2007
DOI: 10.1097/fjc.0b013e3181583d9b
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Effects of Prostaglandin E1 on Vascular ATP-Sensitive Potassium Channels

Abstract: The results indicate that the activation of vascular KATP channels played an important role in the PKA-dependent PGE1-induced vasorelaxation. Furthermore, an electrophysiological experiment demonstrated that PGE1 activated vascular KATP channels via PKA activation.

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Cited by 17 publications
(15 citation statements)
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References 27 publications
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“…Whether β-blockade may trigger coronary spasm or protect the post-ischemic myocardium warrants further investigation. Prostaglandin E 1 is generally regarded to have a myocardial protective effect [10]. However, several anecdotal reports in the Japanese literature have demonstrated a temporal coincidence between prostaglandin E 1 administration and the occurrence of coronary spasm [11][12][13].…”
Section: Discussionmentioning
confidence: 99%
“…Whether β-blockade may trigger coronary spasm or protect the post-ischemic myocardium warrants further investigation. Prostaglandin E 1 is generally regarded to have a myocardial protective effect [10]. However, several anecdotal reports in the Japanese literature have demonstrated a temporal coincidence between prostaglandin E 1 administration and the occurrence of coronary spasm [11][12][13].…”
Section: Discussionmentioning
confidence: 99%
“…As with BK Ca channels and K V channels, vasodilators that signal through the cAMP signaling pathway activate K ATP channels (Akatsuka et al, 1994; Bouchard, Dumont, & Lamontagne, 1994; Dart & Standen, 1993; Eguchi et al, 2007; Jackson, 1993; Kitazono, Heistad, & Faraci, 1993b; Kleppisch & Nelson, 1995; Ming, Parent, & Lavallee, 1997; Nakashima & Vanhoutte, 1995; C. P. Nelson et al, 2011; M.…”
Section: Potassium Channels and Regulation Of Vsm Contractionmentioning
confidence: 99%
“…K ATP channels, working as molecular sensors of cellular metabolism [21] , regulate vascular tone in response to endogenous substances, such as adenosine, noradrenaline and vasopressin [15][16][17][18][19] . We hypothesized that K ATP channels contribute to the BPV after SAD.…”
Section: Discussionmentioning
confidence: 99%
“…However, the definite mechanism by which BPV dramatically increase after SAD surgery is still unclear. ATP-sensitive potassium (K ATP ) channels are critical regulators of vascular tone, forming a focal point for signaling by many vasoactive transmitters, including adenosine, calcitonin gene-related peptide, noradrenaline, insulin, prostaglandin E 1 , and arginine vasopressin [15][16][17][18][19] . It is therefore a molecular sensor, responding to local metabolic need and vasoactive transmitters, altering smooth muscle contractility and so blood flow to retain homeostasis [20][21][22] .…”
Section: Introductionmentioning
confidence: 99%