Hypertension from Obstruction of the Aorta

Abstract

Goldblatt and others have found in chronic experiments that by stenosing the renal arteries and thereby decreasing the blood supply to the kidneys a persistent elevation in blood pressure can be obtained. This phenomenon Goldblatt explains by the hypothesis of a “pressor substance” which he believes is formed as a result of the ischemia of the kidneys. He found also that stenosis of the aorta above the origin of both renal arteries resulted in a persistent elevation of blood pressure while stenosis below the origin of these vessels did not cause hypertension. Rytand, using heart weight increase in rats as evidence of hypertension, obtained similar results. Stenosis of the aorta below the right but above the left renal artery, he found, also produced hypertension; however, if the distal (left) kidney be removed hypertension does not result. Goldblatt's conclusion was that hypertension from experimental aortic stenosis is of the same nature as that due to stenosis of the renal arteries directly, that is, that the stenosis of the aorta caused an elevation of blood pressure by producing renal ischemia. This idea was further expanded by Rytand to the supposition that renal ischemia with its resulting “pressor substance” is the important factor in the elevation of blood pressure so regularly found in the upper extremities in coarctation of the aorta. Inasmuch as these results were obtained in chronic experiments it was felt that it would be interesting to investigate the aortic phenomenon with acute stenosis at similar levels. Using dogs, intraperitoneal nembutal (pentabarbital) as anesthetic and carotid cannula recordings with the kymograph, the following experiments were performed: 1. A screw clamp was placed about the aorta just above the origin of the celiac axis, 2 or 3 cm above the origin of the right (upper) renal artery.