Acetylcholine stimulates the release of prostacyclin by rabbit aorta endothelium

Beetens, Johan; Hove, C. Van; Rampart, M.; Herman, Arnold G.

doi:10.1111/j.2042-7158.1983.tb02924.x

Cited by 32 publications

(14 citation statements)

References 5 publications

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“…Recent studies have suggested that 15 -lipoxygenase products of arachidonic acid relax cat cerebral arteries 23 and rat aorta, 24 mesenteric, and pulmonary arteries. 25 The 5-lipoxygenase metabolites LTC 4 and LTD 4 have been found to relax canine superior mesenteric and renal artery rings in an endotheliumdependent manner. 8 - 9 It has also been demonstrated that LTD 4 -induced relaxation depends on the release of an EDRF which, in a manner similar to that of ACh, subsequently decreases vasomotor tone via activation of guanylate cyclase and generation of cyclic guanosine monophosphate.…”

Section: Discussionmentioning

confidence: 99%

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Endothelium-dependent relaxation of human basilar arteries.

Kanamaru

Waga

Fujimoto

et al. 1989

Stroke

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We studied the effects of acetylcholine and calcium ionophore A23187 on human basilar artery rings. Among 11 arteries, both agents produced significant relaxations in five, A23187 but not acetylcholine caused a response in six, and neither agent was effective in four. After rubbing off the endothelium, the relaxations induced by both agents were significantly attenuated. Indomethacin (a cyclooxygenase inhibitor) and AA861 (a specific inhibitor of 5-lipoxygenase) did not but SKF525A (an inhibitor of cytochrome P450-dependent monooxygenase) did significantly inhibit the acetylcholine-induced relaxation in human basilar arteries. On the other hand, AA861 inhibited while neither indomethacin nor SKF525A had any effect on the A23187-induced relaxation. Our results suggest that different mechanisms may be involved in acetylcholine and A23187-induced relaxations in human basilar arteries. (Stroke 1989;20:1208-1211)

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Section: Discussionmentioning

confidence: 99%

“…7 Moreover, the peptidoleukotrienes LTC 4 and LTD 4 possess the capacity to relax some arterial rings in an endothelium-dependent manner. 8 ' 9 It has also been demonstrated that the decrease in tone in response to ACh and arachidonic acid is attenuated in the presence of SKF525A, an inhibitor of cytochrome P450-dependent monooxygenase.…”

mentioning

confidence: 99%

Endothelium-dependent relaxation of human basilar arteries.

Kanamaru

Waga

Fujimoto

et al. 1989

Stroke

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“…Recently acetylcholine-induced relaxation has been explained by the release of an inhibitory substance (prostacycin) from rabbit aorta endothelium (Beetens et al, 1983). Therefore, the mechanism by which K+ induces relaxation in pig circular muscles might involve the release of inhibitory transmitters from nerve terminals or endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

Potassium induces relaxation and hyperpolarization of circular muscles but contraction of longitudinal muscles of pig duodenum

Kimura

1984

British J Pharmacology

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“…After completion of the surgical procedures and a 60-minute period of equilibration, the dogs received an intravenous bolus infusion of meclofenamate (5 mg/kg) to eliminate the effect of Ach-stimulated prostacyclin production. 9 This was followed by a 30-minute intrarenal infusion of Ach (25 ng/kg/min, Sigma Chemical Co., St. Louis, Missouri) at the end of which 30 additional minutes were allowed for recovery. After this step, the dogs were assigned to one of the following experimental protocols.…”

Section: Methodsmentioning

confidence: 99%

Effects of NG-monomethyl-L-arginine and L-arginine on acetylcholine renal response.

et al. 1990

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Intrarenal infusion of acetylcholine in meclofenamate-treated dogs significantly increased renal blood flow, diuresis, and natriuresis. Intrarenal infusions of either A^'-monomethyl-L-arginine (inhibitor of endothelium-derived relaxing factor formation), or L-arginine (precursor of endothelium-derived relaxing factor formation) did not modify basal levels of those parameters. However, the infusion of A^-monomethyl-L-arginine inhibited the acetylcholineinduced increases in renal blood flow and diuresis without affecting natriuresis, which increased significantly. The infusion of L-arginine failed to further enhance hemodynamic and excretory effects elicited by acetylcholine. I t is well known that the in vitro vascular relaxation induced by acetylcholine (Ach) results from the release of a diffusible relaxing substance, termed endothelium-derived relaxing factor. 1Experimental evidence obtained in these in vitro preparations demonstrates that the endotheliumderived relaxing factor is the free radical nitric oxide.2 -3 Nitric oxide is synthesized from the amino acid L-arginine (L-Arg), 4 and this synthesis is competitively inhibited by A^-monomethyl-L-arginine (LNMMA). 5 The role of nitric oxide in blood pressure regulation has been studied using L N M M A and L-Arg in guinea pigs and rabbits. 6 -7 However, the importance of these actions in vivo is incompletely understood. Ach has been shown to induce the release of endothelium-derived relaxing factor in vitro 1 -2 and when infused intrarenally produces vasodilation accompanied by diuresis and natriuresis. The objective of the present study was to determine whether the vasodilatory and excretory effects of Ach in the dog kidney are mediated by nitric oxide during prostaglandin synthesis inhibition. To address this purpose, we evaluated 1) if the renal vasodilatory and excretory effects of Ach were inhibited in the presence of L N M M A and 2) if these inhibitory effects of L N M M A were abolished by the simultaneous administration of L-Arg. MethodsThe experiment was performed in 16 mongrel dogs of either sex (15-20 kg) anesthetized with sodium pentobarbital (25 mg/kg i.v.). Previously, the dogs had been maintained on a normal diet (sodium 0.42%, potassium 0.71%, calcium 1.6%) and tap water ad libitum. The dogs were ventilated mechanically with a respirator. A femoral artery was cannulated and mean arterial pressure was monitored with a pressure transducer (Statham P23ID, Gould Inc., Hato Rey, Puerto Rico) and recorded on a polygraph (Gould Inc., Cleveland, Ohio). A femoral vein was cannulated for the administration of 2% inulin solution (1 ml/min) and additional anesthetic. The left kidney was exposed through a flank incision, and care was taken not to damage the renal nerves. Renal blood flow (RBF) was measured with a noncannulating electromagnetic flow probe (Carolina Medical Electronics Inc., King, North Carolina) placed around the renal artery. Distal to the flow probe a curved

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Acetylcholine stimulates the release of prostacyclin by rabbit aorta endothelium

Cited by 32 publications

References 5 publications

Endothelium-dependent relaxation of human basilar arteries.

Endothelium-dependent relaxation of human basilar arteries.

Potassium induces relaxation and hyperpolarization of circular muscles but contraction of longitudinal muscles of pig duodenum

Effects of NG-monomethyl-L-arginine and L-arginine on acetylcholine renal response.

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