Actions of Nitroglycerine on the Membrane and Mechanical Properties of Smooth Muscles of the Coronary Artery of the Pig

Ito, Yushi; Kitamura, Kenji; Kuriyama, Hirosi

doi:10.1111/j.1476-5381.1980.tb07925.x

Cited by 58 publications

(18 citation statements)

References 13 publications

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“…In addition, endothelial cells release a yet unidentified endothelium-derived hyperpolarizing factor (EDHF) which, in vascular smooth muscle, causes membrane hyperpolarization by opening K+ channels (Feletou & Vanhoutte, 1988;Chen et al, 1988;1991;Nagao & Vanhoutte, 1992). However EDRF/NO and NO donors which evoke relaxation through the activation of soluble guanylate cyclase (Rapoport & Murad, 1983) also produce smooth muscle cell hyperpolarization in some blood vessels (Ito et al, 1980;Tare et al, 1990;Murphy & Brayden, 'Author for correspondence. 1995).…”

Section: Introductionmentioning

confidence: 99%

Endothelium‐derived factors and hyperpolarization of the carotid artery of the guinea‐pig

Corriu¹,

Félétou²,

Canet³

et al. 1996

British J Pharmacology

163

118

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1 Transmembrane potentials were recorded from isolated carotid arteries of the guinea-pig superfused with modified Krebs-Ringer bicarbonate solution. Smooth muscle cells were impaled from the adventitial side with intracellular glass microelectrodes filled with KCI (30-80 MCI).2 Acetylcholine (1 uM) in the presence of inhibitors of nitric oxide synthase, (Nw-nitro-L-arginine (L-NOARG) 100 gM) and cyclo-oxygenase, (indomethacin 5 tM) induced an endothelium-dependent hyperpolarization (-18.9 + 1.6 mV, n = 15).3 In the presence of these two inhibitors, S-nitroso-L-glutathione (10 gM), sodium nitroprusside (10 gM), 3-morpholinosydnonimine (SIN-1, 10 gM) and iloprost (0.1 gM) induced endotheliumindependent hyperpolarizations of the smooth muscle cells (respectively: -16.0 + 2.3, -16.3 + 3.4, -12.8+2.0 and -14.5+1.5 mV, n=4-6). 4 The addition of glibenclamide (1 uM) did not influence the acetylcholine-induced L-NOARG/ indomethacin-resistant hyperpolarization (-18.0 + 1.8 mV, n = 10). In contrast, the responses induced by S-nitroso-L-glutathione, sodium nitroprusside, SIN-I and iloprost were abolished (changes in membrane potential: -0.8 + 1.1, 1.3 + 3.9, 4.5 + 4.6 and 0.3+ 0.8 mV respectively, n = 4-5). 5 In the presence of NO synthase and cyclo-oxygenase inhibitors, charybdotoxin (0.1 M) or apamin (0.5 gM) did not influence the hyperpolarization produced by acetylcholine. However, in the presence of the combination of charybdotoxin and apamin, the acetylcholine-induced L-NOARG/indomethacinresistant hyperpolarization was converted to a depolarization (4.4 + 1.2 mV, n = 20) while the endothelium-independent hyperpolarizations induced by S-nitroso-L-glutathione, sodium nitroprusside, SIN-I and iloprost were not affected significantly (respectively: -20.4 + 3.4, -22.5 + 4.9, -14.5 + 4.7 and -14.5+0.5 mV, n=4-5). 6 In the presence of the combination of charybdotoxin and apamin and in the absence of L-NOARG and indomethacin, acetylcholine induced a hyperpolarization (-19.5 + 3.7 mV, n = 4). This hyperpolarization induced by acetylcholine was not affected by the addition of indomethacin (-18.3 +4.6 mV, n = 3). In the presence of the combination of charybdotoxin, apamin and L-NOARG (in the absence of indomethacin), acetylcholine, in 5 out of 7 vessels, still produced hyperpolarization which was not significantly smaller (-9.1 + 5.6 mV, n = 7) than the one observed in the absence of L-NOARG. 7 These findings suggest that, in the guinea-pig isolated carotid artery, the endothelium-independent hyperpolarizations induced by NO donors and iloprost involve the opening of KA,P channels while the acetylcholine-induced endothelium-dependent hyperpolarization (resistant to the inhibition of NOsynthase and cyclo-oxygenase) involves the opening of Ca2+-activated potassium channel(s). Furthermore, in this tissue, acetylcholine induces the simultaneous release of various factors from endothelial origin: hyperpolarizing factors (NO, endothelium derived hyperpolarizing factor (EDHF) and prostaglandins) and possibly a depolarizing factor.

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Section: Introductionmentioning

confidence: 99%

Endothelium‐derived factors and hyperpolarization of the carotid artery of the guinea‐pig

Corriu¹,

Félétou²,

Canet³

et al. 1996

British J Pharmacology

163

118

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“…36 -40). Several studies showed that cGMP-mediated relaxation is associated with hyperpolarization of the membrane potential, leading to a decrease in calcium influx (37,41,42). Maxi-K Ca channels have been implicated in this process because they are activated by cGMP kinase and, due to their high conductance, promote effective hyperpolarization (43).…”

Section: Stimulation Of I K(ca) In Cho-cgk Cells Is Reversed By Pro-mentioning

confidence: 99%

Protein Phosphatase 2A Is Essential for the Activation of Ca2+-activated K+ Currents by cGMP-dependent Protein Kinase in Tracheal Smooth Muscle and Chinese Hamster Ovary Cells

Zhou¹,

Ruth²,

Schlossmann³

et al. 1996

Journal of Biological Chemistry

121

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“…Therefore, the actions of nitrate compounds on vascular tissues vary. Ito et al (1980a) studied the effects of NG on electrically quiescent muscle of canine coronary artery and found that NG (10-5 M) modified neither the membrane potential nor the membrane resistance, while at 2-8 x 10-1o M, NG markedly suppressed the contraction induced by excess [K]J or acetylcholine (ACh). They concluded that NG may suppress the Ca releasing mechanism from the storage site rather than the influx of Ca.…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of the nitroglycerine‐induced vasodilation in vascular smooth muscles of the rabbit and pig.

Itoh¹,

Kuriyama²,

Ueno³

1983

The Journal of Physiology

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SUMMARY1. The effects of nitroglycerine (NG) on the mechanical responses of small pieces of intact and skinned smooth muscles of the mesenteric artery, were investigated, as were the Ca fluxes of isolated smooth muscle cells of the coronary artery.2. NG (10-6-10-5 M) inhibited both phasic and tonic components of the K-induced contraction; however, the tonic component was more sensitive to NG. The minimum concentration of NG required to decrease significantly the tonic response evoked by 39 mM-external K was 10-8 M. NG (10-5 M) reduced the number of oscillatory contractions evoked by 10-5 M-noradrenaline (NAd).3. After complete removal of stored Ca, the addition of Ca did not produce contraction in polarized muscle (5 9 mM-external K), yet depolarized muscles (128 mmexternal K) did contract. Addition of NG (10-5 M) with Ca produced no change in the resting tone in polarized muscles but inhibited the contraction in depolarized muscles. After application of NG (10-5 M), caffeine or NAd consistently produced smaller contraction in both polarized and depolarized muscles in Ca-free solution.4. NG (10-5 M) inhibited the Na-free contraction evoked by prolonged treatment with Na-free solution. Contractions evoked by repetitive applications of 10-5 M-NAd or 10 mM-caffeine persisted longer in Na-free, Ca-free (EGTA) solution than those observed in Ca-free Krebs solution, but when NG was added to the Na-free, Ca-free (EGTA) solution, the contractions ceased more rapidly than in the absence of NG.5. In chemically skinned muscles, 10-5 M-NG had no effect on the pCa-tension relationship. The absolute amplitude of Ca-induced contraction was also not affected by 10-5 M-NG. In these muscles, when the amount of stored Ca was estimated from the amplitude of the caffeine-induced contraction, Ca accumulation into and release from store sites were unaffected by 10-5 M-NG.6. The effects of 10-5 M-NG on the accumulation and efflux of 45Ca in isolated cell suspensions prepared from the porcine coronary artery were investigated. The amount of 45Ca taken up by cells after 1-30 min incubation in 45Ca-containing solution, and the 45Ca efflux in Ca-free (EGTA) solution, were not affected by 10-5 M-NG. In the presence of 3 x 10-6 M-acetylcholine (ACh), the efflux of 45Ca into Ca-free (EGTA) solution was accelerated and with the addition of 10-5 M-NG plus 3 x 10-6 M-ACh, this efflux was even further enhanced.The authors' names are in alphabetical order.

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Actions of Nitroglycerine on the Membrane and Mechanical Properties of Smooth Muscles of the Coronary Artery of the Pig

Cited by 58 publications

References 13 publications

Endothelium‐derived factors and hyperpolarization of the carotid artery of the guinea‐pig

Endothelium‐derived factors and hyperpolarization of the carotid artery of the guinea‐pig

Protein Phosphatase 2A Is Essential for the Activation of Ca2+-activated K+ Currents by cGMP-dependent Protein Kinase in Tracheal Smooth Muscle and Chinese Hamster Ovary Cells

Mechanisms of the nitroglycerine‐induced vasodilation in vascular smooth muscles of the rabbit and pig.

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