ACh- and VIP-induced vasorelaxation in rabbit facial artery after carotid artery occlusion.
OBJECTIVE
The influence of carotid artery occlusion (10, 30 and 60 min) on regulatory mechanisms implicated in the vasorelaxant responses of isolated glandular branch of rabbit facial artery to acetylcholine (ACh) and vasoactive intestinal polypeptide (VIP) was examined.


METHODS
In organ bath studies with arterial rings precontracted with phenylephrine (1 microM), before and after carotid artery occlusion, changes in isometric tension were recorded.


RESULTS
Endothelium-dependent vasorelaxation by ACh and endothelium-independent vasorelaxation by VIP were significantly reduced, started from 30 and 10 min of carotid occlusion, respectively. Inhibitory effect of indomethacin on ACh vasorelaxation was enhanced whilst effect of N(G)-nitro-L-arginine reduced, started from 30 min of carotid occlusion. Sodium nitroprusside-induced vasorelaxation was not changed after carotid occlusion. Inhibition of VIP vasorelaxation by L-N(omega)-nitroarginine-2,4-L-diaminobutyric-amide, was reduced, started from 30 min of carotid occlusion. Forskolin enhanced VIP-induced vasorelaxation in control rings but this effect was reduced started from 30 min of occlusion. In the presence of VIP, vasorelaxant effect of ACh was increased; the increase was reduced, started from 10 min of carotid occlusion.


CONCLUSIONS
The present investigation provides evidence for the decreased responsiveness to both, ACh-endothelium-dependent and VIP-endothelium-independent vasorelaxation in rabbit facial artery after carotid occlusion. In addition, the data suggest that ischaemia alters contribution of endothelial nitric oxide (eNO) and prostaglandin to ACh, and vascular smooth muscle's cAMP and neuronal NO to VIP vasorelaxant effects.
Roganović
Jelena
J
Department of Pharmacology, Faculty of Stomatology, University of Belgrade, Belgrade, Serbia.
Radenković
Miroslav
M
Stojić
Dragica
D
D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D001158:Arteries / Q000187:drug effects; D001920:Bradykinin / Q000494:pharmacology; D002340:Carotid Artery Diseases / Q000150:complications*; D017536:Carotid Artery, Common / Q000503:physiopathology; D005576:Colforsin / Q000494:pharmacology; D000242:Cyclic AMP / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000502:physiology; D011464:Epoprostenol / Q000494:pharmacology; D005260:Female; D007213:Indomethacin / Q000494:pharmacology; D007511:Ischemia / Q000150:complications*; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000502:physiology; D009569:Nitric Oxide / Q000494:pharmacology; D019335:Nitroarginine / Q000494:pharmacology; D009599:Nitroprusside / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D011817:Rabbits; D012793:Sialadenitis / Q000209:etiology*; D015398:Signal Transduction; D013363:Submandibular Gland / Q000098:blood supply*; D014660:Vasoactive Intestinal Peptide / Q000494:pharmacology*; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014664:Vasodilation / Q000187:drug effects*; D014665:Vasodilator Agents / Q000494:pharmacology*
D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D009599:Nitroprusside; D005576:Colforsin; D010656:Phenylephrine; D019335:Nitroarginine; D009569:Nitric Oxide; D014660:Vasoactive Intestinal Peptide; D011464:Epoprostenol; D000242:Cyclic AMP; D000109:Acetylcholine; D001920:Bradykinin; D007213:Indomethacin