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Adrenaline receptors

Fig. 2. An adrenaline molecule (1) binds to its binding site on the extracellular site of an adrenaline receptor (2). Thereby, the exchange of GDP by GTP in the Ga subunit of a hetero-trimeric G protein (3) is induced, followed by the dissociation of the Ga and Gpr subunits. G now binds and stimulates its effector adenylate cyclase (4), which produces cyclic AMP (5) from ATP (6). This second messenger starts a cascade of enzymatic reactions, which alter the behavior of the cell via several phosphorylation steps... [Pg.64]

An example of an antagonist medicine Is propranolol, which Is used to treat high blood pressure. It too acts by binding to adrenaline receptor sites, but It does not trigger a response. The propranolol therefore blocks the receptor sites and prevents the action of the body s natural compound. [Pg.80]

The best investigated is the desensitization of the adrenaline receptor type P2 and of rhodopsin. Rhodopsin has the function of a light receptor in the process of vision, ft receives light signals and conducts them to the relevant G-protein, transducin. The key reaction in desensitization of both systems is the phosphorylation of the receptor at the cytoplasmic side by specific protein kinases. [Pg.184]

Members of the Gs subfamily are activated by hormone receptors, by odor receptors and by taste receptors. Gg-proteins mediate, e.g., signal transmission by adrenaline receptors of type P and by glucagon receptors. During perception of taste, the taste receptors are activated, which then pass the signal on via the olfactory G-protein Gou. Perception of sweet taste is also mediated via a Gs-protein. Transmission of the... [Pg.193]

Adrenaline—Receptors. 2. Pharmacogenetics. I. Perez, Dianne M. II.Series. QP364.7.A375 2005 612.4 5—dc22... [Pg.409]

The only exception to this are the nerves which go directly to the adrenal medulla. The neurotransmitter released here is noradrenaline and this stimulates the adrenal medulla to release the hormone adrenaline. This hormone then circulates in the blood system and interacts with noradrenaline receptors as well as other adrenaline receptors not directly fed with nerves. [Pg.208]

The best investigated is the desensitization of the adrenaline receptor type pi and of rhodopsin. Rhodopsin has the function of a light receptor in the process of vision. It... [Pg.192]

The major mechanism for the homologous desensitization of agonist-bound 7-helix transmembrane receptors consists of a two-step process in which the agonist-bound receptor is phosphorylated by a GRK and then binds an arrestin protein which interrupts signaling to the G protein. Well-characterized GRKs (review Pitcher et al., 1998) are those for rhodopsin, rhodopsin kinase and the fil adrenaline receptor, the -adrenergic receptor kinase (/ ARK).The GRKs are protein kinases thatare... [Pg.194]

Hydropathy plot. The hydropathic index is plotted on they axis, with hydrophobic domains at the top and hydrophilic domains at the bottom. The x axis shows the amino-acid residue number from the amino to the carboxy terminus. The protein shown is a 7-transmembrane receptor (the serotonin receptor), analogous to the epinephrine (adrenalin) receptor. The approximate positions of the seven transmembrane segments are indicated by the purple bars. (Original plot graciously provided by... [Pg.139]

We already saw in Topic 41 how the cascade effect leads to a massive and rapid amplification of the initial signal resulting from adrenaline binding to its receptor. We now know also that the subtleties of different responses to adrenaline are in part brought about by the existence of more than one class of adrenaline receptor. There are so-called a- and 3-adrenergic receptors, and some commonly used dmgs are specifically intended to damp down the response to the hormone thus, / blockers are widely used in the control of hypertension or high blood pressure. [Pg.241]

There are two types of cell membrane receptor (a and jS) for adrenaline. -Receptors which are inhibited by -blockers such as propanolol are the main type of receptor in muscle, heart, adipose tissue and many other tissues. They interact with and activate adenylate cyclase in the cell membrane so that the effect of adrenaline on muscle or adipose tissue is to increase the concentration of cAMP in the cell and thus to activate protein kinase. Stimulation of glycogen breakdown by adrenaline in muscle is then mediated by a cascade mechanism similar to that involved in the stimulation of glycogenolysis in liver by glucagon (page 353). Breakdown of triglycerides in adipose tissue, as in liver, occurs as a result of activation of triglyceride lipase by phosphorylation. [Pg.355]

In rat liver, 3-blockers do not completely abolish the response to adrenaline due to the presence of the second type of adrenaline receptor, the a-receptor. a-Receptors are characterized by their sensitivity to phenoxybenzamine. The binding of adrenaline to a-receptors does not increase the cAMP concentration, but nevertheless it stimulates glycogen breakdown by causing an increase in the cytosolic concentration of free Ca ions. This calcium is initially released from the endoplasmic reticulum. The non-phosphorylated form of phos-phorylase kinase is activated by calcium ions so that an increase in cytoplasmic calcium concentration increases the activity of phosphorylase kinase, and hence glycogen breakdown, independently of a change in cAMP. Thus Ca ions act as a second messenger for the a-receptor-mediated effects of adrenaline. In most tissues there are more than a receptors but the ratio varies with both the tissue and the species of animal and also with age. The significance of such variation is not understood. [Pg.355]

Figure 6.11 Interaction of adrenaline with the a-helices in the P2-adrenaline receptor which lead to a conformational change and activation of the coupled G-protein. Figure 6.11 Interaction of adrenaline with the a-helices in the P2-adrenaline receptor which lead to a conformational change and activation of the coupled G-protein.
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. [Pg.282]

The term chiral recognition refers to a process m which some chiral receptor or reagent interacts selectively with one of the enantiomers of a chiral molecule Very high levels of chiral recognition are common m biological processes (—) Nicotine for exam pie IS much more toxic than (+) nicotine and (+) adrenaline is more active than (—) adrenaline m constricting blood vessels (—) Thyroxine an ammo acid of the thyroid gland that speeds up metabolism is one of the most widely used of all prescription... [Pg.295]

Adrenaline (epinephrine) is a catecholamine, which is released as a neurotransmitter from neurons in the central nervous system and as a hormone from chromaffin cells of the adrenal gland. Adrenaline is required for increased metabolic and cardiovascular demand during stress. Its cellular actions are mediated via plasma membrane bound G-protein-coupled receptors. [Pg.42]

The biological actions of adrenaline and noradrenaline are mediated via nine different G-protein-coupled receptors, which are located in the plasma membrane of neuronal and nonneuronal target cells. These recqrtors are divided into two different groups, a-adrenergic receptors and P-adrenergic recqrtors (see P-adrenergic system). [Pg.43]

Non-selective (3-adrenergic receptor agonists, particularly adrenaline (qunephrine), are used in cardiovascular... [Pg.48]

Antidepressants are used in the treatment of neuropathic pain and headache. They include the classic tricyclic compounds and are divided into nonselective nor-adrenaline/5-HT reuptake inhibitors (e.g., amitriptyline, imipramine, clomipramine, venlafaxine), preferential noradrenaline reuptake inhibitors (e.g., desipramine, nortriptyline) and selective 5-HT reuptake inhibitors (e.g., citalopram, paroxetine, fluoxetine). The reuptake block leads to a stimulation of endogenous monoaminer-gic pain inhibition in the spinal cord and brain. In addition, tricyclics have NMDA receptor antagonist, endogenous opioid enhancing, Na+ channel blocking, and K+ channel opening effects which can suppress peripheral and central sensitization. Block of cardiac ion channels by tricyclics can lead to life-threatening arrhythmias. The selective 5-HT transporter inhibitors have a different side effect profile and are safer in cases of overdose [3]. [Pg.77]

Hi-receptors in the adrenal medulla stimulates the release of the two catecholamines noradrenaline and adrenaline as well as enkephalins. In the heart, histamine produces negative inotropic effects via Hr receptor stimulation, but these are normally masked by the positive effects of H2-receptor stimulation on heart rate and force of contraction. Histamine Hi-receptors are widely distributed in human brain and highest densities are found in neocortex, hippocampus, nucleus accumbens, thalamus and posterior hypothalamus where they predominantly excite neuronal activity. Histamine Hrreceptor stimulation can also activate peripheral sensory nerve endings leading to itching and a surrounding vasodilatation ( flare ) due to an axonal reflex and the consequent release of peptide neurotransmitters from collateral nerve endings. [Pg.589]

Examples of sympathomimetic bronchodilators include albuterol (Ventolin), epinephrine (Adrenalin), salme-terol (Serevent), and terbutaline (Brethine). Many of the sympathomimetics used as bronchodilators have die subclassification of beta-2 ((32) receptor agonists (eg, albuterol, salmeterol, and terbutaline). Additional information concerning the various sympathomimetic dragp is given in the Summary Drug Table Bronchodilators. [Pg.334]

Caffeine binds to adenosine receptors in the brain, preventing adenosine from inducing sleep or opening blood vessels. Caffeine also increases levels of dopamine, the neurotransmitter associated with pleasure. This is the chemical mechanism for addiction. The response to adenosine competition causes increased adrenaline flow. [Pg.158]

Ephedrine enhances the release of the hormone norepinephrine in the body, and also binds to the same receptors as that hormone, causing excess calories to be converted to heat instead of being stored as fat. It also raises blood pressure. Epinephrine and norepinephrine are also known as adrenaline and noradrenaline. Ephedrine thus acts to stimulate an adrenaline rush. [Pg.160]

If a series of related chemicals, say noradrenaline, adrenaline, methyladrenaline and isoprenaline, are studied on a range of test responses (e.g. blood pressure, heart rate, pupil size, intestinal motility, etc.) and retain exactly the same order of potency in each test system, then it is likely that there is only one type of receptor for all four of these catecholamines. On the other hand, if, as Ahlquist first found in the 1940s, these compounds give a distinct order of potency in some of the tests, but the reverse (or just a different) order in others, then there must be more than one type of receptor for these agonists. [Pg.58]

Heterologous desensitisation refers to the desensitisation of the response to one agonist by the application of a different agonist. For example, desensitisation of a response to adrenaline by application of 5-HT is mediated by protein kinase A or protein kinase C because these kinases can phosphorylate receptors which are not occupied by agonist. Phosphorylation disrupts the receptor-G-protein interaction and induces the binding of specific proteins, arrestins which enhance receptors internalisation via clathrin-coated pits. Thus desensitisation of G-protein-coupled receptors results in a decrease in the number of functional receptors on the cell surface. [Pg.74]


See other pages where Adrenaline receptors is mentioned: [Pg.304]    [Pg.227]    [Pg.129]    [Pg.185]    [Pg.49]    [Pg.131]    [Pg.267]    [Pg.267]    [Pg.304]    [Pg.227]    [Pg.129]    [Pg.185]    [Pg.49]    [Pg.131]    [Pg.267]    [Pg.267]    [Pg.189]    [Pg.760]    [Pg.42]    [Pg.43]    [Pg.44]    [Pg.45]    [Pg.46]    [Pg.538]    [Pg.562]    [Pg.563]    [Pg.1241]    [Pg.173]    [Pg.180]    [Pg.197]   


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