Increased permeability of the arteries in hypertensive rats: An electron microscopic study

Abstract

Fibrinoid degeneration of the mesenteric arteries in hypertensive rats with bilaterally constricted renal arteries could be ascribed to insudation of blood plasma constituents, especially fibrinogen, into the arterial wall. We investigated electron microscopically what part of the arterial endothelium the blood plasma would pass through, using ferritin or carbon as a tracer. Ferritin (50–100 Å), which was given intravenously to the hypertensive rats, was observed in pinocytotic vesicles and cytoplasm of endothelial cells, in the intercellular space of endothelium, and in the subendothelial space of the mesenteric arteries, whereas intravenously injected carbon particles (200–500 rA) were not found in the pinocytotic vesicles and cytoplasm of endothelial cells, but in the opened intercellular space of endothelium and in the subendothelial space. It was, therefore, considered that there were three pathways of blood plasma insudation into the arterial wall of hypertensive rats, that is, intercellular, transcellular, and transcellular through pinocytotic vesicles. The transcellular permeability seemed to be utilized mainly for permeation of small molecular substances such as albumin, the intercellular permeability in the state of unopened intercellular junction for insudation of fibrinogen, globulin, and albumin, and that in the state of opened junction for insudation of blood cells, fibrinogen, globulin, and albumin. Filaments (50–70 Å thick) were increased in endothelial cells of the mesenteric arteries of hyptertensive rats, and ovoid dense areas were observed there also. These filaments were considered to be involved in the contraction of endothelial cells and subsequently in the opening of the junctions between endothelial cells.