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Effect of amiloride in guinea-pig and rat left atria contraction as affected by frequency of stimulation and [Ca2+]o/[Na+]o ratio: role of Na+/Ca2+ exchange.
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The influence of acidosis on the myocardial uptake and electrocardiographic effects of dysopiramide.
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Effect of ouabain on the response to noradrenaline of guinea-pig intrarenal artery rings.
No full text[Positive inotropic effect of amiloride and inhibition of Na+/Ca2+ exchange: dependence on temperature].
No full textNa+/Ca2+ exchange plays a fundamental role in the regulation of intracellular Ca2+ levels and thus myocardial contractility. The influence of temperature variations on Na+/Ca2+ exchange activity in bovine heart sarcolemmal vesicles has been studied. Furthermore, the temperature dependence of positive inotropic response induced by amiloride, an inhibitor of Na+/Ca2+ exchange activity, has been investigated in isolated guinea-pig left atria driven at 1 Hz. Our results indicate that cooling from 37 degrees to 20 degrees C inhibits Na+/Ca2+ exchange activity in sarcolemmal vesicles, whereas does not change the extent of Na+/Ca2+ exchange inhibition by amiloride. In addition, the positive inotropic effect induced by amiloride in guinea-pig left atria decreases and eventually disappears when temperature is progressively reduced from 35 degrees to 23 degrees C. A possible relationship between the decrease in Na+/Ca2+ exchange activity induced by cooling and the temperature dependence of positive inotropic effect of amiloride is discussed
Endothelin-1-induced arachidonic acid release by cytosolic phospholipase A(2) activation in rat vascular smooth muscle via extracellular signal-regulated kinases pathway
No full textThe present study investigates whether endothelin-1 (ET-1), like noradrenaline (NA), stimulates the release of arachidonic acid (AA) via cytosolic phospholipase A2 (cPLA2) in rat tail artery. In tail artery segments labelled with [3H]AA, ET-1-induced AA release in a concentration-dependent manner with an EC50 of 1.3 nM. The effect of ET-1 was inhibited by bosentan and was insensitive to BQ788, suggesting the involvement of ETA receptor. The stimulation of AA release induced by ET-1 was prevented by arachydonyl trifluoromethyl ketone (AACOCF3), a selective inhibitor of cPLA2 and not by RHC80267, a diacylglycerol lipase inhibitor. Furthermore, PD98059, inhibitor of mitogen-activated protein kinase kinase (MEK) cascade and calphostin C, a protein kinase C (PKC) inhibitor, prevented the stimulation of AA release induced by ET-1 and NA. Immunoblotting of the cytosolic fraction of rat tail arteries stimulated with ET-1 or NA showed an increase in extracellular signal-regulated kinases (ERKs) phosphorylation and this effect was abolished by calphostin C treatment. These findings show that in rat tail artery ET-1 and NA induce a sequential activation of protein kinase C and extracellular signal-regulated kinases that results in stimulation of AA release via cPLA2 activation. This may represent a general pathway by which G-proteins coupled receptors stimulate AA release and its metabolites in vascular smooth muscle
Effect of long-term ouabain treatment on contractile responses of rat aortae
No full textMale Sprague-Dawley rats were infused with 50 microg/kg/day of ouabain for 4 weeks to address the question whether prolonged exposure to the drug affects blood pressure, the in vitro contractile responses to agonists and high K+ of their aortae, and the influence of endothelium on these responses. Systolic blood pressure was not affected by ouabain treatment. The responsiveness of endothelium-intact aortae from ouabain-treated rats to endothelin-1 increased, that to phenylephrine decreased, and that to high K+ was unchanged, as compared with control. The responses of endothelium-free aortae to endothelin-1, phenylephrine, and high K+ were lower in ouabain-treated than in control rats. The removal of endothelium increased the response to phenylephrine and decreased that to high K+ in either control or ouabain-treated rat aortae, whereas it did not affect the response to endothelin-1 in control rat aortae and decreased it in ouabain-treated rat aortae. The response to caffeine was unaffected by either ouabain treatment or endothelium removal. Thus rat ouabain long-term treatment induces opposing effects on the responsiveness of their intact aortae to an alpha-adrenergic agonist and endothelin-1. If these effects observed in the ex vivo experiments occur also in vivo on rat microvasculature, they could balance out and contribute to the lack of effect on systolic blood pressure of prolonged ouabain treatment
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