Regulation and modulation of calcium channels in cardiac, skeletal, and smooth muscle cells

McDonald, Terence F.; Pelzer, Siegried; Trautwein, W.; Pelzer, D

doi:10.1152/physrev.1994.74.2.365

Cited by 962 publications

(774 citation statements)

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“…Passage of divalent cations through the Ca 2+ channel involves interactions of the ion with charged groups within the pore (Josephson et al, 2002). The different ion-channel interaction of Ba 2+ compared to Ca 2+ results in a shift of the Ba 2+ -generated current-voltage relation to the left, a shift amounting to up to 10 mV (McDonald et al, 1994). Moreover, single-channel recordings (Rodriguez-Contreras and Yamoah, 2003) of L-type Ca 2+ channels in hair cells reveal clearly that at any test voltage Ba 2+ results in much greater activation of the channel than Ca 2+ does, i.e., the channel has a much higher open probability in Ba 2+ .…”

Section: Impact Of Experimental Conditionsmentioning

confidence: 99%

Synaptic transmission at retinal ribbon synapses

Heidelberger

Thoreson

Witkovsky

2005

Progress in Retinal and Eye Research

209

231

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The molecular organization of ribbon synapses in photoreceptors and ON bipolar cells is reviewed in relation to the process of neurotransmitter release. The interactions between ribbon synapseassociated proteins, synaptic vesicle fusion machinery and the voltage-gated calcium channels that gate transmitter release at ribbon synapses are discussed in relation to the process of synaptic vesicle exocytosis. We describe structural and mechanistic specializations that permit the ON bipolar cell to release transmitter at a much higher rate than the photoreceptor does, under in vivo conditions. We also consider the modulation of exocytosis at photoreceptor synapses, with an emphasis on the regulation of calcium channels.

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Section: Impact Of Experimental Conditionsmentioning

confidence: 99%

Synaptic transmission at retinal ribbon synapses

Heidelberger

Thoreson

Witkovsky

2005

Progress in Retinal and Eye Research

209

231

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“…This raises the question as to how mesenteric Ca 2 þ channels are able to sustain prolonged Ca 2 þ influx during high K þ . One possibility is through small window currents in the voltage range where steady-state activation and inactivation curves overlap (McDonald et al, 1994;Perez-Reyes, 2003). It has been reported that a T-type window current was responsible for a physiological, steady-state Ca 2 þ entry in human myoblasts (Bijlenga et al, 2000), and window currents in the V m range from À50 to À20 mV were suggested to account for high-K þ -induced, nifedipine-insensitive Ca 2 þ entry and vasoconstriction in rat mesenteric artery (Morita et al, 1999;Itonaga et al, 2002;Inoue & Mori, 2003).…”

Section: Biophysical Characteristics Of Non-l-type Channels In Mesentmentioning

confidence: 99%

“…In the majority of VSMC, excitation-contraction coupling is maintained by L-type Ca 2 þ channels pharmacologically distinguished by their sensitivity to dihydropyridines such as nifedipine (McDonald et al, 1994;Perez-Reyes, 2003). However, in microvascular resistance vessels other types of voltage-dependent Ca 2 þ channels have emerged that were previously believed to function only in the heart or brain tissue.…”

Section: Introductionmentioning

confidence: 99%

“…However, small steady-state Ca 2 þ currents occurring in the voltage 'window' between overlapping steady-state activation and inactivation curves (window currents) may account for sustained Ca 2 þ influx into cells (McDonald et al, 1994;Morita et al, 1999;Perez-Reyes, 2003). A physiological role for T-type window currents has recently been demonstrated in human myoblast terminal differentiation where they mediated the sustained Ca 2 þ entry required for myoblast fusion (Bijlenga et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

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Depolarization‐induced calcium influx in rat mesenteric small arterioles is mediated exclusively via mibefradil‐sensitive calcium channels

Jensen

Salomonsson

Jensen

et al. 2004

British J Pharmacology

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In this study, intracellular Ca2+ was measured as the Fura‐2 ratio (R) of fluorescence excited at 340 and 380 nm (F340/F380) in nonpressurized rat mesenteric small arterioles (Ø (lumen diameter) 10–25 μm). The response to depolarization using 75 mM KCl was an increase in R from a baseline of 0.96±0.01 ([Ca2+]i ∼74 nM) to 1.04±0.01 (∼128 nM) (n=80). The response to 75 mM K+ was reversibly abolished in Ca2+‐free physiological saline solution, whereas phentolamine (10 μM) or tetrodotoxin (1 μM) had no effects. LaCl3 (200 μM) inhibited 61±9% of the response. A [K+]‐response curve indicated that the Ca2+ response was activated between 15 and 25 mM K+. The data suggest that the Ca2+ response was caused by the activation of voltage‐dependent Ca2+ channels. Mibefradil use dependently inhibited the Ca2+ response to 75 mM K+ by 29±2% (100 nM), 73±7% (1 μM) or 89±7% (10 μM). Pimozide (500 nM) use dependently inhibited the Ca2+ response by 85±1%. Nifedipine (1 μM) inhibited the Ca2+ response to 75 mM K+ by 41±12%. The response was not inhibited by calciseptine (500 nM), ω‐agatoxin IVA (100 nM), ω‐conotoxin MVIIA (500 nM), or SNX‐482 (100 nM). Using reverse transcriptase–polymerase chain reaction, it was shown that neither CaV2.1a (P‐type) nor CaV2.1b (Q‐type) voltage‐dependent Ca2+ channels were expressed in mesenteric arterioles, whereas the CaV3.1 (T‐type) channel was expressed. Furthermore, no amplification products were detected when using specific primers for the β1b, β2, or β3 auxiliary subunits of high‐voltage‐activated Ca2+ channels. The results suggest that the voltage‐dependent Ca2+ channel activated by sustained depolarization in mesenteric arterioles does not classify as any of the high‐voltage‐activated channels (L‐, P/Q‐, N‐, or R‐type), but is likely to be a T‐type channel. The possibility that the sustained Ca2+ influx observed was the result of a T‐type window current is discussed. British Journal of Pharmacology (2004) 142, 709–718. doi:10.1038/sj.bjp.0705841

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“…Cd 2 þ has been shown to inhibit smooth muscle NCX (Smith et al, 1987), cardiac NCX (Bers et al, 1980;Trosper & Philipson, 1983), and cloned NCX1 (Iwamoto & Shigekawa, 1998) with K D p33 mM, and has been used (0.2-1 mM) as a prophylactic measure to block NCX in recent studies on cardiomyocytes (Feraille et al, 1997;Gao et al, 2002). Application of Ni 2 þ (3 mM), a weaker inhibitor of I Ca,L (McDonald et al, 1994) and NCX1 (Iwamoto & Shigekawa, 1998) than is Cd 2 þ , also suppressed A23-induced current.…”

Section: S Missan and Tf Mcdonaldmentioning

confidence: 99%

Cardiac Na⁺–Ca²⁺ exchanger current induced by tyrphostin tyrosine kinase inhibitors

Missan

McDonald

2004

British J Pharmacology

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1 Tyrosine kinase (TK) inhibitors genistein and tyrphostin A23 (A23) inhibited Ca 2 þ currents in guinea-pig ventricular myocytes investigated under standard whole-cell conditions (K þ -free Tyrode's superfusate; EGTA-buffered (pCa-10.5) Cs þ dialysate). However, the inhibitors (100 mM) also induced membrane currents that reversed between À40 and 0 mV, and the objective of the present study was to characterize these currents.2 Genistein-induced current behaved like Cl À current, and was unaffected by either the addition of divalent cations (0.5 mM Cd 2 þ ; 3 mM Ni 2 þ ) that block the Na þ -Ca 2 þ exchanger (NCX), or the removal of external Na þ and Ca 2 þ . 3 A23-induced current was independent of Cl À driving force, and strongly suppressed by addition of Cd 2 þ and Ni 2 þ , and by removal of either external Na þ or Ca 2 þ . These and other results suggested that A23 activated an NCX current driven by submembrane Na þ and Ca 2 þ concentrations higher than those in the bulk cytoplasm. 4 Improved control of intracellular Na þ and Ca 2 þ concentrations was obtained by suppressing cation influx (10 mM verapamil) and raising dialysate Na þ to 7 mM and dialysate pCa to 7. Under these conditions, stimulation by A23 was described by the Hill equation with EC 50 6874 mM and coefficient 1.1, tyrphostin A25 was as effective as A23, and TK-inactive tyrphostin A1 was ineffective. Phosphotyrosyl phosphatase inhibitor orthovanadate (1 mM) antagonized the action of 100 mM A23. 5 The results suggest that activation of cardiac NCX by A23 is due to inhibition of genisteininsensitive TK.

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Regulation and modulation of calcium channels in cardiac, skeletal, and smooth muscle cells

Cited by 962 publications

References 0 publications

Synaptic transmission at retinal ribbon synapses

Synaptic transmission at retinal ribbon synapses

Depolarization‐induced calcium influx in rat mesenteric small arterioles is mediated exclusively via mibefradil‐sensitive calcium channels

Cardiac Na⁺–Ca²⁺ exchanger current induced by tyrphostin tyrosine kinase inhibitors

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Regulation and modulation of calcium channels in cardiac, skeletal, and smooth muscle cells

Cited by 962 publications

References 0 publications

Synaptic transmission at retinal ribbon synapses

Synaptic transmission at retinal ribbon synapses

Depolarization‐induced calcium influx in rat mesenteric small arterioles is mediated exclusively via mibefradil‐sensitive calcium channels

Cardiac Na+–Ca2+ exchanger current induced by tyrphostin tyrosine kinase inhibitors

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Resources

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Cardiac Na⁺–Ca²⁺ exchanger current induced by tyrphostin tyrosine kinase inhibitors