Peripheral muscarinic control of norepinephrine release in the cardiovascular system.

  title={Peripheral muscarinic control of norepinephrine release in the cardiovascular system.},
  author={Erich Muscholl},
  journal={The American journal of physiology},
  volume={239 6},
  • E. Muscholl
  • Published 1 December 1980
  • Biology
  • The American journal of physiology
Activation of muscarinic cholinergic receptors located at the terminal adrenergic nerve fiber inhibits the process of exocytotic norepinephrine (NE) release. This neuromodulatory effect of acetylcholine and related compounds has been discovered as a pharmacological phenomenon. Subsequently, evidence for a physiological role of the presynaptic muscarinic inhibition was obtained on organs known to be innervated by the autonomic ground plexus (Hillarp, Acta. Physiol. Scand. 46, Suppl. 157: 1-68… 
Impulse interval-dependent effect of sympathetic nerve stimulation on evoked acetylcholine release from the rabbit perfused atria preparation
The experiments show a facilitation of evoked acetylcholine release by sympathetic activity, confined to a relatively brief interval immediately following the excitation of the noradrenergic terminal, and is unlikely to be mimicked by exogenous drug application.
Different muscarinic receptors mediate autoinhibition of acetylcholine release and vagally-induced vasoconstriction in the rat isolated perfused heart
The results show that the autoinhibition of acetylcholine release in the rat heart is mediated by M2 receptors and the increase in perfusion pressure upon vagus nerve stimulation is caused by a different muscarinic receptor, more sensitive to hexahydrosiladifenidol than to M2-selective antagonists.
Prejunctional modulation of norepinephrine release in the human iris-ciliary body.
Human ocular sympathetic nerves express inhibitory alpha 2-adrenergic, muscarinic, dopaminergic, prostaglandin, and neuropeptide Y receptors and facilitatory angiotensin II receptors that control the impulse-evoked release of 3H-norepinephrine.
Sympathetic nerve stimulation on the perfused rat heart
The rat heart contains inhibitory muscarine receptors modulating noradrenaline release from adrenergic nerve fibres, and the pA2 values of N-methylatropine and pirenzepine at both of these sites did not differ from the presynaptic affinity constants indicating that neither substance revealed differences in structure between neuronal and myocardial musCarine receptors in the rat heart.
Effects of non-depolarizing neuromuscular blocking agents on norepinephrine release from human atrial tissue obtained during cardiac surgery.
The data suggest that the axon terminals of sympathetic nerves in human heart have muscarinic heteroreceptors whose activation by acetylcholine released from the vagal nerve reduces release of NE, and any neuromuscular blocking agent with antimuscarinic actions and capable of increasing the release ofNE may produce tachycardia.
Influence of acetylcholine, peptides, and other vasodilators on endogenous noradrenaline overflow and vasoconstriction in canine blood perfused gracilis muscle.
The SNS evoked NA overflow was not influenced by a moderate mechanical blood flow reduction or by pronounced reductions of vascular resistance induced by either substance P, VIP, nitroglycerin or felodipine, supporting the idea that the transport of NA from nerve terminal to blood is not importantly influenced by moderate decreases in blood flow or vascular tone.
Evidence that M1 muscarinic receptors enhance noradrenaline release in mouse atria by activating protein kinase C
Evidence is provided that activation of protein kinase C is involved in the signal transduction process of McNeil A 343, which enhances noradrenaline release independently of the cyclic AMP system.