抄録
This study was undertaken to demonstrate whether hyperlipidemia altered the arterial reactivity to ergonovine. For this purpose, we compared the contractile responses of isolated aortae, coronary, femoral and carotid arteries form control rabbits (n=18) and Watanabe heritable hyperlipidemic rabbits (WHHL; n=12).
Those helical strips were mounted in tissue baths filled with oxygenated Krebs solution for isometric contraction recording. In the aortae and coronary arteries form WHHL rabbits, the dose-response curves for ergonovine (10-12-10-5M) shifted to the left, whereas those for phenylephrine (10-9-10-4M), post synaptic α-adrenergic agonist, did not. The responsiveness of the carotid and femoral arteries of WHHL rabbits to ergonovine and phenylephrine was not different from those of control rabbits.
In coronary arteries from both groups, 0.1μM cyproheptadine, a serotonergic antagonist, was effective to inhibit 1μM ergonovine induced contractions. In aortae 0.1μM prazosin, a postsynaptic α-adrenergic antagonist, was effective to inhibit ergonovine induced contraction in control rabbits, but not in WHHL rabbits which was inhibited by cyproheptadine.
In carotid and femoral arteries from both groups, 0.1μM prazosin was effective to inhibit ergonovine induced contractions. Thus, aortae and coronary arteries from WHHL rabbits were supersensitive to ergonovine mainly by serotonergic mechanism, whereas femoral and carotid arteries showed similar responses to ergonovine, when compared with those of control vessels, through stimulation of α-adrenergic receptor.
