identified by renal arterial angiography of anesthetized dogs. The effects of renal nerves and prostanoids on the critical stenosis were also examined. The left renal artery was constricted concentrically by a radiolucent con strictor device, and the stenosis of the artery was evaluated by cineangiography with the kidney either innervated or denervated. At this time, renal blood flow, renal perfusion pressure, and systemic blood pressure were serially monitored. In another group of dogs, renal venous and aortic blood samples were taken as the stenosis increased; these were assayed for prostaglandin E2 and plasma re nin activity. The same experiments were done again after treatment with a cyclooxygenase inhibitor, aspirin DL-lysine (54 mg/kg). With the kidney either innervated or denervated, systemic blood pressure began to increase when the stenosis was more than 70% of the diameter of the renal artery; the renal blood flow decreased when the stenosis was more than 75% of the diameter. Aspirin treatment attenuated the increase in blood pres sure but did not affect the autoregulation of the renal blood flow when stenosis was 70% or less. Prostaglandin E2 production increased in the stenotic kidney when the stenosis was more than 70%; aspirin inhibited prostaglandin synthesis and suppressed the stimulation of renin release. These results suggest that whether there is innervation or not, the critical degree of renal arterial stenosis that causes hypertension is more than about 70% of the diameter in the presence of renal prostaglandins; in their absence, the critical point above which hypertension occurs is 75% or more.