Cholinergic stimulation of vascular prostacyclin synthesis

Boeynaems, Jean‐Marie; Galand, Nicole

doi:10.1016/0090-6980(83)90191-0

Cited by 31 publications

(8 citation statements)

References 26 publications

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“…The con tent of 6-keto PGF|a, a major metabolite of PGI2, was increased in the bathing media, to which the mesenteric arteries stimulated by ACh were exposed, suggesting an increased release of PGI2 from the stimulated arteries. Increase in the release of PGI2 by stimula tion of muscarinic receptors are also demon strated in rabbit coeliac and mesenteric ar teries and aortae [9,10]. ACh was proved in the present study to liberate vasodilator sub stances from perfused dog mesenteric arter ies with intact endothelium, since dog coro nary arteries with damaged endothelium re laxed in response to perfusate through the mesenteric artery stimulated by ACh.…”

Section: Discussionmentioning

confidence: 71%

“…The slight but significant relaxation in the vascular preparation, from which en dothelium is removed, is not necessarily considered to be due to an incomplete endo thelial denudation. ACh releases prostaglan din (PG) D from isolated rabbit coeliac and mesenteric arteries and aortae [8][9][10], which appears to be involved in the vasodilator action of ACh. PGI2 is synthesized not only in endothelium but also in subendothelial tissues [11,12].…”

Section: Introductionmentioning

confidence: 99%

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Endothelium-Dependent and -Independent Mechanisms of Action of Acetylcholine in Monkey and Dog Isolated Arteries

Okamura¹,

Minami²,

Toda³

1989

Pharmacology

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In helical strips of monkey coronary and mesenteric arteries and dog mesenteric arteries partially contracted with prostaglandin (PG) F₂_α, the mechanism of action of acetylcholine (ACh) has been analyzed by the use of pharmacological antagonists and by the endothelium-derived relaxing factor (EDRF) bioassay and the 6-keto PGF_1α radioimmunoassay. In conclusion, ACh releases vasodilator substance(s) from endothelium (EDRF) and also PGs from subendothelial tissues. Vasoconstrictor PGs appear to counteract the dilator action of EDRF in monkey coronary arteries, whereas vasodilator PG, possibly PGI₂ appears to facilitate the relaxation caused by EDRF in monkey and dog mesenteric arteries.

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Section: Discussionmentioning

confidence: 71%

Section: Introductionmentioning

confidence: 99%

Endothelium-Dependent and -Independent Mechanisms of Action of Acetylcholine in Monkey and Dog Isolated Arteries

Okamura¹,

Minami²,

Toda³

1989

Pharmacology

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“…19 ' M Further, a contractile product of arachidonic acid metabolism by cyclooxygenase products may mediate the diminished endothelium-dependent relaxations in the SHR. l5 The effects of indomethacin on acethylcholine-induced and A23187-induced relaxations of the thoracic aorta are found in Table 3.…”

Section: Effects Of Indomethacin On Acetylcholine and A23187 Responsesmentioning

confidence: 99%

Impaired endothelium-dependent relaxations in rabbits subjected to aortic coarctation hypertension.

Miller¹,

Pinto

Mullane³

1987

Hypertension

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SUMMARY Rabbits were rendered hypertensive by suprarenal coarctation of the abdominal aorta. Seven days later, endothelium-dependent and endothelium-independent vascular relaxations were examined in vascular rings taken from hypertensive (thoracic aorta, carotid artery) and normotensive (abdominal aorta) regions. Relaxation of phenylephrine-contracted rings in response to endotheliumdependent agonists (acetylcholine, A23187) was impaired, compared with that in sham-operated and intact controls, in regions exposed to the elevated blood pressure (i.e., above the coarctation). Responses to acetylcholine and A23187 in the abdominal aorta, below the coarctation, were not altered. The diminished endothelium-dependent responses in the thoracic aorta were not affected by pretreatment with the cyclooxygenase inhibitor indomethacin. In contrast to acetylcholine and A23187, responses to the endothelium-independent agonist nitroprusside were not attenuated in vessels from hypertensive regions, indicating that the defect occurred in the endothelium. The EC 50 for acetylcholine-induced relaxations of thoracic aorta correlated significantly with mean arterial pressure above the coarctation, indicating that the extent to which endothelium-dependent relaxation is impaired is in proportion to the degree of blood pressure elevation. This study suggests that the diminished relaxations by endothelium-dependent agonists is a local response to the elevation of blood pressure and is not due to a circulating factor. (Hypertension 10: 164-170, 1987) KEY WORDS • endothelium * vascular relaxation * hypertension • endothelium-dependent relaxing factor • acetylcholine • nitroprusside T HE seminal observation by Furchgott and Zawadzki 1 that the presence of the endothelium is essential for the relaxant effects of acetylcholine precipitated a deluge of studies demonstrating mediation of the vascular effects of a variety of autacoids by the endothelium, in a host of different blood vessels in vitro (see References 2-4 for review). Removal of the endothelial layer could ablate the relaxant properties of agents such as adenosine 5'-diphosphate or substance P or convert them to weak contractions, as observed with acetylcholine or thrombin, as well as enhance the contractile activity of agonists such as

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“…Since the vasodilatory effect of EOCA was similarly attenuated by the removal of endothelium and by the inhibition of the cyclooxygenase, this may indicate that EOCA stimulate the release of prostacyclin from the endothelial cells. It has been demonstrated that prostacyclin synthesis by muscarinic agents such ACh is due to the activation of M 3 receptors located on endothelial cells but not on the smooth muscle cells [35, 36]. …”

Section: Discussionmentioning

confidence: 99%

Cardiovascular Effects of the Essential Oil of Croton argyrophylloides in Normotensive Rats: Role of the Autonomic Nervous System

Alves-Santos

Siqueira

Duarte

et al. 2016

Evidence-Based Complementary and Alternative Medicine

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Cardiovascular effects of the essential oil of Croton argyrophylloides Muell. Arg. (EOCA) were investigated in normotensive rats. In saline-pretreated anesthetized or conscious rats, intravenous (i.v.) injection of the EOCA induced dose-dependent hypotension. Dose-dependent tachycardia was observed only in conscious rats. In anesthetized rats, cervical bivagotomy failed to enhance EOCA-induced hypotension but unmasked significant bradycardia. In conscious rats, i.v. pretreatment with methylatropine, but not with atenolol or L-NAME, reduced both hypotensive and tachycardiac responses to EOCA. However, hexamethonium pretreatment reverted the EOCA-induced tachycardia into significant bradycardia without affecting the hypotension. In aortic ring preparations precontracted with phenylephrine, EOCA induced a concentration-dependent relaxation that was significantly reduced by vascular endothelium removal and pretreatment with atropine, indomethacin, or glibenclamide but remained unaffected by pretreatment with L-NAME or TEA. It is concluded that i.v. treatment with EOAC decreased blood pressure probably through an active vascular relaxation rather than withdrawal of sympathetic tone. Muscarinic receptor stimulation, liberation of the endothelium-derived prostacyclin, and opening KATP channels are partially involved in the aortic relaxation induced by EOCA and in turn in the mediation of EOCA-induced hypotension. EOCA-induced tachycardia in conscious rats appears to be mediated reflexly through inhibition of vagal drive to the heart.

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Cholinergic stimulation of vascular prostacyclin synthesis

Cited by 31 publications

References 26 publications

Endothelium-Dependent and -Independent Mechanisms of Action of Acetylcholine in Monkey and Dog Isolated Arteries

Endothelium-Dependent and -Independent Mechanisms of Action of Acetylcholine in Monkey and Dog Isolated Arteries

Impaired endothelium-dependent relaxations in rabbits subjected to aortic coarctation hypertension.

Cardiovascular Effects of the Essential Oil of Croton argyrophylloides in Normotensive Rats: Role of the Autonomic Nervous System

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