Muscles glycogenolysis

P-Adrenoceptors have been subdivided into P - and P2-adrenoceptors. A third subset called nontypical P-adrenoceptors or P -adrenoceptors have been described but are stiU the subject of debate. In terms of the interactions with various subsets of P-adrenoceptors, some antagonists are nonselective in that they antagonize the effects of activation of both P - and P2-adrenoceptors, whereas others are selective for either P - or P2-adrenoceptors. P - and P2-adrenoceptors coexist in almost all organs but generally, one type predominates. The focus herein is on the clinically relevant P -adrenoceptor-mediated effects on heart and on P2-adrenoceptor-mediated effects on smooth muscles of blood vessels and bronchioles, the insulin-secreting tissue of the pancreas, and skeletal muscle glycogenolysis for side effects profile (36). 

These cascades of reactions need time in the range of seconds synaptic transmission through GPCRs is slow. All further postsynaptic changes depend on the type of postsynaptic cell. For example activation of 32-adrenoceptors causes in the heart an increase of the rate and force of contraction in skeletal muscle glycogenolysis and tremor in smooth muscle relaxation in bronchial glands secretion and in sympathetic nerve terminals an increase in transmitter release. 

Spriet, L.L., Soderlund, K., Bergstrom, M., Hultman, E. (1987b). Skeletal muscle glycogenolysis, glycolysis, and pH during electrical stimulation in men. J. Appl. Physiol. 62, 616-621. 

Isoproterenol is the most potent stimulant of skeletal muscle glycogenolysis, followed by epinephrine and norepinephrine. (3z-Adrenoceptors mediate muscle glycogenolysis. Stimulation of skeletal muscle glycogenolysis will raise blood lactic acid levels rather than blood glucose levels because skeletal muscle lacks the enzyme glucose-6-phosphatase, which catalyzes the conversion of glucose-6-phosphate to glucose. 

K. C. Vinnakota, M. L. Kemp, and M. J. Kushmerick. Dynamics of muscle glycogenolysis modeled with pH time-course computation and pH-dependent reaction equilibria and enzyme kinetics. Biophys. J., 91 1264-1287, 2006. 

Other actions—lungs (bronchodilation), liver (glycogenolysis stimulated—T serum glucose), pancreas (-1 insulin release because a2 predominates), muscle (glycogenolysis), fat (t mobilization and use of fat). 

Laurent D, Peterson KF, Russell RR, et al. Effect of epinephrine on muscle glycogenolysis and insulin-stimulated muscle glycogen synthesis in humans. Am J Physiol 1998 274 E130-E138. 

F. 47.9. Activation of muscle glycogenolysis and glycolysis by AMP. As muscle contracts, ATP is converted to ADP and Pj. In the adenylate kinase reaction, two ADP react to form ATP and AMP. The ATP is used for contraction. As AMP accumulates, it activates glycogenolysis and glycolysis. 

An increase in glucagon concentration in the blood, such as occurs during starvation, does not provide a strong stimulus for muscle glycogenolysis but the concomitant hypoinsulinemia inhibits new glycogen synthesis. Therefore, every time muscle glycogen is used in muscle contraction, it is not immediately replaced so the concentration of glycogen in muscles steadily declines over the first few days of starvation. 

The existence of two different adrenergic receptors was first suggested by Ahlquist (1948) Those responses evoked most readily by noradrenaline (norepinephrine), less by adrenaline 7.43), still less by isoprenaline 12.44) and least by A -/-butylnorepinephrine are credited to a-receptors those for which this sequence runs in the reverse direction are credited to jS-receptors. Typical a-responses are constriction of blood-vessels, stimulation of the uterus, relaxation of the intestine. Typical jS-responses are dilatation of blood-vessels, relaxation of the uterus, stimulation of muscle glycogenolysis, production of tachycardia (Levy and Ahlquist, 1961). 

Considerable attention has been given to the activation of adenylcyclase via the action of this enzyme ATP gives rise to cyclic 3, 5 -AMP. According to Sutherland and Rail (1960) this is of fundamental importance for a number of adrenomimetic reactions (positive inotropic action, relaxation of smooth muscle, glycogenolysis, and possibly also lipolysis). Many of the 3, 5 -AMP effects can be mediated via the activation of phosphorylase evoked by 3, 5 -AMP. 

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