The effect of the angiotensin converting enzyme (ACE) inhibitor, captopril, on proteosynthesis in the aorta, acetylcholine-stimulated aortic relaxation and endothelaemia (circulating endothelial cells) was investigated in rabbits with aortic insufficiency. The animals were studied 28 days after experimental intervention. Cardiac volume overload stimulated proteosynthesis in the aorta as reflected by increased ribonucleic acid (RNA) concentration and [14C] leucine incorporation into proteins of the aorta. Moreover, the number of endothelial cells in the blood was increased. The administration of captopril starting from the second day of the haemodynamic overload, partially prevented the increase both in aortic proteosynthesis and in endothelaemia. Despite these alterations, the relaxing ability of the aorta to acetylcholine was not changed either by the haemodynamic overload or by captopril. We conclude that the increase of proteosynthesis in the aorta and of endothelaemia in the early period of chronic cardiac volume overload in rabbits were partially prevented by chronic captopril treatment. Neither aortic insufficiency nor captopril changed the acetylcholine-induced relaxation of the aorta.
The responsiveness of isolated high-pressure (aorta, renal artery) and low-pressure vessels (pulmonary artery) was compared during systemic hypertension induced by chronic inhibition of nitric oxide synthesis by NG-nitro-L-arginine methyl ester (L-NAME) in rats. L-NAME (40 mg/kg/day) was given to animals in their drinking water. After 4 weeks of L-NAME treatment, systolic blood pressure increased by 37 % as compared with that in the control group. Chronic L-NAME treatment resulted in significant reduction of endothelium-dependent relaxation to acetylcholine (10-8 to 3xl0-6 mol/1) in both types of vessels. The reduced relaxation was not influenced by acute pretreatment with indomethacin (10"5 mol/1), however, it was further reduced by acute pretreatment with additional L-NAME (10-4 mol/1). L-arginine (10-4 mol/1) improved the reduced relaxation. Endothelium- independent relaxation to sodium nitroprusside (10-9 to 10-6 mol/1) was unaffected by L-NAME treatment. /3-adrenoceptor-mediated relaxation to isoprénaline (10“8 to 3xl0-6 mol/1) was also not influenced by chronic L-NAME treatment Similar alterations in the responsiveness of high- and low- pressure vessels indicate rather the decisive role of nitric oxide restriction than that of elevated blood pressure in their development