Captopril attenuates proteosynthesis in the aorta and decreases endothelaemia in rabbits with aortic insufficiency.
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.
Department of Pathophysiology, Faculty of Medicine, Bratislava, Slovak Republic.
F
F
Simko
O
O
Pechánová
I
I
Bernátová
A
A
Holécyová
J
J
Simko
R
R
Sochorová
D000109:Acetylcholine / Q000494:pharmacology; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D001011:Aorta / Q000473:pathology*; D002216:Captopril / Q000494:pharmacology*; D004730:Endothelium, Vascular / Q000187:drug effects*; D009126:Muscle Relaxation / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D014176:Protein Biosynthesis; D012313:RNA / Q000378:metabolism; D011817:Rabbits
D000806:Angiotensin-Converting Enzyme Inhibitors; D012313:RNA; D002216:Captopril; D000109:Acetylcholine