Acetylcholine-induced vasoconstrictor response of coronary vessels in rats: A possible contribution of M2 muscarinic receptor activation

Nasa, Yoshihisa; Kume, Hiroko; Takeo, Satoshi

doi:10.1007/bf02767046

Cited by 14 publications

(3 citation statements)

References 37 publications

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“…Co-administration of nifedipine with Tiotropium bromide also shows significant reduction in coronary flow. Muscarinic receptor activation has previously been associated with acetylcholine mediated vasoconstriction in rodent coronary vessels (Nasa et al, 1997),…”

Section: Discussionmentioning

confidence: 99%

Tiotropium bromide, a long acting muscarinic receptor antagonist triggers intracellular calcium signalling in the heart

Cassambai

Mee

Renshaw

et al. 2019

Toxicology and Applied Pharmacology

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Section: Discussionmentioning

confidence: 99%

Tiotropium bromide, a long acting muscarinic receptor antagonist triggers intracellular calcium signalling in the heart

Cassambai

Mee

Renshaw

et al. 2019

Toxicology and Applied Pharmacology

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“…Case 4 in Table 2, who also smoked tobacco, was later found to have severe occlusion of both left anterior descending and right coronary arteries. The muscarinic alkaloids of betel can induce coronary vasospasm (10,18) and the concomitant ingestion of alcohol in these patients may also aggravate vasospasm hours after exposure (25). However, epidemiologic studies are needed to clarify whether there is any association between betel and AMI.…”

Section: Reprintsmentioning

confidence: 98%

“…Arecoline is the most potent at M1-2-3 and arecaidine at M2 (8,9). In addition, arecoline possesses weak ganglionic nicotine agonism (10).…”

Section: Introductionmentioning

confidence: 99%

Acute Toxicities of Betel Nut: Rare but Probably Overlooked Events

Deng

Ger

Tsai

et al. 2001

Journal of Toxicology: Clinical Toxicology

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Betel nut chewing has long been a social habit in Taiwan and other Asian and tropical countries. It produces various autonomic and psychoneurologic effects including tachycardia, flushing, warmth, cholinergic activation, alertness, and euphoria. Although the oral carcinogenic effects are well known, data concerning its acute toxicity are few. To better understand the toxicity of betel nut, cases reported to the Taiwan Poison Control Center as probable or possible betel nut-related toxicity (January 1988-June 1998) were reviewed. In the 17 cases suitable for review (14 males, 3 females, age 21 to 60 years), the most common manifestations were tachycardia/palpitations (7); tachypnea/dyspnea (6); hypotension and sweating (5); vomiting, dizziness, and chest discomfort (4); abdominal colic, nausea, numbness, and coma (3); and acute myocardial infarction and related manifestations (2). The reported quantity of betel nut used was low (1 to 6 nuts), except an extract of 100 betel nuts was used in 1 case and 66 chewed in another. Most cases recovered within 24 hours after the exposure. One patient developed probable acute myocardial infarction and ventricular fibrillation and died despite repeated cardiac defibrillation. Although betel nut chewing is widespread, significant toxicity as reported to a poison center is rare. Because most betel nut-related effects are transient and mild in nature, the incidence of such events is likely to be underreported. Nevertheless, betel nut chewing can produce significant cholinergic, neurological, cardiovascular, and gastrointestinal manifestations. It is possible that it may aggravate cardiac diseases in susceptible patients but this hypothesis must be further investigated. Treatment is symptomatic. With timely support, rapid and complete recovery is anticipated but a small risk of major complications cannot yet be discounted.

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