Morphogenesis of hypertensive vascular lesions.
Accelerated hypertension is a convenient model for studying the pathomechanism of hypertensive vascular lesions. It has not been settled, however, whether such lesions are really equivalent to those developing slowly in the course of experimental hypertensive vascular disease. In the present study, early vascular lesions of accelerated hypertension have been compared with those of hypertensive vascular disease by using two complementary techniques: small-molecule plasma-protein label (Ferrlecit) and a macromolecular tracer protein (horse ferritin). Two kinds of vascular lesions have been distinguished. Non-destructive vascular lesions exhibit necrotic smooth-muscle cells with intracellular deposition of Ferrlecit-labelled plasma proteins and intact basement-membrane barrier to the macromolecular tracer. Destructive vascular lesions, in turn, are characterized by the breakdown of the basement-membrane barrier to the macromolecular tracer. Incipient destructive lesions are identified as dissecting microaneurysms initiated by small ruptures of the basement membrane framework. Both non-destructive vascular lesions and incipient destructive vascular lesions end in confluent medial destruction that precedes the formation of fibrinoid necrosis. The localization and morphology of vascular lesions is identical both in hypertensive vascular disease and in accelerated hypertension. Circumstantial evidence strongly suggests that non-destructive vascular lesions are caused by arterial contraction. Nevertheless, the possibility that non-destructive lesions are but abortive forms of destructive ones cannot be excluded.
D000818:Animals; D001485:Basement Membrane / Q000473:pathology; D003331:Coronary Vessels / Q000473:pathology; D006977:Hypertension, Renal / Q000150:complications*; D006978:Hypertension, Renovascular / Q000150:complications* / Q000473:pathology; D007422:Intestines / Q000098:blood supply; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000473:pathology; D010179:Pancreas / Q000098:blood supply; D051381:Rats; D011919:Rats, Inbred Strains; D012077:Renal Artery / Q000473:pathology; D014652:Vascular Diseases / Q000209:etiology* / Q000473:pathology