Click here to close
Hello! We notice that you are using Internet Explorer, which is not supported by Xenbase and may cause the site to display incorrectly.
We suggest using a current version of Chrome,
FireFox, or Safari.
Naunyn Schmiedebergs Arch Pharmacol
2005 Feb 01;3712:133-40. doi: 10.1007/s00210-005-1018-x.
Show Gene links
Show Anatomy links
Cross-talk between beta(1)-adrenoceptors and ET(A) receptors in modulation of the slow component of delayed rectifier K(+) currents.
Lin C
,
Nagai M
,
Ishigaki D
,
Hayasaka K
,
Endoh M
,
Ishii K
.
???displayArticle.abstract???
Delayed rectifier K(+) currents (I(K)) play a critical role in determining cardiac action potential duration (APD). Modulation of I(K) affects cardiac excitability critically. There are three components of cardiac delayed rectifier, and the slowly activating component (I(Ks)) is influenced strongly by a variety of stimuli. Plasma levels of noradrenaline and endothelin are elevated in heart failure, and arrhythmias are promoted by such humoral abnormalities through modulation of ion channels. It has been reported that protein kinase A (PKA) and protein kinase C (PKC) modulate I(Ks) from human minK in a complex manner. In the present study, we coexpressed human minK with the human beta(1)-adrenoceptor (hbeta(1)AR) and the endothelin receptor subtype A (hET(A)R) in Xenopus oocytes and investigated the effects of receptor activation on the currents (I(Ks)) flowing through the oocytes. ET-1 modulated I(Ks) biphasically: a transient increase followed by a decrease. The PKC inhibitor chelerythrine completely inhibited the effects of ET-1. Intracellular EGTA abolished the transient increase by ET-1 and partially inhibited the subsequent decrease in the currents. When I(Ks) was increased by 10(-6) M isoproterenol (ISO), ET-1 did not increase but rather decreased the current to an even greater extent than under control conditions. In addition, the effects of ISO on I(Ks) were suppressed by ET(A)R stimulation. These data indicate that I(Ks) can be regulated by cross-talk between the ET(A)R and beta(1)AR systems in addition to direct regulation by each receptor system.
Barhanin,
K(V)LQT1 and lsK (minK) proteins associate to form the I(Ks) cardiac potassium current.
1996, Pubmed,
Xenbase
Barhanin,
K(V)LQT1 and lsK (minK) proteins associate to form the I(Ks) cardiac potassium current.
1996,
Pubmed
,
Xenbase
Busch,
Regulation by second messengers of the slowly activating, voltage-dependent potassium current expressed in Xenopus oocytes.
1992,
Pubmed
,
Xenbase
Chu,
Signal transduction and Ca2+ signaling in contractile regulation induced by crosstalk between endothelin-1 and norepinephrine in dog ventricular myocardium.
2003,
Pubmed
Damron,
Arachidonic acid and endothelin potentiate Ca2+ transients in rat cardiac myocytes via inhibition of distinct K+ channels.
1993,
Pubmed
Folander,
Cloning and expression of the delayed-rectifier IsK channel from neonatal rat heart and diethylstilbestrol-primed rat uterus.
1990,
Pubmed
,
Xenbase
Habuchi,
Endothelin enhances delayed potassium current via phospholipase C in guinea pig ventricular myocytes.
1992,
Pubmed
Honoré,
Cloning, expression, pharmacology and regulation of a delayed rectifier K+ channel in mouse heart.
1991,
Pubmed
,
Xenbase
Kaczmarek,
Properties and regulation of the minK potassium channel protein.
1997,
Pubmed
,
Xenbase
Lo,
Independent and exclusive modulation of cardiac delayed rectifying K+ current by protein kinase C and protein kinase A.
1998,
Pubmed
,
Xenbase
McMurray,
Plasma endothelin in chronic heart failure.
1992,
Pubmed
Minami,
Plasma norepinephrine concentration and plasma dopamine-beta-hydroxylase activity in patients with congestive heart failure.
1983,
Pubmed
Murakoshi,
Receptor-mediated modulation of rat KV1.2 in Xenopus oocytes.
1994,
Pubmed
,
Xenbase
Noble,
Outward membrane currents activated in the plateau range of potentials in cardiac Purkinje fibres.
1969,
Pubmed
Pedersen,
Angiotensin II, aldosterone and arginine vasopressin in plasma in congestive heart failure.
1986,
Pubmed
Sahara,
Characterization of protein kinase C in Xenopus oocytes.
1992,
Pubmed
,
Xenbase
Sakai,
Endogenous endothelin-1 participates in the maintenance of cardiac function in rats with congestive heart failure. Marked increase in endothelin-1 production in the failing heart.
1996,
Pubmed
Salata,
IK of rabbit ventricle is composed of two currents: evidence for IKs.
1996,
Pubmed
,
Xenbase
Sanguinetti,
Coassembly of K(V)LQT1 and minK (IsK) proteins to form cardiac I(Ks) potassium channel.
1996,
Pubmed
,
Xenbase
Sanguinetti,
Delayed rectifier outward K+ current is composed of two currents in guinea pig atrial cells.
1991,
Pubmed
Steinberg,
Protein kinase C isoform diversity in the heart.
1995,
Pubmed
Tohse,
Alpha 1-adrenoceptor stimulation enhances the delayed rectifier K+ current of guinea pig ventricular cells through the activation of protein kinase C.
1992,
Pubmed
Uretsky,
Primary prevention of sudden cardiac death in heart failure: will the solution be shocking?
1997,
Pubmed
Van Wagoner,
Phenylephrine suppresses outward K+ currents in rat atrial myocytes.
1996,
Pubmed
Varnum,
The min K channel underlies the cardiac potassium current IKs and mediates species-specific responses to protein kinase C.
1993,
Pubmed
,
Xenbase
Walsh,
Regulation of a heart potassium channel by protein kinase A and C.
1988,
Pubmed
Wang,
Sustained depolarization-induced outward current in human atrial myocytes. Evidence for a novel delayed rectifier K+ current similar to Kv1.5 cloned channel currents.
1993,
Pubmed
Washizuka,
Endothelin-1 inhibits the slow component of cardiac delayed rectifier K+ currents via a pertussis toxin-sensitive mechanism.
1997,
Pubmed
Yazawa,
Mechanism of receptor-mediated modulation of the delayed outward potassium current in guinea-pig ventricular myocytes.
1990,
Pubmed
Zhang,
K+ currents expressed from the guinea pig cardiac IsK protein are enhanced by activators of protein kinase C.
1994,
Pubmed
,
Xenbase