Possible opioid receptor function changes in isolated atria of the spontaneously hypertensive rat

Wong, So C.; Ingenito, Alphonse J.

doi:10.1016/0306-3623(93)90440-9

Cited by 7 publications

(2 citation statements)

References 15 publications

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“…Opioids reportedly decrease the spontaneous beating rate of isolated rat atria (Wong and Ingenito, 1993), and induce bradycardia through increasing vagal tone in anaesthetised dogs (Urthaler et al, 1975). While in vivo responses may be modulated by vagal tone, in vitro responses may involve inhibitory ‘cross-talk’ between opioid receptors and β-adrenoceptors.…”

Section: Discussionmentioning

confidence: 99%

Chronic β 1 -adrenoceptor blockade impairs ischaemic tolerance and preconditioning in murine myocardium

Hoe

Schilling

Busija

et al. 2016

European Journal of Pharmacology

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β-adrenoceptor antagonists are commonly used in ischaemic heart disease (IHD) patients, yet may impair signalling and efficacy of ‘cardioprotective’ interventions. We assessed effects of chronic β1-adrenoceptor antagonism on myocardial resistance to ischemia-reperfusion (IR) injury and the ability of cardioprotective interventions [classic ischaemic preconditioning (IPC); novel sustained ligand-activated preconditioning (SLP)] to reduce IR injury in murine hearts. Young male C57Bl/6 mice were untreated or received atenolol (0.5 g/l in drinking water) for 4 weeks. Subsequently two cardioprotective stimuli were evaluated: morphine pellets implanted (to induce SLP, controls received placebo) 5 days prior to Langendorff heart perfusion, and IPC in perfused hearts (3 × 1.5 min ischemia/2 min reperfusion). Atenolol significantly reduced in vivo heart rate. Untreated control hearts exhibited substantial left ventricular dysfunction (~50% pressure development recovery, ~20 mmHg diastolic pressure rise) with significant release of lactate dehydrogenase (LDH, tissue injury indicator) after 25 min ischemia/45 min reperfusion. Contractile dysfunction and elevated LDH were reduced >50% with IPC and SLP. While atenolol treatment did not modify baseline contractile function, post-ischaemic function was significantly depressed compared to untreated hearts. Atenolol pre-treatment abolished beneficial effects of IPC, whereas SLP protection was preserved. These data indicate that chronic β1-adrenoceptor blockade can exert negative effects on functional IR tolerance and negate conventional IPC (implicating β1-adrenoceptors in IR injury and IPC signalling). However, novel morphine-induced SLP is resistant to inhibition by β1-adrenoceptor antagonism.

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Section: Discussionmentioning

confidence: 99%

Chronic β 1 -adrenoceptor blockade impairs ischaemic tolerance and preconditioning in murine myocardium

Hoe

Schilling

Busija

et al. 2016

European Journal of Pharmacology

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show abstract

“…For example, obstructive cholestasis seems associated with naltrexone-sensitive bradycardia [74]. Enhanced OPR-mediated chronotropy is significantly associated with hypertension [75]. K-opioid receptor stimulation has a protective effect in hypoxic pulmonary hypertension [76].…”

Section: Opioidsmentioning

confidence: 99%