VOLUME, SURFACE, AND JUNCTIONS OF RAT AORTIC ENDOTHELIUM DURING EXPERIMENTAL-HYPERTENSION - A MORPHOMETRIC AND FREEZE-FRACTURE STUDY

  • 1 January 1982
    • journal article
    • research article
    • Vol. 46  (5) , 489-504
Abstract
Three models of hypertension were induced in Wistar rats: aortic ligature between renal arteries, uninephrectomy and Na-rich diet, and uninephrectomy, 0.9% NaCl as drinking fluid and s.c. administration of deoxicorticosterone acetate (DOCA). The aortic endothelium was studied during the early (7-10 days) and late (40 days) phases of these models: volume, surface, and ratios of tight and gap junctions to lateral membrane surface by means of morphometric analysis using thin-sectioning EM and organization of tight and gap junctions by mean of freeze fracture EM. Compared with normotensive rats the volume of the endothelial cell layer was increased in all hypertensive situations with the exception of the late group after aortic ligature, and the increase was most marked early after aortic ligature and early and late after DOCA. Endothelial surface to volume ratio was markedly decreased early after aortic ligature and early and late after DOCA, and the volume ratio was markedly decreased early after aortic ligature and early and late after DOCA; the ratio of luminal, abluminal, and lateral to total endothelial surface remained unchanged in all hypertensive situations. In all hypertensive situations the ratio of tight junctions to lateral membrane surface increased, whereas the ratio of gap junctions to lateral membrane surface showed no significant change; in all hypertensive situations lateral endothelial plasma membranes contained, in addition to zonular and macular type tight junctions, many small aggregates of intramembrane particles in the P face and particle-free grooves in the E face; these structures were particularly numerous early after aortic ligature and early and late after DOCA. In all hypertensive situations (most early and late after DOCA and least after Na-rich diet) gap junctions were irregularly shaped in contrast to those of normotensive animals. Different types of hypertension produce different degrees of hypertrophy of the endothelial cell layer; hypertension increases the ratio of tight junctions to lateral endothelial membrane surface; the presence of small aggregates of intramembrane particles (probably representing assembly and/or disassembly of tight junctions) in the lateral endothelial plasma membranes is responsible for this phenomenon, and hypertension does not change the ratio of gap junctions to lateral membrane surface but results in abnormal gap junction morphology.