Adrenergic receptors in the coronary circulation

Comparative Effects of Propranolol and Practolol in the Early Stages of Experimental Canine Myocardial Infarction

“…There is considerable evidence for the release of noradrenaline into the circulation following coronary artery occlusion and, although in the early stages (up to 1 h after occlusion) this amine induces active coronary vasoconstriction in the ischaemic area (for references see Moore & Parratt, 1973), noradrenaline later increases blood flow in the ischaemic region (Marshall & Parratt, 1973a), an effect not solely related to increased perfusion pressure. The administration of propranolol would block vascular 62-adrenoceptors in the ischaemic region (as it certainly does in the normal coronary circulation; Parratt & Grayson, 1966) and unmask a vasoconstrictor effect of released noradrenaline on vascular a-adrenoceptors present within this region (Parratt, 1967). This would adequately explain the active increase in resistance to flow (from 1.07 + 0.38 to 2.35 + 0.48 units; P <0.025) within the developing infarct following propranolol administration.…”

Sensitization of Noradrenaline Responses by Inhibitors of Extraneuronal Uptake in a Coronary Artery Preparation

“…However, responses were enhanced about 3-fold by 173-oestradiol and the haloalkylamine GD-131, two known inhibitors of extraneuronal uptake.The coronary blood vessels of diverse species generally respond to the sympathetic nerve transmitter, noradrenaline, with 3-adrenoceptor mediated relaxation, although under in vivo conditions the intensity of the overall effect may be related to the metabolic state of the heart (Gaal, Kattus, Kolin & Ross, 1966;Parratt, 1967 give a stock concentration of 10 mg/ml. The volume of propylene glycol usually added to the muscle chambers was 0.015 ml and when used alone it had no effect on the basal tone of strips or on their responses to potassium or noradrenaline.…”

“…However, no information is available on the relative importance of neuronal and extraneuronal mechanisms in terminating responses to noradrenaline in the coronary vasculature. The overall effect of noradrenaline on coronary vessel blood flow in vivo is dilator but the mechanisms involved have been controversial due to the multiplicity of factors such as extravascular compression, heart rate and myocardial metabolism which can override the direct effect (Parratt, 1967). It now appears likely that the direct effect is in most cases inhibitory, mediated by 3-adrenoceptor activation and antagonized by ,B-adrenoceptor blocking agents (Gaal et al, 1966;Bohr, 1967;Parratt, 1967).…”

“…The overall effect of noradrenaline on coronary vessel blood flow in vivo is dilator but the mechanisms involved have been controversial due to the multiplicity of factors such as extravascular compression, heart rate and myocardial metabolism which can override the direct effect (Parratt, 1967). It now appears likely that the direct effect is in most cases inhibitory, mediated by 3-adrenoceptor activation and antagonized by ,B-adrenoceptor blocking agents (Gaal et al, 1966;Bohr, 1967;Parratt, 1967). The population of a-adrenoceptors appears small to negligible in most preparations of coronary artery strips tested in vitro (Bohr, 1967).…”

Synergistic Actions of Nitrite-&beta;-Adrenergic Blocking Agents in the Therapy of Angina Pectoris

“…Some debate exists over the effects of /J-blockers on the coronary vascular tree. Significant vasoconstriction and widening of the arterial minus coronary sinus oxygen difference have been observed in the anesthetized animal [54], but not convincingly in conscious man or animals [40,55].…”