Norepinephrine and Acetylcholine Transmitter Mechanisms in Large Cerebral Arteries of the Pig

Lee, Tony Jer‐Fu; Kinkead, Lewis R.; Sarwinski, S.

doi:10.1038/jcbfm.1982.50

Cited by 72 publications

(52 citation statements)

References 21 publications

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“…In the present study, relaxation of the basilar arteries induced by isoproterenol that acts on both presynaptic and postsynaptic b-adrenoceptors, however, was not appreciably affected by physostigmine, galantamine, or neostigmine. Therefore, ChEI inhibition of vasodilation induced by nicotine or choline in the present study was not likely due to any possible ChEI effect on presynaptic b 2 -adrenoceptors or postsynaptic b 1 -adrenoceptors (Lee et al, 1982;Lee, 2000). Moreover, relaxation induced by sodium nitroprusside, which is known to release NO on entering the smooth muscle cells (Ignarro et al, 1981), was not affected by these three ChEIs either.…”

Section: Discussionmentioning

confidence: 74%

“…The SCG is the origin of the cerebral perivascular sympathetic nerves in all species including the pig (Lee et al, 1982). Cultured porcine SCG neurons have been found to contain a7-nAChRs, which mediate calcium influx on activation by nicotinic agonists, like those found in cerebral perivascular sympathetic nerve terminals (Si and Lee, 2002).…”

Section: Discussionmentioning

confidence: 99%

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Cholinesterase Inhibitor Blockade and its Prevention by Statins of Sympathetic α7-nAChR-Mediated Cerebral Nitrergic Neurogenic Vasodilation

Mozayan

Chen

et al. 2006

J Cereb Blood Flow Metab

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Cholinesterase inhibitors (ChEIs) have been used to treat Alzheimer's disease (AD). The efficacy of these drugs, however, is less than satisfactory. The possibility that ChEIs may have effects unrelated to ChE activity, such as negatively modulate neuronal nicotinic acetylcholine receptors (nAChRs) was evaluated. Since a7-nAChRs on cerebral perivascular sympathetic neurons mediate cerebral parasympathetic-nitrergic vasodilation, effects of physostigmine, neostigmine, and galantamine on a7-nAChR-mediated dilation in isolated porcine basilar arterial rings denuded of endothelium was examined using in vitro tissue bath technique. The results indicated that these ChEIs blocked vasodilation induced by choline (0.3 mmol/L), nicotine (0.1 mmol/L), and transmural nerve stimulation (TNS). The ChEI inhibition of dilation induced by TNS but not by choline or nicotine was prevented by atropine (0.1 lmol/L) pretreatment. Furthermore, using confocal microscopy, significant calcium influx induced by choline and nicotine in cultured porcine superior cervical ganglion (SCG) cells was attenuated by ChEIs. In a7-nAChR-expressed Xenopus oocytes, nicotine-induced inward currents were attenuated by a-bungarotoxin and ChEIs. Moreover, ChEI inhibition of nicotine-and choline-induced dilation was prevented by pretreatment with mevastatin and lovastatin (10 lmol/L), which did not affect ChEI inhibition of TNS-induced relaxation. These findings suggest that ChEIs inhibit the a7-nAChRs located on postganglionic sympathetic nerve terminals of SCG origin, causing a decreased release of nitric oxide in the neighboring nitrergic nerves and cerebral vasodilation. Inhibition of a7-nAChRs leading to a potential cerebral hypoperfusion may contribute to the limitation of ChEIs and question the validity of using a ChEI alone in treating AD. The efficacy of ChEIs may be improved by concurrent use of statins.

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Section: Discussionmentioning

confidence: 74%

Section: Discussionmentioning

confidence: 99%

Cholinesterase Inhibitor Blockade and its Prevention by Statins of Sympathetic α7-nAChR-Mediated Cerebral Nitrergic Neurogenic Vasodilation

Mozayan

Chen

et al. 2006

J Cereb Blood Flow Metab

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“…lntraparenchymal vessels have been more difficult to study because of their location and small size. The responsiveness of these smaller vessels has been inferred from studies of Duckles, 1979;Lee et a!. , 1982).…”

mentioning

confidence: 99%

“…Studies of human cerebral vessels are scarce and important because of the difficulty of carrying out physiological investigations with human tissues and considerable species variations in animals (Duckles et a!., 1977;Duckles, 1979;Lee et a!. , 1982).…”

mentioning

confidence: 99%

α-Adrenoreceptors and Muscarine Receptors in Human Pial Arteries and Micro Vessels: A Receptor Binding Study

Ferrari-Dileo

Potter

1985

J Cereb Blood Flow Metab

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Summary: Human pial arteries and intraparenchymal microvessels were isolated for enzyme assays and radio ligand binding studies of receptors, Special attention was paid to contamination with brain tissue, which was as sessed by luxol staining and cerebroside assays for myelin and by scanning electron microscopy, The amount of contamination was �1% for pial vessels and 14% for microvessel preparations, Significant levels of

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“…The endogenous catecholamine is exclusively norepinephrine (NE) (3,4), which can be released experimentally upon electrical stimulation of these nerves (5 -7). Transmural nerve stimulation (TNS)-induced constriction in isolated cerebral arteries of rabbits and dogs, however, was not blocked by a-adrenoceptor antagonists (1,8,9).…”

Section: Sympathetic Adrenergic Innervation In the Cerebral Circulationmentioning

confidence: 99%

Pharmacology and Physiology of Perivascular Nerves Regulating Vascular Function

Lee

2002

Japanese Journal of Pharmacology

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ABSTRACT-The presence of close apposition between the adrenergic and the non-adrenergic or nitrergic nerve terminals in large cerebral arteries in several species is well documented. The axo-axonal distance between these different types of nerve terminals is substantially closer than the synaptic distance between the adventitial nerve terminals and the outermost layer of smooth muscle in the media. This feature suggests that a functional axo-axonal interaction between nerve terminals is more likely to occur than that between the nerve and muscle. Thus, transmitters released from one nerve terminal may modulate release of transmitters from the neighboring nerve terminals, resulting in a neurogenic response. We have reported that nicotine-induced nitric oxide (NO)-mediated neurogenic vasodilation is dependent on intact sympathetic innervation in porcine and cat cerebral arteries. Evidence also has been presented to indicate that nicotine acts on a 7-nicotinic receptors located on sympathetic nerve terminals, resulting in release of norepinephrine which then diffuses to act on b2-adrenoceptos located on the neighboring nitrergic nerve terminals to release NO and therefore vasodilation. The predominant facilitatory effect of b2-adrenoceptors in releasing NO is compromised by presynaptic a2-adrenoceptors located on the same nerves. Activation of cerebral sympathetic nerves may cause NO-mediated dilation in large cerebral arteries at the base of the brain.

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Norepinephrine and Acetylcholine Transmitter Mechanisms in Large Cerebral Arteries of the Pig

Cited by 72 publications

References 21 publications

Cholinesterase Inhibitor Blockade and its Prevention by Statins of Sympathetic α7-nAChR-Mediated Cerebral Nitrergic Neurogenic Vasodilation

Cholinesterase Inhibitor Blockade and its Prevention by Statins of Sympathetic α7-nAChR-Mediated Cerebral Nitrergic Neurogenic Vasodilation

α-Adrenoreceptors and Muscarine Receptors in Human Pial Arteries and Micro Vessels: A Receptor Binding Study

Pharmacology and Physiology of Perivascular Nerves Regulating Vascular Function

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