Inhibition of voltage-gated K<sup>+</sup>current in rat intrapulmonary arterial myocytes by endothelin-1

Shimoda, Larissa A.; Sylvester, J. T.; Sham, James S.K.

doi:10.1152/ajplung.1998.274.5.l842

Cited by 92 publications

(86 citation statements)

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“…The discrepancy between these reports (19) and our data may result from developmental differences between animal models used in these studies (neonatal vs. adult pigs) or the use of endothelin preconstriction in our study. Indeed, endothelin-induced vasoconstriction is mediated in part via K V -, K Ca -, and K ATPchannel inhibition (25,26,35), as is likely the case with most vasoconstrictors (29). Our data suggest that adenosine may overcome the endothelin-mediated inhibition of K V but not K ATP channels.…”

Section: Discussionmentioning

confidence: 99%

Gender-specific K⁺-channel contribution to adenosine-induced relaxation in coronary arterioles

Heaps

Bowles

2002

Journal of Applied Physiology

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Heaps, Cristine L., and Douglas K. Bowles. Gender-specific K ϩ -channel contribution to adenosine-induced relaxation in coronary arterioles. J Appl Physiol 92: 550-558, 2002. First published October 5, 2001 10.1152/ japplphysiol.00566.2001.-We examined the contribution of K ϩ -channel activity on basal tone and adenosine-mediated relaxation of coronary arterioles isolated from sexually mature male and female miniature swine. Arterioles (ϳ100-200 m ID) isolated from the apical region of the heart were cannulated and studied using videodimensional analysis under constant intraluminal pressure. Coronary arterioles from male and female pigs demonstrated similar levels of basal tone and reductions in basal diameter in response to the K ϩ -channel blockers 4-aminopyridine (4-AP; 1 mM), tetraethylammonium (1 mM), and glibenclamide (Glib; 10 M), with 4-AP producing significantly greater constriction than tetraethylammonium or Glib. After endothelin-induced preconstriction, relaxation responses to adenosine were not significantly different between coronary arterioles of male and female pigs. Inhibition of 4-AP-sensitive channels significantly impaired adenosine-mediated relaxation in arterioles from male but not female pigs. However, inhibition of K ϩ channels with iberiotoxin (100 nM) or Glib had no effect on adenosine-induced relaxation in either sex. Results obtained in the presence of nitric oxide synthase inhibition suggest a potential interaction of 4-AP-sensitive channels and nitric oxide at low adenosine concentrations. In conclusion, our data indicate that 4-AP-sensitive channels 1) contribute significantly to basal tone in coronary arterioles of both male and female pigs, 2) contribute to adenosine-mediated relaxation in male but not female pigs, and 3) can contribute to adenosine-induced relaxation independent of nitric oxide production in male pigs. These data are consistent with a significant role for voltage-dependent K ϩ channels in adenosine-mediated relaxation of coronary arterioles from males. potassium channel; smooth muscle; endothelium; nitric oxide synthase; endothelin ADENOSINE IS AN ENDOGENOUS vasodilator that produces vascular smooth muscle relaxation through a variety of mechanisms that act to reduce intracellular Ca 2ϩ levels and decrease Ca 2ϩ sensitivity of the contractile apparatus. K ϩ -channel activation has been identified as an important component of adenosine-mediated relaxation (7,13,19,31). Increased K ϩ -channel activity hyperpolarizes smooth muscle and thereby reduces smooth muscle contraction via reduced Ca 2ϩ entry through voltage-dependent Ca 2ϩ channels.Both Ca 2ϩ -activated K ϩ (K Ca ) channels and ATPsensitive K ϩ (K ATP ) channels have been reported to contribute to adenosine-mediated relaxation in vascular smooth muscle. Price and colleagues (7, 31) have demonstrated significant roles for K Ca channels in both basal tone and adenosine-mediated relaxation in pressurized canine coronary arterioles. In contrast, Kuo and colleagues (13,19) reported that inhibition of K ATP chan...

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Section: Discussionmentioning

confidence: 99%

Gender-specific K⁺-channel contribution to adenosine-induced relaxation in coronary arterioles

Heaps

Bowles

2002

Journal of Applied Physiology

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“…Intensive studies on the biochemical/physiological role of PKC over several decades have revealed that PKC activation closely linked to cell growth, cell cycle, differentiation, hormone release, reactive oxygen species (ROS) generation, and ion channels modulation (16)(17)(18)(19). Thus, PKC inhibitors are indispensable for studies on PKC-related signaling pathways.…”

Section: Biological Actions Of Pkc Inhibitors On Ion Channelsmentioning

confidence: 99%

“…For example, PKC activation leads to the activation of L-type Ca 2+ channels, Cl − channels, and nonselective cation channels in vascular smooth muscle (20)(21)(22). Generally, K + channels in vascular smooth muscle, including voltage-dependent K + (Kv), ATP-sensitive K + (KATP), and inward rectifier K + (Kir), are inhibited by PKC activation (18,23,24). However, several PKC inhibitors are known to directly affect the ion channels independently of PKC-related signaling pathways, making it difficult to right interpretation of the experimental results.…”

Section: Biological Actions Of Pkc Inhibitors On Ion Channelsmentioning

confidence: 99%

Direct effect of protein kinase C inhibitors on cardiovascular ion channels

Son

Hong²,

Kim³

et al. 2011

BMB Reports

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“…The same group, however, also showed that Kv channel inhibition by thromboxane A2 is mediated by the activation of PKCζ (Cogolludo et al, 2003;Ko et al, 2008). Regarding the inhibitory effects of endothelin-1 on pulmonary Kv channels, both Ca 2+ -dependent and -independent subtypes of PKC are involved (Shimoda et al, 1998) (Fig. 2).…”

Section: Effects Of Vasoconstrictors On Kv Channel In Pasmcs: Role Ofmentioning

confidence: 99%

Patho-, physiological roles of voltage-dependent K+ channels in pulmonary arterial smooth muscle cells

Park

Firth

Han

et al. 2010

J. Smooth Muscle Res.

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In this review, we demonstrate the basic properties, modulation of, and pathological changes in voltage-dependent K + (Kv) channels that are expressed in pulmonary arterial smooth muscle cells (PASMCs). Pulmonary Kv channels are thought to play a crucial role in the maintenance of resting membrane potentials, and therefore the vascular tone of the pulmonary arteries. Although the molecular identity of pulmonary Kv channels is not clear, Kv1.1, Kv1.2, Kv1.5, Kv2.1, Kv9.3, and Kv3.1 subtypes are expressed in PASMCs. In addition, resistant PASMCs contain greater amount of Kv channels as compared to conduit PASMCs. This heterogenetic expression of Kv channels is consistent with regional differences in the contractile response to hypoxia. Similar to other K + channels, pulmonary Kv channels can also be modulated by several vasoconstrictors concomitant with the activation of protein kinase C (PKC). Alterations in Kv channel function have several additional and interrelated consequences, including the regulation of cell proliferation and apoptosis, which ultimately lead to pulmonary vascular remodeling. Increased pulmonary vasoconstriction in pulmonary arterial hypertension is attributable to decreased expression and activity of Kv channels in smooth muscle cells. Kv channels play a central role in the maintenance of cellular homeostasis and ion channels, and consequential signaling cascades. Therefore, Kv channels are potential therapeutic targets for the treatment of pulmonary vascular disease.

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Inhibition of voltage-gated K⁺current in rat intrapulmonary arterial myocytes by endothelin-1

Cited by 92 publications

References 41 publications

Gender-specific K⁺-channel contribution to adenosine-induced relaxation in coronary arterioles

Gender-specific K⁺-channel contribution to adenosine-induced relaxation in coronary arterioles

Direct effect of protein kinase C inhibitors on cardiovascular ion channels

Patho-, physiological roles of voltage-dependent K+ channels in pulmonary arterial smooth muscle cells

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Inhibition of voltage-gated K+current in rat intrapulmonary arterial myocytes by endothelin-1

Cited by 92 publications

References 41 publications

Gender-specific K+-channel contribution to adenosine-induced relaxation in coronary arterioles

Gender-specific K+-channel contribution to adenosine-induced relaxation in coronary arterioles

Direct effect of protein kinase C inhibitors on cardiovascular ion channels

Patho-, physiological roles of voltage-dependent K+ channels in pulmonary arterial smooth muscle cells

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Inhibition of voltage-gated K⁺current in rat intrapulmonary arterial myocytes by endothelin-1

Gender-specific K⁺-channel contribution to adenosine-induced relaxation in coronary arterioles

Gender-specific K⁺-channel contribution to adenosine-induced relaxation in coronary arterioles