Inward-rectifying K+ current

Increases inwardly rectifying K+ current, PLC activation with increased IPs and elevated [Ca2+]j observed in recombinant systems PLC activation with increased IPs and elevated [Ca2+]j to observed in recombinant systems. PLC activation with increased IPs and elevated [Ca2+]j observed in recombinant systems. ... 

Adenosine is a nucleoside that occurs naturally throughout the body. Its half-life in the blood is less than 10 seconds. Its mechanism of action involves activation of an inward rectifier K+ current and inhibition of calcium current. The results of these actions are marked hyperpolarization and suppression of calcium-dependent action potentials. When given as a bolus dose, adenosine directly inhibits atrioventricular nodal conduction and increases the atrioventricular nodal refractory period but has lesser effects on the sinoatrial node. Adenosine is currently the drug of choice for prompt conversion of paroxysmal supraventricular tachycardia to sinus rhythm because of its high efficacy (90-95%) and very short duration of action. It is usually given in a bolus dose of 6 mg followed, if necessary, by a dose of 12 mg. An uncommon variant of ventricular tachycardia is adenosine-sensitive. The drug is less effective in the presence of adenosine receptor blockers such as theophylline or caffeine, and its effects are potentiated by adenosine uptake inhibitors such as dipyridamole. 

The potassium channels present in neuronal membranes could also be affected by phenothiazine derivatives. In the study performed by Ogata et al. [255] it was shown that CPZ (9) interfered with several types of potassium channels present in membranes of neurons of the newborn rat cultured dorsal root ganglia. Reversible reduction of the amplitude was found for transient and delayed rectified K+ currents, while inward rectified K+ current remained unaffected by CPZ (9). The block of delayed rectified K+ current by CPZ (9) was, however, less potent than block of the transient one. The hyper-polarizing shift of the steady-state inactivation curve for transient K+ current indicated that CPZ (9) binds preferably to the channels in the inactivated state. 

In contrast to many other potassium channels (see below), the inward rectifying K+ channels in guinea pig ventricular myocytes were directly blocked by genistein (42) and daidzein (40) [312]. Both flavonoids inhibited inward rectifying K+ current in a dose-dependent manner. The opposite effect (i.e., stimulation) was observed when the influence of naringenin (33) on the Ca2+-activated K+ channels of rat tail artery myocytes was studied [313]. Channel activation was dose-dependent and reversible after flavonoid wash-out. The final conclusion of this work was that the vasorelaxant effect of naringenin (33) could be due to activation of Ca2+-activated K+ channels. 

Penington NJ, Kelly JS, Fox AP. Whole-cell recordings of inwardly rectifying K+ currents activated by 5-HT1A receptors on dorsal raphe neurones of the adult rat. J Physiol 1993 469 387-405. 

Ishibashi H, Kuwano K, Takahama K. Inhibition of the 5-HT1A receptor-mediated inwardly rectifying K+ current by dextromethorphan in rat dorsal raphe neurones. Neuropharmacology 2000 39 2302-2308. 

Arcangeli A, Bianchi L, Becchetti A, Faravelli L, Coronnello M, Mini E, Olivotto M, Wanke E (1995) A novel inward-rectifying K+ current with a cell-cycle dependence governs the resting potential of mammalian neuroblastoma cells. J Physiol 489 455-471... 

Hida H, Takeda M, Soliven B (1998) Ceramide inhihits inwardly rectifying K+ currents via a Ras- and Raf-l-dependent pathway in cultured oligodendrocytes. J Neurosci 18 8712-8719. 

Knoflach F, Kemp JA (1998) Metabotropic glutamate group II receptors activate a G protein-coupled inwardly rectifying K current in neurones of the rat cerebellum. J Physiol 509 347-354. 

Bauer CK, Engeland B, Wulfsen I, Ludwig J, Pongs O, Schwarz JR. RERG is a molecular correlate of the inward-rectifying K current in clonal rat pituitary cells. Receptors Channels 1998 6(l) 19-29. 

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