The cellular pathology of experimental hypertension. 7. Structure and permeability of the mesenteric vasculature in angiotensin-induced hypertension.
Acute hypertension was produced in rats by the infusion of angiotensin amide for 2 to 4 hours. These animals were injected intravenously prior to sacrifice with either colloidal carbon or iron dextran particles. The mesenteric vessels from hypertensive and control animals were processed for electron microscopy. Ultrastructural alterations are found in dilated segments of small arteries. Initially there is severe contraction of medial smooth muscle cells and the formation of processes of smooth muscle cytoplasm. This is followed by lysis of cell processes and bodies, and passage of plasma and colloidal iron into the media. Subsequently, carbon, platelets, fibrin and cellular debris are seen within these foci of medial necrosis. These changes appear as a sequence whose severity reflects the duration of the angiotensin infusion and degree of elevation of the systolic pressure. The morphologic alterations are discussed in relation to the generalized increase in vascular permeability that is associated with the hypertensive state.
D000804:Angiotensin II; D000818:Animals; D002247:Carbon Isotopes; D002467:Cell Nucleus; D003102:Colloids; D003593:Cytoplasm; D004727:Endothelium / Q000473:pathology; D006973:Hypertension / Q000139:chemically induced / Q000473:pathology*; D007811:Lanthanum; D008297:Male; D008638:Mesenteric Arteries / Q000473:pathology*; D008854:Microscopy, Electron; D009119:Muscle Contraction; D009130:Muscle, Smooth / Q000473:pathology; D010539:Permeability; D051381:Rats; D013194:Staining and Labeling
D002247:Carbon Isotopes; D003102:Colloids; D000804:Angiotensin II; D007811:Lanthanum