2001
DOI: 10.1038/sj.bjp.0704256
|View full text |Cite
|
Sign up to set email alerts
|

Suppression of K+‐induced hyperpolarization by phenylephrine in rat mesenteric artery: relevance to studies of endothelium‐derived hyperpolarizing factor

Abstract: In intact mesenteric arteries, increasing [K + ] o by 5 mM hyperpolarized both endothelial and smooth muscle cells. Subsequent exposure to 10 mM phenylephrine depolarized both cell types which were then repolarized by a 5 mM increase in [K + ] o . In endothelium-denuded vessels, increasing [K + ] o by 5 mM hyperpolarized the smooth muscle but K + had no e ect after depolarization by 10 mM phenylephrine. On subsequent exposure to iberiotoxin plus 4-aminopyridine, the repolarizing action of 5 mM K + was restored… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1

Citation Types

6
48
0

Year Published

2003
2003
2019
2019

Publication Types

Select...
6
2

Relationship

0
8

Authors

Journals

citations
Cited by 50 publications
(54 citation statements)
references
References 12 publications
6
48
0
Order By: Relevance
“…It should be noted that the effect of non-selective gap junction inhibitors such as 18α-glycyrrhetinic acid and carbenoxolone were also tested for their effect on EDHF-mediated responses; however, responses to 18α-glycyrrhetinic acid were very inconsistent, and carbenoxolone resulted in potent vasodilation, consistent with previous findings [37]. It is important to recognise that responses to 40 Gap27 were obtained in the presence of phenylephrine, which has been demonstrated to increase the gap junction component of an EDHF response, whilst decreasing any contribution made by endothelium-derived potassium to the EDHF response [35]. To study this effect in the absence of the 40 Gap27, it would be beneficial to obtain control concentration- Fig.…”
Section: Discussionsupporting
confidence: 61%
“…It should be noted that the effect of non-selective gap junction inhibitors such as 18α-glycyrrhetinic acid and carbenoxolone were also tested for their effect on EDHF-mediated responses; however, responses to 18α-glycyrrhetinic acid were very inconsistent, and carbenoxolone resulted in potent vasodilation, consistent with previous findings [37]. It is important to recognise that responses to 40 Gap27 were obtained in the presence of phenylephrine, which has been demonstrated to increase the gap junction component of an EDHF response, whilst decreasing any contribution made by endothelium-derived potassium to the EDHF response [35]. To study this effect in the absence of the 40 Gap27, it would be beneficial to obtain control concentration- Fig.…”
Section: Discussionsupporting
confidence: 61%
“…26 The efflux of K ϩ ions through Ca 2ϩ -dependent K ϩ channels has been suggested to result in a sufficient increase in the subendothelial K ϩ concentration to activate inwardly rectifying K ϩ channels and/or the Na-K-ATPase in smooth muscle cells. 10,[27][28][29] There are, however, other means of transferring hyperpolarization from one cell type to another. For example, hyperpolarizing factor(s) such as EETs could be released from endothelial cells.…”
Section: Discussionmentioning
confidence: 99%
“…So both KCl and PE would be expected to depolarize endothelial cells, either directly or indirectly via smooth muscle cells [38]. If there is a large effect of voltage on Ca 2+ influx, these depolarizing effects on the endothelial cells should, if anything, act to decrease Ca 2+ by reducing the driving force for Ca 2+ entry into the endothelial cells [39,40].…”
Section: Regulation Of Endothelial Ca 2+ Events Via Myoendothelial Gamentioning
confidence: 99%