Nonpenetrating Abdominal Trauma as Cause of Renal Vascular Hypertension

Abstract

THE POSSIBILITY that systolic and diastolic hypertension can be caused by partial ischemia of a kidney or of parts of it is now generally accepted. The basic investigations of Goldblatt et al¹ have clearly demonstrated that reduced blood pressure in the juxtaglomerular apparatus leads to increased renin production, with subsequent increased production of angiotensin I, which by the converting enzyme is rapidly transformed into the highly pressor active angiotensin II. Congenital or acquired narrowing of the renal artery, thrombosis, or external pressure on the renal artery may lead to the mobilization of this mechanism. Boyd and Lewis,² and later Howard et al,³ have called attention to the fact that incomplete infarction of the kidney with ischemic areas in which some, although markedly diminished, blood flow and pressure persist may lead to hypertension and that nephrectomy may relieve the hypertension. The mechanism by which the decreased blood pressure