Effects of K+Channel Blockers on Acetylcholine-Induced Vasodilation in Guinea-pig Choroid

Tamai, Kazushi; Suzuki, Hiroyoshi; Hashitani, Hikaru; Shirai, Shoichiro; Ogura, Yuichiro

doi:10.1006/exer.1999.0674

Cited by 4 publications

(2 citation statements)

References 33 publications

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“…Thirdly, our data strongly suggest the important involvement of the Kir and K v 1.6 channels in mediating endothelium-dependent dilation to ACh. Previous studies have shown that K + released from the endothelium can act as an EDHF by activating K Ca and stimulating Na + /K + -ATPase and Kir channel in guinea pig choroidal arterioles and rat hepatic arteries, respectively 51 52 . Therefore, we examined the possible role of potassium channels in endothelium-dependent vasodilation of the mouse ophthalmic artery.…”

Section: Discussionmentioning

confidence: 99%

The Gatekeepers in the Mouse Ophthalmic Artery: Endothelium-Dependent Mechanisms of Cholinergic Vasodilation

Manicam

Staubitz

Brochhausen

et al. 2016

Sci Rep

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Cholinergic regulation of arterial luminal diameter involves intricate network of intercellular communication between the endothelial and smooth muscle cells that is highly dependent on the molecular mediators released by the endothelium. Albeit the well-recognized contribution of nitric oxide (NO) towards vasodilation, the identity of compensatory mechanisms that maintain vasomotor tone when NO synthesis is deranged remain largely unknown in the ophthalmic artery. This is the first study to identify the vasodilatory signalling mechanisms of the ophthalmic artery employing wild type mice. Acetylcholine (ACh)-induced vasodilation was only partially attenuated when NO synthesis was inhibited. Intriguingly, the combined blocking of cytochrome P450 oxygenase (CYP450) and lipoxygenase (LOX), as well as CYP450 and gap junctions, abolished vasodilation; demonstrating that the key compensatory mechanisms comprise arachidonic acid metabolites which, work in concert with gap junctions for downstream signal transmission. Furthermore, the voltage-gated potassium ion channel, Kv1.6, was functionally relevant in mediating vasodilation. Its localization was found exclusively in the smooth muscle. In conclusion, ACh-induced vasodilation of mouse ophthalmic artery is mediated in part by NO and predominantly via arachidonic acid metabolites, with active involvement of gap junctions. Particularly, the Kv1.6 channel represents an attractive therapeutic target in ophthalmopathologies when NO synthesis is compromised.

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Section: Discussionmentioning

confidence: 99%

The Gatekeepers in the Mouse Ophthalmic Artery: Endothelium-Dependent Mechanisms of Cholinergic Vasodilation

Manicam

Staubitz

Brochhausen

et al. 2016

Sci Rep

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“…In the iris-ciliary body of the eye, it is possible that there are several types of K + channels (ATP-sensitive, voltage-sensitive, Ca 2+ -activated) that could be involved in norepinephrine release. Actions of K + channel blockers have been studied on the sympathetic nerves of the rat vas deferens [14] and on acetylcholine-induced vasodilation of guinea-pig choroids [20]. Furthermore, 4-AP-stimulated norepinephrine release has been demonstrated in the rat hippocampus [21].…”

Section: Discussionmentioning

confidence: 99%

4-Aminopyridine Transiently Increases Intraocular Pressure in Rabbits

Socci

Chu²,

Bayorh³

et al. 2003

Pharmacology

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The purpose of this study is to determine the mechanisms of action involved in the ocular hypertension induced by 4-aminopyridine (4-AP), a voltage-dependent potassium (K⁺) channel blocker, in rabbits. Topical application of 4-AP elevated intraocular pressure (IOP). This action caused increases in the aqueous flow rate as well as aqueous levels of protein and norepinephrine. In isolated iris-ciliary body preparations, 4-AP (0.01, 0.1, 1 mmol/l) caused dose-related increases in field-stimulated norepinephrine release by 43, 222 and 243%, respectively. Taken together, the IOP-elevating effect evoked by 4-AP was associated with enhancement of aqueous norepinephrine levels and norepinephrine release from sympathetic nerves of the iris-ciliary body. These results demonstrate that the 4-AP-sensitive K⁺ channels in sympathetic nerves and the ciliary epithelium are the potential sites of action of the 4-AP-induced ocular hypertension.

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The endothelium-derived hyperpolarising factor (EDHF) in isolated bovine choroidal arteries

Delaey

Boussery

Breyne

et al. 2007

Experimental Eye Research

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Effects of K+Channel Blockers on Acetylcholine-Induced Vasodilation in Guinea-pig Choroid

Cited by 4 publications

References 33 publications

The Gatekeepers in the Mouse Ophthalmic Artery: Endothelium-Dependent Mechanisms of Cholinergic Vasodilation

The Gatekeepers in the Mouse Ophthalmic Artery: Endothelium-Dependent Mechanisms of Cholinergic Vasodilation

4-Aminopyridine Transiently Increases Intraocular Pressure in Rabbits

The endothelium-derived hyperpolarising factor (EDHF) in isolated bovine choroidal arteries

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