Adrenergic receptors for glycogenolysis and cardiac contractile force Public Deposited

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  • It is common to characterize adrenergic receptors by placing them in one of two categories, alpha or beta. The receptors responsible for adrenergically induced increase in cardiac contractile force and glycogenolysis are usually classified as beta receptors, but such a classification is not definitely established. Therefore, an attempt was made in the present study to characterize the nature of the receptors responsible for increases in cardiac contractile force and glycogenolysis induced by various adrenergic amines, The effects of rapid injections of phenylephrine and norepinephrine (amines which excite only alpha receptors) and epipinephrine (amine which excites alpha and beta receptors) and isoproterenol (amine which excites beta receptors) were measured in dogs, on blood pressure and cardiac contractile force before and after phenoxybenzamine or Hydergine (alpha receptor blocking agents) or dichloroisoproterenol (beta receptor blocking agent) or d-tubocurarine (neuromuscular blocking agent). Cardiac contractile force was measured by a strain gauge sutured on the ventricule wall and average blood pressure was measured from the carotid artery. Phenoxybenzamine did not alter the cardiac contractile effects of any of the amines and d-tubocurarine did not alter the cardiovascular responses of any of the amines. Hydergine inhibited the cardiac contractile force response of phenylephrine and norepinephrine, and dichloroisoproterenol inhibited this response of all four of the amines. Phenoxybenzamine and Hydergine blocked the blood pressure responses of all of the amines except isoproterenol. Dichloroisoproterenol blocked the blood pressure response of only isoproterenol. These results show that both alpha or beta adrenergic amines can increase cardiac contractile force and that dichloroisoproterenol can inhibit this response of all four of the amines, while Hydergine can produce a selective blockade with two of the amines. This led to the conclusion that the cardiac receptor responsible for adrenergically induced increases in cardiac contractile force can be excited by either alpha or beta adrenergic amines and it is therefore suggested that this receptor be reclassified as an undifferentiated receptor. The glycogenolytic effects of adrenergic amines, in dogs, were determined by measuring the elevation of serum levels of of glucose and lactic acid produced by slow infusions of the four adrenergic amines before and after blocking agents. Serum levels of glucose and lactic acid were significantly elevated by epinephrine and isoproterenol, but not by phenylephrine or norepinephrine. Dichloroisoproterenol or Hydergine significantly reduced the hyperglycemic and hyperlactic acidemic responses of epinephrine, but d-tubocurarine or phenoxybenzamine did not. The hyperglycemic and hyperlactic acidemic responses of isoproterenol were inhibited by d-tubocurarine or dichloroisoproterenol, but not by Hydergine. These results show that only adrenergic amines which could excite beta receptors (epinephrine and isoproterenol) elevated serum levels of glucose and lactic acid, and that Hydergine, an alpha blocking agent, inhibited the effects of epinephrine, but dichloroisoproterenol inhibited the effects of both epinephrine and isoproterenol. These results suggest that adrenergically induced glycogenolysis, in the dog, occurs by excitation of a receptor that is closely related to the beta receptor, but cannot be categorically identified as a beta receptor. Isoproterenol stimulated glycogenolysis, as determined by glucose uptake and lactic acid production, in isolated liver and skeletal muscle tissues, from dog. Dichloroisoproterenol inhibited these effects of isoproterenol in only skeletal muscle. These results indicate that isoproterenol is an effective glycogenolytic agent in both types of tissues and that d-tubocurarine can separate isoproterenol induced glycogenolysis in liver and skeletal muscle by selectively inhibiting the amine's effect in skeletal muscle. Phenoxybenzamine, by itself, significantly elevated serum glucose levels in intact dogs. Since this effect was not observed in adrenalectomized animals, it was concluded that the hyperglycemia induced by phenoxybenzamine occurred from a release of epinephrine from the adrenal glands. The present study has been concerned with the proposal that all adrenergically induced responses occur due to the excitation of either of two receptors. It seems more likely that each particular physiological or biochemical response induced by adrenergic amines has its own particular receptor and that categorically identifying adrenergic receptors as either alpha or beta is an over-simplification of what is an extremely complex system.
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