Effects of lysophosphatidylcholine on resting potassium conductance of isolated guinea pig ventricular cells

Kiyosue, Tatsuto; Arita, Makoto

doi:10.1007/bf00640917

Cited by 74 publications

(32 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Nevertheless the detergent effects of lysophospholipids have been implicated as causative factors of arrhythmogenesis during ischaemia (Corr et al, 1981;1984; by affecting a wide variety of membrane-linked processes, particularly by inhibiting the conductance of the inward rectifier K+ channel (Clarkson & Ten Eick, 1983;Kiyosue & Arita, 1986). The threshold concentration for affecting K+ conductance in guinea-pig myocytes was found to be 10pM (Kiyosue & Arita, 1986), which was the threshold concentration for the effects of LPC in the present study. Tachycardia followed by asystole would be expected from an agent affecting K+ conductance and this parallels the excitability changes seen in ischaemic tissue (Corr et al, 1987).…”

Section: Discussionsupporting

confidence: 48%

Interaction of palmitoyl carnitine with calcium antagonists in myocytes

Patmore¹,

Duncan²,

Spedding³

1989

British J Pharmacology

View full text Add to dashboard Cite

1 Beating of aggregates of embryonic chick myocytes, in primary culture, was quantified by use of a motion-detector and video-recorder technique. Interactions of palmitoyl carnitine, a putative endogenous ligand at Ca2 + channels, with calcium antagonists were investigated. 2 Bay K 8644 (1-100nM) and palmitoyl carnitine (0.2-30 M) increased edge movement of the aggregates; beats fused so that there was an increase in baseline 'tone'. The concentrations required to produce a 50% increase in edge movement were 2.5 nm for Bay K 8644 and 2Mm for palmitoyl carnitine. Higher concentrations (20-30pM) of palmitoyl carnitine caused tachycardia of abrupt onset but resulted in cessation of beating. The effects of palmitoyl carnitine were not stereo-selective in that the (+)-and (-)-isomers were equieffective. Lysophosphatidyl choline (LPC) had no effect in concentrations up to 1OMm but higher concentrations caused tachycardia followed by cessation of beating. High concentrations of both palmitoyl carnitine and LPC (100pM) caused break-up of the aggregates, presumably as a result of detergent effects.3 Palmitoyl carnitine (1-100pM) reversed the inhibitory effects of nisoldipine (0.3/jiM), diltiazem (10Mm) and verapamil (1 gM). Ouabain was ineffective in reversing the effects of nisoldipine, differentiating the effects of palmitoyl carnitine from those of Na+/K+ATPase inhibition. In contrast, palmitoyl carnitine did not reverse the inhibitory effects of pimozide (2 Mm) or lidoflazine (7jiM); palmitoyl carnitine showed a similar profile to Bay K 8644 in this respect. 4 These findings indicate that the effects of palmitoyl carnitine closely resemble those of Bay K 8644 and can be differentiated from those of lysophospholipids. As palmitoyl carnitine accumulates in the sarcolemma during myocardial ischaemia, the mode of action in the Ca2 + channel may have clinical relevance for the use of calcium antagonists in ischaemia.

show abstract

Section: Discussionsupporting

confidence: 48%

Interaction of palmitoyl carnitine with calcium antagonists in myocytes

Patmore¹,

Duncan²,

Spedding³

1989

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…37 In ventricular myocytes, LPC modulates the Na ϩ current by PKC-dependent and tyrosine kinasedependent phosphorylation. 10 However, a controversy still exists, because LPC and PKC isoforms are not tissuespecific. Therefore, to determine whether LPC might suppress atrial release of ANP through PKC, several inhibitors for PKC or PI3 kinase were used.…”

Section: Discussionmentioning

confidence: 99%

“…After loading with 2 mol/L fura 2-AM (Molecular Probes) for 20 minutes at room temperature, atrial myocytes were attached to a perfusion chamber coated with matrix gel, stimulated at 1 Hz, and perfused with HEPES buffer containing Ca 2ϩ at a concentration of 1 mmol/L at a rate of 0.7 mL/min for 5 minutes. LPC (10,30, or 100 mol/L; nϭ8 to 10) was perfused for 5 minutes. Three types of LPCs (nϭ8 to 10)-stearoyl-LPC, lauroyl-LPC, and myristoyl-LPC-were also used.…”

Section: Measurement Of Intracellular Ca 2؉ Concentration In Single Amentioning

confidence: 99%

“…[2][3][4][5][6][7][8] A marked increase in LPC levels observed within 10 minutes of myocardial ischemia 9 produces potent, reversible, and localized effects in the heart. 3,4 LPC causes membrane depolarization as a result of decreases in potassium conductance 3,10 and modulates the cardiac Na ϩ current through protein kinase C (PKC)-dependent phosphorylation. 11 Therefore, LPC has been implicated in arrhythmogenesis during ischemia.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Decreases in ANP Secretion by Lysophosphatidylcholine Through Protein Kinase C

et al. 2003

View full text Add to dashboard Cite

Abstract-Lysophosphatidylcholine (LPC) is an endogenous phospholipid released from the cell membrane during ischemia, and it has potent, local effects on cardiac tissues. LPC has been implicated in arrhythmogenesis during ischemia by increasing intracellular Ca 2ϩ . However, it is not known whether LPC influences atrial release of atrial natriuretic peptide (ANP). The aim of this study was to investigate the effect of LPC on ANP secretion from isolated, perfused, beating rat atria. LPC (10 and 30 mol/L) caused decreases in ANP secretion in a dose-dependent manner, with slight increases in intra-atrial pressure and extracellular fluid (ECF) translocation. Therefore, the ANP secretion in terms of ECF translocation was markedly decreased by LPC. The order of the suppressive effect of ANP release was stearoyl-LPCϾLPCϾmyristoyl-LPCϭlauroyl-LPC. Staurosporine and wortmannin significantly attenuated suppression of the ANP release and an increase in intra-atrial pressure by LPC. High extracellular Mg 2ϩ also attenuated the LPC-induced suppression of ANP release. However, other protein kinase C inhibitors such as chelerythrine, GF 109203X, and tamoxifen citrate did not affect LPC-induced suppression of ANP release. In single atrial myocytes, LPC caused increases in intracellular Ca 2ϩ in a dose-dependent manner. The order of an increase in intracellular Ca 2ϩ by LPC was stearoyl-LPCϾLPCϾmyristoyl-LPCϭlauroyl-LPC. An increase in intracellular Ca 2ϩ by LPC was attenuated by staurosporine. These results suggest that LPC-induced suppression of ANP release through protein kinase C/Ca 2ϩ and phosphoinositol-3-kinase might in part play an important role in the development of hypertension.

show abstract

“…LPC decreases IK1 by decreasing the single channel conductance (Kiyosue & Arita, 1986;Sato et al 1993). LPC has also been reported to open non-selective pores permeable to Na¤, K¤, Ca¥ and NMDG, but not to aspartate, in guineapig ventricular cells (Magishi et al 1996).…”

Section: Implications Of Vrest-dependent Electroporationmentioning

confidence: 98%

Low K⁺‐induced hyperpolarizations trigger transient depolarizations and action potentials in rabbit ventricular myocytes

Akuzawa-Tateyama

Tateyama

Ochi

1998

The Journal of Physiology

View full text Add to dashboard Cite

The effects of large reductions of [K+]o on membrane potential were studied in isolated rabbit ventricular myocytes using the whole‐cell patch clamp technique. Decreasing [K+]o from the normal level of 5.4 mm to 0.1 mm increased resting membrane potential (Vrest) from −75.6 ± 0.3 to −140.3 ± 1.9 mV (means ± s.e.m; n= 127), induced irregular, transient depolarizations with mean maximal amplitudes of 19.5 ± 1.5 mV and elicited action potentials in 56.7 % of trials. The action potentials exhibited overshoots of 37.9 ± 1.5 mV (n= 72) and sustained plateaux. Addition of 0.1 mm La3+ in the presence of 0.1 mm[K+]o significantly increased Vrest but decreased the amplitude of transient depolarizations and suppressed the firing of action potentials. Replacement of external Na+ or Cl− with N‐methyl‐D‐glucamine or aspartate, respectively, or internal dialysis with 10 mm EGTA or BAPTA had little effect on low [K+]o‐induced membrane potential changes. Hyperpolarizing voltage clamp pulses to potentials between −110 and −200 mV activated irregular inward currents that increased in amplitude and frequency with increasing hyperpolarization and were depressed by 0.1 mm La3+. The generation of transient depolarizations by low [K+]o can be explained as being a consequence of decreasing the inward rectifier K+ current (IK1) and the appearance of inward currents reflecting electroporation resulting from strong electric fields across the membrane.

show abstract

Effects of lysophosphatidylcholine on resting potassium conductance of isolated guinea pig ventricular cells

Cited by 74 publications

References 26 publications

Interaction of palmitoyl carnitine with calcium antagonists in myocytes

Interaction of palmitoyl carnitine with calcium antagonists in myocytes

Decreases in ANP Secretion by Lysophosphatidylcholine Through Protein Kinase C

Low K⁺‐induced hyperpolarizations trigger transient depolarizations and action potentials in rabbit ventricular myocytes

Contact Info

Product

Resources

About

Effects of lysophosphatidylcholine on resting potassium conductance of isolated guinea pig ventricular cells

Cited by 74 publications

References 26 publications

Interaction of palmitoyl carnitine with calcium antagonists in myocytes

Interaction of palmitoyl carnitine with calcium antagonists in myocytes

Decreases in ANP Secretion by Lysophosphatidylcholine Through Protein Kinase C

Low K+‐induced hyperpolarizations trigger transient depolarizations and action potentials in rabbit ventricular myocytes

Contact Info

Product

Resources

About

Low K⁺‐induced hyperpolarizations trigger transient depolarizations and action potentials in rabbit ventricular myocytes