α-2 G protein-coupled receptor bound (Jie 2) adrenergic receptor and G-protein hetero king (or adrenergic receptor) is a (GPCR). It consists of sub-type three high homology, including 2C-adrenergic Jie Jie 2A-, and 2B-Jie. Several species of non-human Jie 2 in the peripheral nervous system and norepinephrine (noradrenaline) and epinephrine (adrenaline) center – expressing four Jie 2D-adrenergic receptor as well. Catecholamines as a signal of adrenergic receptor.

2 Jie – the adrenergic receptor, classically, to inhibit vascular prejunctional terminal release of norepinephrine (noradrenaline), it is located in the form of negative feedback. It multimeric Jie 1 it – so as to be located with the adrenergic receptors are located in vascular smooth muscle cells on such found  in veins or arteries skin in some vessels. Jie 2 – adrenergic receptor Connect the epinephrine with high affinity slightly, is associated with the norepinephrine emitted epinephrine release and sympathetic postganglionic fibers from (adrenaline) by the adrenal cortex [edit]. 1 Jie it – it not only has some common features in common with the adrenergic receptor, has the effect of certain of its own. Jie 2 – In general, agonists of adrenergic receptor (activator) is used in veterinary anesthetic that affect sedation, muscle relaxation and analgesia by which they act on the central nervous system (CNS).

Of inhibitory protein G α subunit – is separated from the protein G, Wang is associated with adenylate cyclase (also known as adenylate cyclase or adenylate cyclase) to. Resulting in a decrease in cAMP produced from ATP, which leads to inactivation of adenylyl cyclase. This leads to a reduction of intracellular cAMP. For example, protein kinases, can not be such that it can not be phosphorylated by PKA, proteins such as phosphorylase kinase activated by cAMP of. Specifically, phosphorylase kinase is responsible for the phosphorylation and activation of enzymes necessary to breakdown glycogen phosphorylase, the more glycogen. So at this point, the downstream effect of inactivation of adenylate cyclase, reduces the degradation of glycogen.
Relaxation of gastrointestinal motility is a presynaptic inhibition to suppress the release of neurotransmitter from further homotropic effect.

classic α2-adrenergic receptor, to inhibit vascular prejunctional terminal release of norepinephrine (noradrenaline), it is located in the form of negative feedback. It to be located with the richer α1 adrenergic receptors, which are arranged in vascular smooth muscle cells on such found in veins or arteries skin in some vessels. norepinephrine that connects epinephrine affinity slightly higher α2-adrenergic receptor, was released epinephrine release and sympathetic postganglionic fibers from (adrenaline) by the adrenal cortex is associated with it is [edit]. Not only have some common features in common with the α1-adrenergic receptor, this has the effect of certain of itself. agonists of α2-adrenergic receptor (activator) is used in veterinary anesthetic that affect sedation, muscle relaxation and analgesia by generally they act on the central nervous system.

Of inhibitory protein G α subunit – is separated from the protein G, Wang is associated with adenylate cyclase (also known as adenylate cyclase or adenylate cyclase) to. Resulting in a decrease in cAMP produced from ATP, which leads to inactivation of adenylyl cyclase. This leads to a reduction of intracellular cAMP. For example, protein kinases, can not be such that it can not be phosphorylated by PKA, proteins such as phosphorylase kinase activated by cAMP of. Specifically, phosphorylase kinase is responsible for the phosphorylation and activation of enzymes necessary to breakdown glycogen phosphorylase, the more glycogen. So at this point, the downstream effect of inactivation of adenylate cyclase, reduces the degradation of glycogen. Relaxation of gastrointestinal motility is a presynaptic inhibition to suppress the release of neurotransmitter from further homotropic effect.

A2-receptor is an important regulator of the cardiovascular system. A2-agonist intravenous induces a biphasic response of blood pressure to phase a temporary high blood pressure blood pressure is below the reference value. After Oral administration of A2 agonist is used to treat hypertension in hypertensive patients hypotensive effect is dominant. In mice, the phase of the pressure responding is mediated by the receptor subtypes A2-two different. Low blood pressure long-term while mediated by A2A receptors, A2B receptor is responsible for the high blood pressure of the initial phase. Therefore, A2A receptor is a therapeutic target for antihypertensive drugs subtype-selective. Some data, A2a receptor receptor also indicates that it may be involved in mediating vasoconstriction by A2 agonist in mice. Rather than A2C and A2B deficient mice and wild-type mice, bolus injection of noradrenaline caused transient hypertension in mice lacking the A2A receptor. I shows the structural similarity with dexmedetomidine of specifica2-adrenergic receptor agonists as imidazoline type in the intravenous anesthetic etomidate. In vivo, it indicates that the hypnotic effect of etomidate does not require the A2A receptor subtype in mice, higher intraperitoneal injection of etomidate in A2A receptor-deficient mice and wild-type and recovery time loss of righting reflex. Instead of blood pressure in wild-type mice, intravenous injection of etomidate is, due to a temporary increase in mice lacking the A2B receptor. Etomidate is outside the body, A2B-A2C more A2A receptor and high efficiency – to inhibit the binding of radiolabeled A2 antagonist in A2 receptor subtypes and recombinant receptor. In addition, ERK1 / 2 phosphorylation etomidate of extracellular signal-related kinase in a2Breceptors expression is increased rapidly in HEK293 cells. These results, indicating that act as agonists of the A2-adrenergic receptors occurs in vivo as an increase etomidate, the main blood a2Breceptor mediated. May contribute to the stability of the cardiovascular system of a patient after induction of anesthesia with etomidate This effect of etomidate.

α2-adrenergic receptors mediate the various effects of the biology of norepinephrine and epinephrine of endogenous catecholamines. α2-adrenergic receptors, α2A, α2B, α2C, sub-three different types have been identified from various species. for subtype-selective ligands are missing, there are many unclear points until recently biological functions of specific receptor subtypes of these. mouse gene targets carrying a deletion in the gene encoding the α2-receptor subtypes have different add significant new insights into the physiological significance of diversity adrenergic receptors. It has emerged different strategies two to regulate adrenergic signal transduction. For example, it is controlled by the α2-receptor subtypes two opposing, increased α2B subtypes, blood pressure, while sympathetic outflow, several biological functions reduces blood pressure α2A-receptors. Are regulated by α2-receptor subtypes synergistic biological functions of the other. The feedback loop inhibitory presynaptic to regulate the release of neurotransmitters from nerve adrenaline firm, it requires two receptor subtypes, the α2C and α2A. Similarly, sensitivity to pain is controlled in any of three α2-receptor subtypes several levels. Research to improve the understanding of the importance of the receptor protein specific function of α2-subtype closely related to significantly further, will highlight new therapeutic strategies for the development of subtype-selective drugs.