Experimental study demonstrates interactions in systemic hemodynamics in anesthetized cats, highlighting both receptor types’ roles.
On anesthetized cats following M-cholinoreceptors blockade acetylcholine injection caused, in contrast with intact animals, the increasing of the arterial pressure, cardiac output, total peripheral resistance, heart rate and myocardial contractility. After acetylcholine injection in the condition of the N-cholinoreceptors blockade the systemic hemodynamic parameters decreased more, comparing with the intact animals. Thus, N-mimetic effects of acetylcholine are augmented following M-cholinoreceptors blockade; meanwhile M-mimetic effects of acetylcholine on the heart and vessels are increased following N-cholinoreceptors blockade. After the blockade of muscarinic or nicotinic receptors adrenaline injection caused more evaluated increasing of the systemic hemodynamic parameters comparing with intact animals. However, if we injected adrenalin in cats following M-cholinoreceptors blockade combined with inhibition of acetylcholinesterase by proserine, the systemic hemodynamic parameters increased more, comparing with animals with only M-cholinoreceptors blockade. If we injected adrenalin in cats following N-cholinoreceptors blockade combined with inhibition of acetylcholinesterase, the systemic hemodynamic parameters increased less, than in animals with only N-cholinoreceptors blockade. Thus, we concluded that there is reciprocal interaction between muscarininc and nicotinic cholinergic mechanisms in the processes of the nervous regulation of the systemic circulation.
No takes yet. Share an insight, caveat, or question.
Loseѵ et al. (2011) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: