Pharmacological modulation of voltage-dependent calcium channels in intact cells

Porzig, H.

doi:10.1007/bfb0031020

Cited by 69 publications

(41 citation statements)

References 258 publications

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“…These data, in conjunction with those showing nifedipine also inhibited the p-opioid-induced Ins(1,4,5)P3 response (Smart et al, 1995), indicate that p-opioids open L-type VSCCs, allowing Ca2`influx to stimulate PLC activity (Cockcroft & Thomas, 1992) in SH-SY5Y cells. Whilst opioids generally close VSCCs (Porzig, 1990), there is evidence that they can also open L-type VSCCs, as seen with b-opioids in NG108-15 cells (Jin et al, 1992) and K-opioids in astrocytes (Eriksson et al, 1993).…”

Section: Source Of Reagentsmentioning

confidence: 99%

“…However, SH-SY5Y cells possess only L-and N-type VSCCs (Morton et a!., 1992;Reeve et al, 1994), and we have previously shown that nifedipine dose-dependently inhibits the fentanyl-induced Ins(1,4,5)P3 response (Smart et al, 1995), suggesting that, in SH-SY5Y cells, p-opioid-induced Ca21 influx occurs via Ltype VSCCs. Opioids have also been reported to open L-type VSCCs in astrocytes (Eriksson et al, 1993) and NG108-15 cells (Jin et al, 1992), although it should be noted that opioids generally close VSCCs (Porzig, 1990).…”

Section: Introducdonmentioning

confidence: 99%

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Desensitization of the μ‐opioid activation of phospholipase C in SH‐SY5Y cells: the role of protein kinases C and A and Ca²⁺‐activated K⁺ currents

Smart

Lambert

1995

British J Pharmacology

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1 In SH-SY5Y cells, y-opioids cause a rapidly desensitizing activation of phospholipase C (PLC), that appears secondary to Ca2" influx via L-type voltage-sensitive Ca2" channels (VSCCs). The aim of the present study was to characterize the mechanisms of desensitization of the p-opioid-induced inositol (1,4,5) Blockade of Ca2+-activated K+ currents with 4-aminopyridine (2 mM) or iberiotoxin (10 nM) had no effect on fentanyl-induced Ins(1,4,5)P3 formation but further increased the Ro 31-8220-enhanced response.6 All three mechanisms had additive, or even supra-additive, effects, but only at later (120-300 s) time points. In addition, fentanyl-induced Ins(1,4,5)P3 formation, even if enhanced by H-89, Ro 31-8220 and/ or 4-aminopyridine, was inhibited by nifedipine (1 nM-10 I*M). 7 In conclusion, desensitization of the p-opioid-induced activation of PLC is multifactorial, involving protein kinases C and A and Ca2'-activated K+ efflux, but the L-type VSCC is of critical importance and may be a possible common site of action.

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Section: Source Of Reagentsmentioning

confidence: 99%

Section: Introducdonmentioning

confidence: 99%

Desensitization of the μ‐opioid activation of phospholipase C in SH‐SY5Y cells: the role of protein kinases C and A and Ca²⁺‐activated K⁺ currents

Smart

Lambert

1995

British J Pharmacology

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“…Next, we tested a number of organic Ca2" channel blockers for their ability to inhibit Mg2" refill in magnesium-depleted cells (17)(18)(19). Nifedipine, a 1,4 dihydropyridine derivative, inhibited the Mg2" influx pathway ( Figure 3.…”

mentioning

confidence: 99%

“…These results suggest that protein synthesis is partially involved with the adaptation of transport sites in cTAL cells after placement in magnesium-free media. Mg2+ influx was determined in magnesium-depleted cells as illus- (17)(18)(19)44). It should also be noted that Mg2" does not share the Ca2" channel in cardiac or vascular smooth muscle cells (reviewed in reference 44).…”

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confidence: 99%

Intracellular Mg2+ and magnesium depletion in isolated renal thick ascending limb cells.

Quamme¹

1991

J. Clin. Invest.

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IntroductionMagnesium reabsorption and regulation within the kidney occur principally within the cortical thick ascending limb (cTAL) cells of the loop of Henle. Fluorometry with the dye, mag-fura- Homeostasis of total body magnesium occurs principally within the kidney by epithelial cells of the cortical segment of the thick ascending limb (cTAL)' of Henle's loop (1-3). Shareghi and Agus (4), using in vitro perfused tubules, provided evidence for passive magnesium transport probably moving through the paracellular pathway. These early observations were supported by the findings ofde Rouffignac and colleagues (1, 5). However, the later investigators also showed that magnesium transport may be altered in the absence of voltage and resistance changes and NaCl absorption, suggesting that magnesium transport may be active in nature (5).Although we have considerable understanding of transepithelial magnesium movement and some ofthe factors that control transport, little is known about the intracellular regulation ofmagnesium (1-5). This, has been due in part to the lack ofan adequate radiotracer of magnesium or other suitable quantitative methods (2, 6). More important was the deficiency of an adequate means of assessing free Mg2" activity. The recent development of fluorescent dyes for Mg2" should allow a better understanding of cellular free Mg2" movements (7). It is the free Mg2" concentration ([Mg2J]i) that is thought to be important in determining plasma membrane transport and entry into biochemical processes rather than total magnesium, much of which is bound to intracellular ligands (6).

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“…However, raloxifene did not significantly shift the steady-state activation or inactivation curves. This contrasts with the known effects of 17b-oestradiol and dihydropyridine Ca 2 þ channel antagonists, which produce a leftward shift of the steady-state inactivation curves (Nakajima et al, 1999a, b;Porzig, 1990). Raloxifene therefore does not appear to preferentially exert inhibitory actions on activated or inactivated states of the L-type Ca 2 þ channel and consequently its mechanism of Ca 2 þ channel antagonism may be different to that of 17b-oestradiol.…”

Section: Discussionmentioning

confidence: 85%

Raloxifene acutely suppresses ventricular myocyte contractility through inhibition of the L‐type calcium current

Liew

Stagg

MacLeod

et al. 2004

British J Pharmacology

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1 The selective oestrogen (ER) receptor modulator, raloxifene, is widely used in the treatment of postmenopausal osteoporosis, but may also possess cardioprotective properties. We investigated whether it directly suppresses myocyte contractility through Ca 2 þ channel antagonism in a similar way to 17b-oestradiol. 2 Cell shortening and Ca 2 þ transients were measured in single guinea-pig ventricular myocytes fieldstimulated (1 Hz, 371C) in a superfusion chamber. Electrophysiological recordings were performed using single electrode voltage-clamp. 3 Raloxifene decreased cell shortening (EC 50 2.4 mM) and the Ca 2 þ transient amplitude (EC 50 6.4 mM) in a concentration-dependent manner. At a concentration of 1 mM, raloxifene produced a 3372% (mean7s.e.m) and 2472% reduction, respectively (Po0.001, n ¼ 14 for both parameters). 4 These inhibitory actions were not observed in myocytes that had been incubated with the specific antagonist, ICI 182,780 (10 mM) (n ¼ 11). 5 Raloxifene (1 mM) shortened action potential durations at 50 and 90% repolarisation (Po0.05 and o0.001, respectively; n ¼ 27) and decreased peak L-type Ca 2 þ current by 45%, from À5.170.5 pA/pF to À2.870.3 pA/pF (Po0.001, n ¼ 18). 6 Raloxifene did not significantly alter sarcoplasmic reticulum Ca 2 þ content, as assessed by integrating the Na þ /Ca 2 þ exchanger currents following rapid caffeine application. 7 The present study provides evidence for direct inhibitory actions of raloxifene on ventricular myocyte contractility, mediated through Ca 2 þ channel antagonism.

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Pharmacological modulation of voltage-dependent calcium channels in intact cells

Cited by 69 publications

References 258 publications

Desensitization of the μ‐opioid activation of phospholipase C in SH‐SY5Y cells: the role of protein kinases C and A and Ca²⁺‐activated K⁺ currents

Desensitization of the μ‐opioid activation of phospholipase C in SH‐SY5Y cells: the role of protein kinases C and A and Ca²⁺‐activated K⁺ currents

Intracellular Mg2+ and magnesium depletion in isolated renal thick ascending limb cells.

Raloxifene acutely suppresses ventricular myocyte contractility through inhibition of the L‐type calcium current

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Pharmacological modulation of voltage-dependent calcium channels in intact cells

Cited by 69 publications

References 258 publications

Desensitization of the μ‐opioid activation of phospholipase C in SH‐SY5Y cells: the role of protein kinases C and A and Ca2+‐activated K+ currents

Desensitization of the μ‐opioid activation of phospholipase C in SH‐SY5Y cells: the role of protein kinases C and A and Ca2+‐activated K+ currents

Intracellular Mg2+ and magnesium depletion in isolated renal thick ascending limb cells.

Raloxifene acutely suppresses ventricular myocyte contractility through inhibition of the L‐type calcium current

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Desensitization of the μ‐opioid activation of phospholipase C in SH‐SY5Y cells: the role of protein kinases C and A and Ca²⁺‐activated K⁺ currents

Desensitization of the μ‐opioid activation of phospholipase C in SH‐SY5Y cells: the role of protein kinases C and A and Ca²⁺‐activated K⁺ currents