Aortic response to renovascular hypertension.
In the early phase of malignant renal hypertension induced by aortic ligature, a transient activation of transmural aortic permeability is observed. The transmural permeability shows its maximum during the first week of hypertension returning in the third week to normal or even subnormal values, whereas the blood pressure is still rising. The permeability disturbance precedes the structural transformation of the arterial wall. Although the aortic segments above and below the ligature are exposed to different blood pressure and hemodynamic stresses their patterns of permeability disturbance are the same. If the kidney below the aortic ligature is removed no permeability disturbance can be observed. Aortic wall PGI2-formation both above and below the ligature is elevated in the first phase of hypertension. The PGI2-synthesis returns to normal values during the 5th week. Our data suggest that in the early phase of renovascular hypertension there is an increased aortic antiaggregatory activity and that PGI2 is probably not the compound responsible for increased transmural permeability. Moreover, the blood pressure and the hemodynamic forces have no decisive importance in the induction of the aortic transmural permeability disturbance.
D000818:Animals; D001011:Aorta / Q000503:physiopathology*; D001692:Biological Transport; D001794:Blood Pressure; D002199:Capillary Permeability; D011464:Epoprostenol; D006977:Hypertension, Renal / Q000503:physiopathology*; D006978:Hypertension, Renovascular / Q000503:physiopathology*; D007501:Iron; D008026:Ligation; D008297:Male; D009392:Nephrectomy; D051381:Rats
D011464:Epoprostenol; D007501:Iron