P-Adrenoreceptors

K, Values for Inhibition of 125l-lodohydroxybenzylpindolol Binding to P-Adrenoreceptors in Turkey Erythrocyte... 

Two main subtypes of P adrenoreceptors, P and P2, have been identified in the periphery and in the CNS (Minneman et ak, 1979 Palacios and Kuhar, 1980). Both are located at postsynaptic terminals and have been cloned. In the periphery, P receptors are located in myocardial tissue, and P2 receptors are located in pulmonary bronchi and bronchioli, as well as in some blood vessels. P Adrenoceptors are the major subtype throughout the brain, except for the cerebellum, where P2 receptors are predominant. Areas that contain high concentrations of P adrenoceptors include the superfi-... 

The three P-adrenoreceptor subtypes have varying localizations and functional properties. The brain contains both Pj and Pj receptors the density of Pj receptors varies in different brain areas to a much greater extent than does that of Pj receptors. Pj receptors predominate in the cerebral cortex Pj receptors are more common in the cerebellum. Likewise, there is a coexistence of Pj and Pj receptors in the heart, with both receptor subtypes being coupled to the electrophysiological effects of catecholamines upon the myocardium. Pj receptors tend to predominate in the lung. 

There are two principal groups of receptors for epinephrine and NE, so-called adrenoreceptors, which are divided into a- and P-adrenoreceptors. a-adrenoreceptors are subdivided into oti and oc2, whereas the P-adrenoreceptors into Pi, P2 and P3. All the adrenoreceptors are coupled to different G protein subtypes. More specifically, oci-adrenoreceptors is coupled to Gq, a2-adrenoreceptors to Gi, and all the P-adrenoreceptors to Gs. Briefly, activation of Gs and G, stimulates and reduces the production of cAMP, respectively. cAMP functions as a second messenger that can activate the protein kinase A (PKA), which in turn, can transfer the signals to the nucleus. 

Activation of P-ARs by isoproterenol enhances the expression of COX-2 and iNOS in a human urothelial cell line (Harmon et al., 2005). Since activation of P-adrenoreceptors leads to an increase in cAMP and a subsequent PKA activation, the authors investigated whether the increase in these inflammatory markers was due to activation of this pathway. However, this increase is independent of PKA, since PKA inhibitors did not reduce the augmentation in COX-2 and iNOS expression. 

The production of reactive oxygen species (ROS) is associated with cytotoxicity. In the CNS, microglia are an important source of these species. In neonatal hamster microglia stimulated with phorbol myristate acetate, a PKC activator, isoproterenol reduces the production of superoxide anion and this decrease was blocked by a P-adrenoreceptors antagonist (Colton and Chernyshev, 1996). 

As described previously, activation of P-adrenoreceptors leads to the accumulation of cAMP and activation of PKA. This suggests that the effects of NE and other P-adrenoreceptors agonists are mainly mediated via activation of PKA. This is supported by the fact, that the effects of NE is mimicked by P agonists or by compounds that increase... 

Depletion of NE may cause deterioration of AD pathology in different animal models (Heneka et al., 2002) (Kalinin et al., 2007) (Heneka et al., 2006). Animals who received amyloid-P injections into the cortex and chronic DSP4 to induce LC neuronal cell death led to induction of inflammatory changes within the CNS of AD animals. An increase in iNOS, IL-ip, and IL-6 expression compared to control animals was measured in the brain. However, COX-2 expression was transiently reduced in the AD animals. Co-injection with NE or the P-adrenoreceptors agonist isoproterenol attenuated the inflammatory response in the amyloid-P and DSP4 injected animals. The inflammatory response caused by NE depletion seems to be due to reduced levels of NF-kB inhibitory IkB proteins and of heat shock protein 70 (Heneka et al., 2003). 

Radiolabelled cis-flupenthixol can be used as a ligand specific for the dopamine receptor linked to adenylyl cyclase in the rat striatum (64). Its affinity for the dopamine receptor in the anterior pituitary has not been measured. (Previously (65) the two categories of dopamine receptors were designated as a-dopaminergic" and P-dopaminergic. This has led to confusion with the a and p adrenoreceptors. The new designations should prevent further confusion.)... 

Tab. 4.16 Structures of P-adrenoreceptor-blocking agents. (Reprinted from Tab. 1 of ref. 54 with permission from the American Chemical Society)...

Correct answer = A. A bidirectional block can decrease arrhythmias caused by reentry. All antiarrhythmic drugs exert some negative inotropic effect and decrease cardiac output. The i side effects of this group of drugs are serious and include arrhythmias that can lead to sudden death. Some antiarrhythmic drugs affect K+ or Ca++ channels, or p adrenoreceptors. 

P-Adrenoreceptor blockers Antidepressants Neuroleptics An tiarrhy thmic drugs Miscellaneous... 

Adrenaline is only capable of producing platelet aggregation in the presence of other platelet agonists (Steen cr of, 1993 Lanza et al, 1988), and is therefore not a tme agonist. Platelets have stimulatory Uj adrenoreceptors and inhibitory p adrenoreceptors, but the adrenoreceptors predcnnhiates. The adrenoreceptor is coupled via G proteins to adenylyl cyclase, while ffie a, adrenoreceptor (present in about 30 %) has Ireen proposed to be... 

R)-salbutamol P-adrenoreceptor blocker for bronchial asthma Sultanol... 

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