Adrenaline muscle

Adrenaline (muscle) or glucagon (liver) bind to receptor and adenylate cyclase Is stimulated to make cyclic AMP... 

M.p. 103°C. Noradrenaline is released in the adrenal medulla with adrenaline, and also at the sympathetic nerve endings. Its release from a nerve fibre is followed by binding to a receptor molecule on the next nerve or muscle fibre, probably causing a change in the electrical charge of the receptor-cell membrane. Biosynthetically it normally serves as a precursor for adrenaline. 

Epinephrine (adrenalin) 0.1 to 0.5 mg may be given by subcutaneous or intramuscular injection. Hypotension and shock may be treated with fluids and vasopressors. Bronchodilators are given to relax the smooth muscles of the bronchial tubes. Antihistamines may be given to block the effects of histamine. 

Bulbring E, T omita T 1969 Effect of calcium, barium and manganese on the action of adrenaline in the smooth muscle of the guinea-pig taenia coli. Proc R Soc Lond B Biol Sci 172 121-136 Marchant JS, Taylor CW 1998 Rapid activation and partial inactivation of inositol trisphosphate receptors by inositol trisphosphate. Biochemistry 37 11524-11533 Somlyo AV, Horiuti K, Trentham DR, Kitazawa T, Somlyo AP 1992 Kinetics of Ca2+ release and contraction induced by photolysis of caged D-myo-inositol 1,4,5-trisphosphate in smooth muscle the effects of heparin, procaine, and adenine nucleotides. J Biol Chem 267 22316-22322... 

Most hormones are produced naturally in the body (e.g. adrenaline (II) is formed in the adrenal glands). From there, the hormone enters the bloodstream and is consumed chemically (a physiologist would say metabolized ) at the relevant sites in the body - in fact, adrenaline accumulates and is then broken down chemically in the muscles and lungs. Adrenaline is generated in equal amounts in men and women,... 

Reversible phosphorylation is the main control mechanism of liver phosphorylase allosteric effects being much less pronounced. This is in contrast with muscle phosphorylase, which is also controlled by phosphorylation, stimulated by an adrenaline-... 

Furthermore, as well as CaCM-induced phosphorylation, MLCK is also subject to control via a cAMP-dependent protein kinase, PKA. Phosphorylated MLCK binds CaCM only weakly, thus contraction is impaired. This explains the relaxation of smooth muscle when challenged with adrenaline (epinephrine), a hormone whose receptor is functionally linked with adenylyl cyclase (AC), the enzyme that generates cAMP from ATP. 

The situation in muscle is different. Here the responsible hormones are adrenaline (epinephrine), and noradrenaline (norepinephrine) ... 

Many years later. Sir James Black identified fhe beta adrenergic receptor in heart muscle. Adrenaline increases heart rate by activating the beta adrenergic receptor in this organ. Within a decade. Black and his colleagues had synthesized a molecule known as propranolol, marketed as Inderal. 

This is not the end of the story about beta blockers. Subsequent research demonstrated that there are two subclasses of beta receptors, termed beta-1 and beta-2. Both are activated by adrenaline. Both are blocked by propranolol. Beta-1 receptors are found mostly in heart muscle but not much in the lungs, whereas beta-2 receptors are found mostly in the lungs but not much in the heart. These facts provided the opportunity for better drugs. Here is the argument. 

Hormones can modify the concentration of precursors, particularly the lipolytic hormones (growth hormone, glucagon, adrenaline) and cortisol. The lipolytic hormones stimulate lipolysis in adipose tissue so that they increase glycerol release and the glycerol is then available for gluconeogenesis. Cortisol increases protein degradation in muscle, which increases the release of amino acids (especially glutamine and alanine) from muscle (Chapter 18). 

The function of adrenaline is to mobilise all fuels that can be used by muscle to provide ATP to support physical activity in response to stress (i.e. fight or flight response). And to increase sensitivity of regulation of enzymes involved in control of the rate of processes that generate ATP. The biochemical effects in the heart increase cardiac output, in preparation for fight or flight . 

These compounds competitively inhibit phosphodiesterase, resulting in an increase in cyclic AMP (see Box 14.3) and subsequent release of adrenaline. This leads to the major effects a stimulation of the central nervous system (CNS), a relaxation of bronchial smooth muscle, and induction of diuresis. These effects vary in the three compounds. Caffeine is the best CNS stimulant, and has weak diuretic action. Theobromine has little stimulant action, but has more diuretic activity and also muscle relaxant properties. Theophylline also has low stimulant action and is an effective diuretic, but it relaxes smooth muscle better than caffeine or theobromine. 

Skeletal muscle glycogen delivers glucose primarily as a response to contractile stress. Regulation occurs through both modification of the enzyme phosphorylase, primarily by the action of epinephrine-adrenaline and allosteric regulation of phosphorylase related to a demand for ATP. 

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