Endothelium in functional aortic changes of coarctation hypertension

D. R. Bell and D. F. Bohr Department of Physiology, University of Michigan, Ann Arbor 48109-0622. Eleven coarctation hypertensive (CH), twelve sham control (C), and seven one-kidney, one-clip (1K,1C) rats were used to examine the role of pressure and the endothelium in vascular sensitivity changes to acetylcholine (ACh), serotonin (5-HT), and norepinephrine (NE) in chronic arterial hypertension. Terminal mean carotid artery pressures were CH = 156 +/- 5 mmHg, C = 99 +/- 3 mmHg, and 1K,1C = 159 +/- 5 mmHg. Femoral artery pressures were CH = 100 +/- 3 mmHg, C = 98 +/- 4 mmHg, and 1K,1C = 154 +/- 4 mmHg, respectively. Isometric tension recordings were made from helically cut strips of thoracic and abdominal aortas, with and without functional endothelium, from the three groups of rats. Sensitivity to relaxation by acetylcholine, expressed as -log of 50% effective dose, was significantly depressed in thoracic aortas from CH and 1K,1C rats and abdominal aortas from 1K,1C rats but not from abdominal aortas of CH rats. A similar relationship between the groups was seen for 5-HT contractions. Sensitivity to NE was enhanced in thoracic and abdominal aortas of hypertensive rats. Inactivation of aortic endothelia abolished ACh responses, did not alter 5-HT relationships between the three groups, and abolished the differences in sensitivity to NE in thoracic aortas. The data suggest that pressure and the endothelium may play a role in vascular sensitivity changes in hypertension.