The role of M4-subtype of cholinoreceptors in acethilinecholine vasoconstriction

  • N.Ya. Kovalenko Institute of General Pathology and Pathophysiology RAMS, 8, Baltyiskaya str., Moscow, 125315, Russia
  • D.D. Matsievsky Institute of General Pathology and Pathophysiology RAMS, 8, Baltyiskaya str., Moscow, 125315, Russia
  • V.K. Reshetnyak Institute of General Pathology and Pathophysiology RAMS, 8, Baltyiskaya str., Moscow, 125315, Russia
Keywords: M4-cholinoreceptors, tropicamide, vessels, acetylcholine vasoconstriction, ultrasonic

Abstract

In experiments on rats using high frequency ultrasonic measurement technique and selective M4- cholinoreceptor antagonist tropicamide it was shown that i/v injection of the cholinolitic block agent in large doses exceeding of its selective threshold (1 mg/kg) causes pronounced inhibition of the cardiovascular system in rats. Severe transitory hypotension and bradycardia are developed, general vascular resistance, minute cardiac output, are decreased. The block of M4-cholinoreceptors with smaller doses of tropicamide (0,1—0,001 mg/kg) causes transitory dose-depended effect on hemodynamic — system blood pressure and vascular resistance , pulse, minute cardiac output, as soon as velocity of aortic blood flow, strike cardiac output are increased on the contrary. The following decrease the dose of the high selective M4cholinolitic antagonist (0,0001 mg/kg) reveals that its negative chronotropic effect are not detected practically but tropicamide vessel action (decrease of system blood pressure and vascular resistance) are preserved distinctly. The obtained data are discussed in aspect of the possible involvement of M4-muscarinic receptor subtype in acetylcholine -induced vasoconstriction in rats.

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Published
2013-08-12
How to Cite
Kovalenko N., Matsievsky D., Reshetnyak V. The role of M4-subtype of cholinoreceptors in acethilinecholine vasoconstriction // Patologicheskaya Fiziologiya i Eksperimental’naya Terapiya (Pathological physiology and experimental therapy). 2013. VOL. 57. № 3. PP. 23–26.
Section
Original research