Effects of Adrenergic Activators and Inhibitors on the Coronary Circulation

Parratt, J. R.

doi:10.1007/978-3-642-67505-8_19

Cited by 21 publications

(11 citation statements)

References 284 publications

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“…They showed that p-oxprenolol (in contrast to oxprenolol itself) caused no blockade of the vascular (12) effects of isoprenaline whereas blockade of the myocardial (01) effects of isoprenaline was comparable with that of oxprenolol. The present results, albeit in a different species, agree precisely with this ( (Parratt, 1980).…”

Section: Relevance Ofcardioselectivitysupporting

confidence: 93%

The effect of β‐adrenoceptor blocking agents, with differing ancillary properties, on the arrhythmias resulting from acute coronary artery ligation in anaesthetized rats

Campbell

Parratt

1983

British J Pharmacology

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The effects of several P-adrenoceptor blocking agents, ((+), (-) and (±)-oxprenolol, poxprenolol, practolol, propranolol and timolol) were investigated on the ventricular arrhythmias occurring within the first 30 min of acutely ligating the main left coronary artery in anaesthetized rats. The degree of cardiac and vascular 3-adrenoceptor blockade was also assessed. 2 All the compounds exhibited antiarrhythmic activity under these conditions. The degree of cardiac P-adrenoceptor blockade required for this protection was less for the cardioselective agents, p-oxprenolol and practolol, than for the non-selective 3-adrenoceptor blocking agents. 3 A comparison of the two isomers of oxprenolol demonstrated that the (-)-isomer markedly suppressed ischaemic arrhythmias (ventricular ectopic beats, incidence and duration of ventricular tachycardia and duration of ventricular fibrillation) more effectively than the (+)-isomer. 4 Compounds possessing intrinsic sympathomimetic activity (ISA) caused less marked haemodynamic changes (in equivalent f-blocking doses) than those that did not possess this ancillary property.5 The membrane stabilizing activity of oxprenolol and p-oxprenolol did not appear to contribute to the antiarrhythmic activity of these agents; however, the membrane stabilizing activity of propranolol may contribute to its effectiveness. 6 In all the drugs studied, the main pharmacological property required to suppress early postischaemic arrhythmias is blockade of cardiac f-adrenoceptors.

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Section: Relevance Ofcardioselectivitysupporting

confidence: 93%

The effect of β‐adrenoceptor blocking agents, with differing ancillary properties, on the arrhythmias resulting from acute coronary artery ligation in anaesthetized rats

Campbell

Parratt

1983

British J Pharmacology

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“…First, AP did not change, so the decreased ejection fraction could not be attributed to increased afterload (28) or to baroreceptor reflexinhibition of contractile function (29). Second, a direct negative inotropic effect of NPY would not be expected to cause the magnitude of decrease in CBF that was observed in the present study (30), and a negative inotropic effect would not cause the decrease in intramyocardial pH seen in group I or ST-T wave changes as seen in group VI. Further, if data from another study from this lab (31) are plotted on Fig.…”

Section: Resultsmentioning

confidence: 61%

Neuropeptide-Y. A peptide found in human coronary arteries constricts primarily small coronary arteries to produce myocardial ischemia in dogs.

Maturi

Greene²,

Speir³

et al. 1989

J. Clin. Invest.

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(LVEF), measured by radionuclide angiography, decreased from 0.52±0.08 to 0.42±0.12 U (n = 5, P < 0.01) during NPY. NPY-induced vasoconstriction was also associated with ST-T wave changes on the electrocardiogram (ECG) in eight of nine other animals (group V). In another group of six dogs (group IV), the change in small vessel resistance accounted for 94% of the increase in total resistance, so that the primary vasoconstrictor effect of NPY was exerted on small coronary arteries. Thus, NPY, a peptide found in human coronary arteries, caused constriction of primarily small coronary arteries that was severe enough to produce myocardial ischemia as determined by ECG ST-T wave changes, and decreases in intramyocardial pH and LVEF in dogs.

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“…Evidence shows that activation of ␣ 1 -and ␣ 2 -receptors in vivo results in constriction of the coronary vessels, 15,17,26 whereas activation of ␤ 1 -and ␤ 2 -receptors elicits dilations. 17,[21][22][23][24][25] In vivo investigation of the mechanism of action of NE infused in the coronary circulation has been hampered somewhat by the actions of NE on various adrenoceptors and tissues.…”

Section: Sun Et Al ␤ 2 -Adrenoceptors In Human Coronary Circulation 553mentioning

confidence: 99%

Norepinephrine Elicits β ₂ -Receptor–Mediated Dilation of Isolated Human Coronary Arterioles

et al. 2002

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Background-The exact role of adrenoceptors in norepinephrine (NE)-mediated regulation of the human coronary circulation has yet to be elucidated. Thus, the goals of this study were to characterize the adrenoceptors involved in the responses to NE in isolated human coronary arterioles and small arteries. Methods and Results-Arterioles (nϭ39) and small arteries from the left ventricle of explanted human hearts were isolated and cannulated. Vessels from the hearts of 21 patients were studied: 15 males and 6 females, aged 0.5 to 63 years. Nineteen patients were considered to be New York Heart Association class 4. All hearts exhibited hypertrophy (190Ϯ20%). The passive diameter of arterioles was 167Ϯ8 m (range 97 to 323 m). NE (10 Ϫ7 to 3ϫ10 Ϫ7 mol/L) elicited concentration-dependent dilations (47Ϯ4 m) that were unaffected by endothelium removal, N -nitro-Larginine (10 Ϫ4 mol/L, an NO synthase inhibitor), or practolol (10 Ϫ6 mol/L, a ␤ 1 -receptor blocker). However, administration of propranolol (10 Ϫ5 mol/L, a combined ␤ 1 -and ␤ 2 -blocker) or butoxamine (10 Ϫ6 mol/L, a ␤ 2 -receptor blocker) completely eliminated the NE-induced dilation. Constrictions to NE (2 of 39 vessels) were inhibited by prazosin (10 Ϫ6 mol/L, an ␣ 1 -receptor blocker). Methoxamine (10 Ϫ9 to 10 Ϫ5 mol/L, an ␣ 1 -agonist) had no effect, whereas U44619, a thromboxane mimetic, elicited dose-dependent constriction of vessels. Conclusions-Our data indicate that isolated human coronary arterioles and small arteries dilate to NE via ␤ 2 -receptors on smooth muscle. These findings are important to our understanding of the mechanisms action of NE in the human coronary circulation. (Circulation. 2002;106:550-555.)

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Effects of Adrenergic Activators and Inhibitors on the Coronary Circulation

Cited by 21 publications

References 284 publications

The effect of β‐adrenoceptor blocking agents, with differing ancillary properties, on the arrhythmias resulting from acute coronary artery ligation in anaesthetized rats

The effect of β‐adrenoceptor blocking agents, with differing ancillary properties, on the arrhythmias resulting from acute coronary artery ligation in anaesthetized rats

Neuropeptide-Y. A peptide found in human coronary arteries constricts primarily small coronary arteries to produce myocardial ischemia in dogs.

Norepinephrine Elicits β ₂ -Receptor–Mediated Dilation of Isolated Human Coronary Arterioles

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Effects of Adrenergic Activators and Inhibitors on the Coronary Circulation

Cited by 21 publications

References 284 publications

The effect of β‐adrenoceptor blocking agents, with differing ancillary properties, on the arrhythmias resulting from acute coronary artery ligation in anaesthetized rats

The effect of β‐adrenoceptor blocking agents, with differing ancillary properties, on the arrhythmias resulting from acute coronary artery ligation in anaesthetized rats

Neuropeptide-Y. A peptide found in human coronary arteries constricts primarily small coronary arteries to produce myocardial ischemia in dogs.

Norepinephrine Elicits β 2 -Receptor–Mediated Dilation of Isolated Human Coronary Arterioles

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Norepinephrine Elicits β ₂ -Receptor–Mediated Dilation of Isolated Human Coronary Arterioles