Effects of procaine on pharmaco-mechanical coupling mechanisms activated by acetylcholine in smooth muscle cells of porcine coronary artery.

Ueno, Hikaru; Sumimoto, Kotoko; Hashimoto, Toshihiko; Hirata, Masato; Kuriyama, Hirosi

doi:10.1161/01.res.60.3.356

Cited by 19 publications

(14 citation statements)

References 41 publications

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“…12 In contrast, ACh, which is often used in assessing coronary endothelial function, is one of the agonistinduced stimulators of endothelial NO. It has its effect on vasculature, mediated by muscarinic receptors present on the endothelium, leading to the phosphorylation of endothelial NO synthase through the phosphatidylinositol 3-kinase pathway in conduit vessels, 21,22 while other factors such as prostacylin and endothelium-dependent hyperpolarizating factor also contribute to ACh-induced vasodilation at the level of the resistance vessel. 23 With respect to the relationship between agonist-and shear stress-induced NO release, our previous study has demonstrated that FMD of the coronary artery in response to an intracoronary infusion of adenosine does not change before or after the administration of L-NMMA, while ACh-induced dilation of the coronary artery was blocked by this dose of L-NMMA.…”

Section: Flow-mediated Dilation Of the Brachial Artery And Acetylcholmentioning

confidence: 99%

Relationship between endothelial function in the coronary and brachial arteries

et al. 2005

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SummaryBackground: Endothelial dysfunction is the first step in the progression to atherosclerosis, but little is known regarding whether there is a correlation in endothelial function between the coronary and peripheral arteries.Hypothesis: We investigated the relationship between coronary and peripheral endothelial function.Methods: In 41 patients (mean age 63 years; 23 men, 18 women) with angiographically normal coronary arteries, changes in brachial artery diameter in response to hyperemic flow and sublingual nitroglycerin (NTG) were measured by high-resolution ultrasonography. During coronary angiography, acetylcholine (ACh, 3 and 30 µg/min) and NTG were infused into the left coronary ostium. The diameter of the coronary artery was quantitatively measured and coronary blood flow (CBF) was calculated by quantitative angiography and Doppler flow velocity measurements. Changes in these parameters in response to each drug infusion were expressed as the percent change from the baseline values.Results: Flow-mediated dilation (FMD) of the brachial artery was 5.0 ± 3.5% and correlated positively not only with the change in coronary diameter (ACh at 30 µg/min, r = 0.31, p < 0.05) but also with the change in CBF (ACh at 3 µg/min, r = 0.39, p < 0.05; ACh at 30 µg/min, r = 0.46, p < 0.01). Multi-

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Section: Flow-mediated Dilation Of the Brachial Artery And Acetylcholmentioning

confidence: 99%

Relationship between endothelial function in the coronary and brachial arteries

et al. 2005

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“…Effects of drugs that inhibit Ca2' release from intracellular storage sites Procaine inhibits the release of Ca21 from internal stores (Endo, 1977;Ueno, Sumimoto, Hashimoto, Hirata & Kuriyama, 1987). It reduced both the slow IPSP and noradrenaline hyperpolarization in a dose-dependent manner without affecting The slow IPSP and the noradrenaline hyperpolarization were reversibly reduced by procaine (A and B), while the fast EPSP and the slow EPSP were not reduced (C).…”

Section: B Slow Ipsp and Intracellular Processmentioning

confidence: 99%

Mechanisms underlying intracellular signal transduction of the slow IPSP in submucous neurones of the guinea‐pig caecum.

Mihara¹,

Hirai²,

Katayama³

et al. 1991

The Journal of Physiology

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SUMMARY1. Intracellular recordings were obtained from submucous plexus neurones of the guinea-pig caecum.2. The resting membrane conductance displayed two types of inward rectification: one which developed at potentials more negative than -70 mV, and another that occurred at potentials more negative than the potassium equilibrium potential. The former inward rectification was blocked by extracellular caesium (Cs'; 1-2 mM) and the latter was blocked by Cs' (1-2 mM) or barium (Ba2"; 30-100 /lM).3. The noradrenaline-induced current measured by subtraction of the currentvoltage (I-V) relation before and after adding the agonist also showed an inward rectification around the resting potential. Ba2l (30-100 ,UM) blocked both the outward and inward current induced by noradrenaline. The noradrenaline current was not affected by Cs+ (1-2 mM). Both the slow IPSP and the slow IPSC (inhibitory postsynaptic current) were reduced by Ba2+, but not by Cs+.4. During the intracellular injection of guanosine 5'-O-(3-thiotriphosphate) (GTPy-S), multiple repetitive stimulation or repeated applications of noradrenaline produced irreversible membrane hyperpolarizations with a decreased membrane input resistance, until the membrane had approached the potassium equilibrium potential.5. Pertussis toxin (1-40 ,ug/ml) abolished both the slow IPSP and the noradrenaline hyperpolarization without affecting the nicotinic fast EPSP or the slow EPSP.6. Superfusion with a Ca2+-free, high-Mg2+ (12 mM) solution caused a membrane depolarization associated with an increased input resistance. It eliminated the Ca2+ spikes, the slow after-hyperpolarizations following the spikes, and the synaptic potentials within 3 min. Prolonged exposure (longer than 20 min) to this solution resulted in a progressive decline of the noradrenaline hyperpolarization.

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“…It is more likely that local anaesthetics act on Ca release channels in a structure-specific manner and some of them inhibit the desensitization of the Ca-induced Ca release mechanism. This idea is supported by reports that local anaesthetics act widely on Ca channels including voltage-dependent Ca channels in plasma membrane and IP3-induced and Ca-induced Ca release channels in intracellular Ca stores (Spedding & Berg, 1985;Ahn & Karaki, 1988;Ueno et al, 1987).…”

Section: Discussionmentioning

confidence: 73%

“…We found in smooth muscle of guinea-pig taenia caecum that histamine-induced homologous desensitization was prevented by some local anaesthetics under normal physiological conditions and that their effects were produced by their specific action rather than by their nonspecific membrane-stabilizing effect (Hishinuma & Uchida, 1987). Local anaesthetics were also shown to have some effects on voltage-dependent Ca channels in the plasma membrane (Spedding & Berg, 1985), on inositol trisphosphate (OP3)-induced and Ca-induced Ca release channels in intracellular Ca stores (Ahn & Karaki, 1988;Ueno et al, 1987) and on K+ channels in smooth muscle cells (Ohya et al, 1987).…”

Section: Introductionmentioning

confidence: 99%

Blockade by the local anaesthetic, tetracaine, of desensitization of Ca‐induced Ca release after muscarinic stimulation in smooth muscle

Hishinuma

Uchida

1991

British J Pharmacology

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1 Desensitization of contractile responses dependent on release of intracellularly stored Ca elicited by carbachol, histamine or caffeine was measured after desensitizing treatment with carbachol or histamine in the presence or absence of local anaesthetics in Ca-free solution containing 2mm EGTA in the smooth muscle of guinea-pig taenia caecum. 2 Histamine-induced homologous desensitization was inhibited by tetracaine and procainamide. Dibucaine did not exert an inhibitory effect on the desensitization. This is consistent with our previous findings concerning the effects of local anaesthetics on the densitization of histamine H -receptors measured under normal physiological conditions. 3 Carbachol induced a functional change of intracellular Ca stores which resulted in heterologous desensitization. Tetracaine completely blocked carbachol-induced desensitization of the caffeine-elicited contraction, but in the case of carbachol-induced desensitization of carbachol-and histamine-elicited contractions, this blocking effect of tetracaine was very weak and absent, respectively. The other local anaesthetics used did not affect the desensitization. These results suggest that the Ca-induced and inositol trisphosphate-induced Ca release mechanisms were both desensitized by carbachol and that the desensitization of the Ca-induced Ca release mechanism was selectively blocked by tetracaine.

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Effects of procaine on pharmaco-mechanical coupling mechanisms activated by acetylcholine in smooth muscle cells of porcine coronary artery.

Abstract: The action of procaine on pharmaco-mechanical coupling activated by application of acetylcholine (ACh) was investigated using collagenase-treated dispersed intact and skinned smooth muscle cells and intact muscle tissues of the porcine coronary artery. ACh reduced stored 45

Cited by 19 publications

References 41 publications

Relationship between endothelial function in the coronary and brachial arteries

Relationship between endothelial function in the coronary and brachial arteries

Mechanisms underlying intracellular signal transduction of the slow IPSP in submucous neurones of the guinea‐pig caecum.

Blockade by the local anaesthetic, tetracaine, of desensitization of Ca‐induced Ca release after muscarinic stimulation in smooth muscle

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