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Hypertensive arteriolar necrosis revisited
1Department of Medical Physiology, Panum Institute, University of Copenhagen, Denmark. finng@centrum.dk
Arteriolar necrosis is the histopathological hallmark of malignant hypertension. In the period from 1940 to 1980, intensive studies of the pathogenesis of hypertensive fibrinoid necrosis were carried out. From studies of mesenteric vessels in animals with experimental hypertension it was discovered that arteriolar necrosis is preceded by an abnormal vascular reaction pattern consisting of alternating constriction and localized dilatations. The development of the abnormal reaction pattern is followed by endothelial hyperpermeability resulting in transsudation of plasma and macromolecules into the wall of the arteriole. The hyperpermeability, and, in turn, arteriolar necrosis, is exclusively found in the dilated segments of the vessel. The abnormal vascular reaction pattern can be induced experimentally by various techniques such as infusion of angiotensin II or stimulation of perivascular nerves, and it can be demonstrated in all target organs. Since 1980 a remarkable falling-off in the research on the pathogenesis of hypertensive arteriolar necrosis has been noted. Recent studies in this area utilizing current knowledge and major advances in microvascular research methods are very few in number. As of today, the chain of pathogenetic processes leading eventually to the all-important lesion of arteriolar fibrinoid necrosis remains poorly understood.
Arteriolar necrosis is the histopathological hallmark of malignant hypertension. In the period from 1940 to 1980, intensive studies of the pathogenesis of hypertensive fibrinoid necrosis were carried out. From studies of mesenteric vessels in animals with experimental hypertension it was discovered that arteriolar necrosis is preceded by an abnormal vascular reaction pattern consisting of alternating constriction and localized dilatations. The development of the abnormal reaction pattern is followed by endothelial hyperpermeability resulting in transsudation of plasma and macromolecules into the wall of the arteriole. The hyperpermeability, and, in turn, arteriolar necrosis, is exclusively found in the dilated segments of the vessel. The abnormal vascular reaction pattern can be induced experimentally by various techniques such as infusion of angiotensin II or stimulation of perivascular nerves, and it can be demonstrated in all target organs. Since 1980 a remarkable falling-off in the research on the pathogenesis of hypertensive arteriolar necrosis has been noted. Recent studies in this area utilizing current knowledge and major advances in microvascular research methods are very few in number. As of today, the chain of pathogenetic processes leading eventually to the all-important lesion of arteriolar fibrinoid necrosis remains poorly understood.