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Aim:To study the effects of urotensin Ⅱ(UⅡ)on the carotid sinus baroreflex(CSB).Methods:The functional curve of carotid sinus baroreflex was measuredby recording changes in arterial pressure in anesthetized male rats with perfusedisolated carotid sinus.Results:UⅡ at the concentration of 3 nmol/L had no effecton the CSB,while at the concentration of 30,300 and 3000 nmol/L inhibited theCSB,shifting the functional curve of the baroreflex upward and to the right.Therewas a marked decrease in peak slope and reflex decrease in blood pressure.Theseeffects of UⅡ were concentration-dependent.Pretreatment with verapamil(anantagonist of the L-type calcium channel,10 μmol/L)partially eliminated the.aboveeffects of UⅡ(300 nmol/L)on the CSB.Pretreatment with BIM-23127(3 μmol/L),an antagonist of human and rat UⅡ receptors,abolished the actions of UⅡ on theCSB.Pretreatment with N~G-nitro-L-arginine methyl ester(L-NAME)100 μmol/L didnot affect the inhibitory effects of UⅡ(300 nmol/L)on the CSB.Conclusion:These data suggest that UⅡ exerts an inhibitory action on the isolated CSB.Suchan action of UⅡ is predominantly mediated by the UⅡ receptors in vascular smoothmuscles,resulting in the opening of L-type calcium channels.
Aim: To study the effects of urotensin II (UII) on the carotid sinus baroreflex (CSB). Methods: The functional curve of carotid sinus baroreflex was measured by recording changes in arterial pressure in anesthetized male rats with perfusedisolated carotid sinus. Results: UII at the concentration of 3 nmol / L had no effect on the CSB while at the concentration of 30,300 and 3000 nmol / L inhibited theCSB, shifting the functional curve of the baroreflex upward and to the right. Here a marked decrease in peak slope and reflex decrease in blood pressure. The effects of UII were concentration-dependent. Treatment with verapamil (anantagonist of the L-type calcium channel, 10 μmol / L) was eliminated. The effects of UⅡ (300 nmol / L) on the CSB.Pretreatment with BIM -23127 (3 μmol / L), an antagonist of human and rat U II receptors, abolished the actions of U Ⅱ on the CSB.Pretreatment with N-G-nitro-L-arginine methyl ester (L-NAME) 100 μmol / L didnot affect the inhibitory effects of UII (300 nmol / L) on the CSB.Conclusion: These data suggest that UII exerts an inhibitory action on the isolated CSB. Sudan action of UII is predominantly mediated by the UII receptors in vascular smooth muscle, resulting in the opening of L-type calcium channels.