Presynaptic M2-muscarinic receptors on noradrenergic nerve endins and endothelium-derived M3 receptor in cat cerebral arteries

Alonso, María J.; Arribas, Silvia M.; Marı́n, Jesús; Balfagón, Gloria; Salaíces, Mercedes

doi:10.1016/0006-8993(91)91438-7

Cited by 24 publications

(15 citation statements)

References 38 publications

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“…As described earlier (Section III.A.8. ) on cerebral arteries and in the literature on cat cerebral artery (Alonso et al, 1991), dog mesenteric artery (Zhang et al, 1997b), saphenous vein (O'Rourke andVanhoutte, 1987), and guinea pig carotid artery (Casado et al, 1994), M 2 muscarinic receptors would be responsible for the inhibitory action (Fig. 6).…”

Section: Interaction Of Nitrergic Cholinergic and Adrenergic Nementioning

confidence: 76%

“…The vasoconstrictor response to adrenergic nerve stimulation is attenuated by prejunctional actions of acetylcholine on the M 2 muscarinic subtype in canine saphenous vein (O'Rourke and Vanhoutte, 1987), feline cerebral artery (Alonso et al, 1991), and guinea pig carotid artery (Casado et al, 1994) or M 2 and M 3 subtypes in the bovine cerebral artery (Ferrer et al, 1992). In vasculature in which the vascular size is under predominant control of adrenergic nerves over nitrergic nerves, vasodilatation due to decreased adrenergic nerve function would be induced by neurogenic acetylcholine.…”

Section: E Antimuscarinic Agentsmentioning

confidence: 99%

See 1 more Smart Citation

The Pharmacology of Nitric Oxide in the Peripheral Nervous System of Blood Vessels

Toda

Okamura

2003

Pharmacological Reviews

275

228

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Section: Interaction Of Nitrergic Cholinergic and Adrenergic Nementioning

confidence: 76%

Section: E Antimuscarinic Agentsmentioning

confidence: 99%

The Pharmacology of Nitric Oxide in the Peripheral Nervous System of Blood Vessels

Toda

Okamura

2003

Pharmacological Reviews

275

228

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“…The ACh-induced contraction of endothelium-removed preparations was significantly protected against the phenoxybenzamine-effect only by pretreatment with pFHHSiD (2 gM; Figure 7b and (Armstead et al, 1988;Hu & El-Fakahany, 1990) and PD142505 (Schwarz et al, 1994) (Duckles, 1988). However, in arterial preparations derived from either the dog or cat (Rubanyi et al, 1987;Dauphin & Hamel, 1990;Alonso et al, 1991) (Furchgott & Zawadzki, 1980;Angus et al, 1983), several of the autoradiographic or radioligand binding studies failed to detect the presence of muscarinic receptors on endothelial cells of blood vessels (Stephenson et al, 1988;Yamada et al, 1990;De Michele et al, 1991). In contrast, autoradiographic investigations in the rabbit thoracic aorta (Tsukahara et al, 1989) and radioligand binding experiments performed in the bovine thoracic aorta (Brunner & Kukovetz, 1991;Traish et al, 1994) have shown the presence of M1 and/or M3 receptors on endothelial cells.…”

Section: Effects Of Muscarinic Antagonistsmentioning

confidence: 99%

M₁ and M₃ muscarinic receptors in human pulmonary arteries

Norel

Walch

Costantino³

et al. 1996

British J Pharmacology

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1 Acetylcholine (ACh) and the M, agonists (McN-A-343 or PD142505) relaxed human isolated pulmonary arteries which were pre-contracted with noradrenaline (10 ,gM). In preparations where the endothelium had been removed ACh induced a contractile response whereas the M1 agonists (McN-A-343 or PD142505) had no effect. 2 ACh-and McN-A-343-induced relaxations were abolished after treatment of endothelium-intact preparations with the drug combination N0-nitro-L-arginine (L-NOARG: 0.1 mM) and indomethacin (1.7 giM). 3 The affinity (pKB value) for pirenzepine was higher in human pulmonary arteries when tissues were relaxed with McN-A-343 as compared with ACh (pKB values, 7.71+0.30 (n=4) and 6.68+0.15 (n=8), respectively). In addition, the affinity for pFHHSiD against McN-A-343-and ACh-induced relaxations was 6.86+0.13 (n=3) and 7.35+0.11 (n=9), respectively. 4 The low affinities for methoctramine in human isolated pulmonary arteries with the endothelium either intact or removed, suggested the lack of involvement of M2 and M4 receptors in the ACh responses.5 Phenoxybenzamine (3 /M: 30 min) abolished both ACh contraction and relaxation in human pulmonary artery. The ACh contraction was present when the phenoxybenzamine treatment was preceded by incubation with pFHHSiD (2 gM) but not with pirenzepine (1 gM). In addition, the ACh relaxation was present when preparations were treated with either pFHHSiD (2 gM) or pirenzepine (1 gM), before exposure to phenoxybenzamine.6 These results in human isolated pulmonary arteries support the notion that only M3 receptors, on smooth muscle, mediate the ACh-induced contraction whereas M3 and M, receptors are involved in the endothelium-dependent ACh-induced relaxation.

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“…(Komori & Suzuki, 1987;Orphanos & Catravas, 1989;Garcia-Villalon et al, 1991), the M2 subtype (Hynes et al, 1986;Duckles, 1988) and the M3 subtype (McCormack et al, 1988;Duckles & Garcia-Villalon, 1990;Dauphin & Hamel, 1990;Brunner et al, 1991;Jaiswal et al. 1991;Garcia-Villalon et al, 1991;Alonso et al, 1991;Shimizu et al, 1993). Each muscarinic receptor subtype may contribute to the local control of vascular reactivity.…”

Section: Relaxationmentioning

confidence: 99%

“…The M3 muscarinic receptors mediate endothelium-dependent relaxation in pial arterioles of mice (Shimizu et al, 1983), the rabbit ear artery (Duckles & Garcia-Villalon, 1990), the rat pulmonary artery (McCormack et al, 1988), the bovine coronary artery (Brunner et al, 1991), the rabbit aorta (Jaiswal et al, 1991), the rabbit pial artery (Garcia-Villalon et al, 1991) and the cat cerebral artery (Dauphin & Hamel, 1990;Alonso et al, 1991). In addition, activation of different muscarinic receptor subtypes in the same preparation can cause the release of different endothelial vasoactive factors; indeed, in the rabbit saphenous artery, the release of EDRF and that of endothelium-derived hyperpolarizing factor are mediated by activation of M2 and Ml subtypes, respectively (Komori & Suzuki, 1987).…”

Section: Introductionmentioning

confidence: 99%

Mediation by M₃‐muscarinic receptors of both endothelium‐dependent contraction and relaxation to acetylcholine in the aorta of the spontaneously hypertensive rat

Boulanger

Morrison

Vanhoutte

1994

British J Pharmacology

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1 Experiments were designed to characterize the subtype(s) of endothelial muscarinic receptor that mediate(s) endothelium-dependent relaxation and contraction in the aorta of spontaneously hypertensive rats (SHR). 2 Rings of SHR aorta with endothelium were suspended in organ baths for the measurement of isometric force. Ecothiopate (an inhibitor of acetylcholinesterase) was present throughout the experiments. Endothelium-dependent contraction to acetylcholine was studied in quiescent aortic rings in the presence of N0-nitro-L-arginine (to prevent the formation of nitric oxide). Endothelium-dependent relaxation to acetylcholine was obtained during contraction to phenylephrine and in the presence of indomethacin (to inhibit cyclo-oxygenase activity). Responses to acetylcholine were assessed against the non-preferential muscarinic receptor antagonist, atropine, and the preferential antagonists pirenzepine (M,), methoctramine (M2) and 4-diphenylacetoxy-N-methylpiperidine methobromide (4-DAMP; M3).3 The potency of acetylcholine in inducing endothelium-dependent contraction was 6.54 ± 0.07 (EC5,,). Atropine, pirenzepine, methoctramine and 4-DAMP displayed competitive antagonism towards the endothelium-dependent contraction to acetylcholine. The pA2 values for these muscarinic receptor antagonists were estimated from Arunlakshana-Schild plots to be (-logM) 9.48 ± 0.07, 6.74 ± 0.22, 6.30 ± 0.20 and 9.39 ± 0.22 respectively. The potency of acetylcholine in inducing endotheliumdependent relaxation was 7.82 ± 0.09 (ICW). Atropine, pirenzepine and 4-DAMP displayed competitive antagonism towards the endothelium-dependent relaxation to acetylcholine but methoctramine had no effect. The pA2 values for atropine and 4-DAMP for the relaxation to acetylcholine were estimated from Arunlakshana-Schild plots to be (-log M) 9.15 ± 0.23 and 9.63 ± 0.28, respectively. These results suggest that the muscarinic M3 receptor subtype mediates both endothelium-dependent relaxation and contraction to acetylcholine in SHR aorta.

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Presynaptic M2-muscarinic receptors on noradrenergic nerve endins and endothelium-derived M3 receptor in cat cerebral arteries

Cited by 24 publications

References 38 publications

The Pharmacology of Nitric Oxide in the Peripheral Nervous System of Blood Vessels

The Pharmacology of Nitric Oxide in the Peripheral Nervous System of Blood Vessels

M₁ and M₃ muscarinic receptors in human pulmonary arteries

Mediation by M₃‐muscarinic receptors of both endothelium‐dependent contraction and relaxation to acetylcholine in the aorta of the spontaneously hypertensive rat

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Presynaptic M2-muscarinic receptors on noradrenergic nerve endins and endothelium-derived M3 receptor in cat cerebral arteries

Cited by 24 publications

References 38 publications

The Pharmacology of Nitric Oxide in the Peripheral Nervous System of Blood Vessels

The Pharmacology of Nitric Oxide in the Peripheral Nervous System of Blood Vessels

M1 and M3 muscarinic receptors in human pulmonary arteries

Mediation by M3‐muscarinic receptors of both endothelium‐dependent contraction and relaxation to acetylcholine in the aorta of the spontaneously hypertensive rat

Contact Info

Product

Resources

About

M₁ and M₃ muscarinic receptors in human pulmonary arteries

Mediation by M₃‐muscarinic receptors of both endothelium‐dependent contraction and relaxation to acetylcholine in the aorta of the spontaneously hypertensive rat