Effects of sotalol, (−)-propranolol and prazosin on reperfusion-induced arrhythmias and increased cardiac norepinephrine release

Lamontagne, Daniel; Yamaguchi, Nobuharu; Nadeau, Réginald; Champlain, Jacques de; Godin, D; Campeau, Nicole

doi:10.1016/0014-2999(86)90680-1

Cited by 18 publications

(12 citation statements)

References 19 publications

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“…Generally, during sustained myocardial ischemia, NE accumulation within the ischemic myocardium is mainly the result of a locally induced nonexocytotic release of NE (Schömig 1990). Nonexocytotic release of NE during ischemia contributes to the genesis of malignant arrhythmias (Godin et al 1985;Lamontagne et al 1986;Yamaguchi et al 1990;Schömig 1990) and accelerates the development of myocardial injury (Nadeau and de Champlain 1979). This finding also suggests that sympathetic nerve terminals themselves are involved in the adaptation to ischemia in a manner comparable with that of myocardial tissue.…”

Section: Discussionmentioning

confidence: 88%

Transient ischemia inhibits nonexocytotic release of norepinephrine following sustained ischemia in rat heart: is bradykinin involved?

Feng

Yamaguchi²,

Foucart³

et al. 1997

Can. J. Physiol. Pharmacol.

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Previous studies have demonstrated that transient ischemia inhibits the release of norepinephrine (NE) following a sustained ischemia. However, the mechanism underlying this inhibition is unknown. Therefore, this study was designed to investigate whether bradykinin (BK) may be involved in the inhibition of NE release following ischemic preconditioning. The effects of transient ischemia, exogenous BK, and kinin receptor blockers on NE release after a prolonged ischemia were tested in the isolated rat heart preparation. Three cycles of 5-min ischemia and reperfusion resulted in the reduction of NE release from 115.3 +/- 14.5 to 51.6 +/- 9.3 pmol.g-1 (p < 0.05) after 30 min of subtotal global ischemia. This effect was not prevented by the administration of either Lys-[Leu8]-des-Arg9-BK (1 mumol.L-1), a B1 antagonist, or HOE-140 (1 mumol.L-1), a B2 antagonist. Three cycles of 5-min BK or des-Arg9-BK infusion also resulted in a dose-dependent inhibition of NE release after 30 min of ischemia. The inhibitory effects of BK (1 mumol.L-1) or des-Arg9-BK (0.5 mumol.L-1) were blocked by Lys-[Leu8]-des-Arg9-BK (1 mumol.L-1), but not by HOE-140 (1 mumol.L-1). The results show that transient ischemia and BK protect sympathetic nerve endings in the isolated rat heart. The inhibition of NE release by pretreatment with BK is mediated by the activation of B1 receptors, whereas preconditioning provided by transient ischemia may be mediated by a different, yet unknown, mechanism in the rat heart.

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Section: Discussionmentioning

confidence: 88%

Transient ischemia inhibits nonexocytotic release of norepinephrine following sustained ischemia in rat heart: is bradykinin involved?

Feng

Yamaguchi²,

Foucart³

et al. 1997

Can. J. Physiol. Pharmacol.

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“…Catecholamines and their oxidation by-products are known to contribute to the deleterious effects accompanying reperfusion (Lamontagne et al 1986;Yamaguchi et al 1990). The release of noradrenaline in ischemic myocardium, with a rapid washout into the coronary effluent upon reperfusion, has been described several years ago.…”

Section: Discussionmentioning

confidence: 99%

The cardioprotective effect of dual metallopeptidase inhibition: respective roles of endogenous kinins and natriuretic peptides

Dumoulin

Adam

Burnett³

et al. 2005

Can. J. Physiol. Pharmacol.

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The objective of the present study was to assess the cardioprotective effect of dual NEP-ACE inhibition in relation to endogenous cardiac bradykinin (BK), its active metabolite des-Arg9-BK, endogenous brain natriuretic peptides (BNP), and cGMP. Rats were treated with the dual metallopeptidase inhibitor, omapatrilat, or the ACE inhibitor, ramipril, for 7 d (1 mg.kg(-1).d(-1)). Hearts were then isolated and subjected to a zero-flow ischemia and reperfusion (except controls), in the absence or presence of either a B2-receptor antagonist (Hoe-140), a B1-receptor antagonist (Lys-Leu8-des-Arg9-BK), or the GC-A/GC-B-receptor antagonist (HS-142-1). Chronic omapatrilat and ramipril increased the amount of endogenous BK collected upon reperfusion, but only ramipril increased that of des-Arg9-BK. Only omapatrilat increased both peak BNP and peak cGMP upon reperfusion, those increases being blocked by Hoe-140. Chronic omapatrilat (but not ramipril) decreased the total noradrenaline and lactate dehydrogenase release during the reperfusion period. Importantly, only omapatrilat improved the functional recovery of the ischemic reperfused heart, with a reduced left ventricular end-diastolic pressure, and improved developed left ventricular pressure. All cardio protective effects of omapatrilat were blocked by Hoe-140 and by HS-142-1, but not by the B1-receptor antagonist. In conclusion, a chronic treatment with a dual metallopeptidase inhibitor demonstrated a cardioprotective action not observed with an ACE inhibitor in a context of severe ischemia in rat isolated hearts, which was mediated by both endogenous BK and BNP.

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“…Recently, much attention has been drawn to the involvement of catecholamines in cardiac arrhythmia in ischemic or reperfused myocardium (23)(24)(25)(26), and both clinical and experimental studies have suggested that in such abnormal hearts, increased circulating catecholamine values might play an arrhy thmogenic role (25)(26)(27).…”

Section: Discussionmentioning

confidence: 99%

Effects of betaxolol, a new beta 1 selective blocker, on canine ventricular arrhythmias.

Mitsuhashi¹,

Akiyama²,

Hashimoto³

1987

Jpn.J.Pharmacol

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Abstract-Antiarrhythmic effects of a new beta 1 selective adrenoceptor blocker, betaxolol, were examined in comparison with those of atenolol using two canine ventricular arrhythmia models (adrenaline arrhythmia and digitalis arrhythmia). Both betaxolol and atenolol suppressed adrenaline arrhythmia, and the minimum effective plasma concentration of betaxolol for this arrhythmia model was deter mined to be less than 10 ng/ml.However, on digitalis arrhythmia, both beta blockers were ineffective, even though the high doses used in these experiments, 3 mg/kg for betaxolol and 5 mg/kg for atenolol, showed significant hypotensive effects.The present results suggest that betaxolol and atenolol may be expected to be clinically effective on arrhythmias related to increased sympathetic tone.

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Effects of sotalol, (−)-propranolol and prazosin on reperfusion-induced arrhythmias and increased cardiac norepinephrine release

Cited by 18 publications

References 19 publications

Transient ischemia inhibits nonexocytotic release of norepinephrine following sustained ischemia in rat heart: is bradykinin involved?

Transient ischemia inhibits nonexocytotic release of norepinephrine following sustained ischemia in rat heart: is bradykinin involved?

The cardioprotective effect of dual metallopeptidase inhibition: respective roles of endogenous kinins and natriuretic peptides

Effects of betaxolol, a new beta 1 selective blocker, on canine ventricular arrhythmias.

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