Adrenergic receptors modulators

Abdulla D, Renton KW. 2005. Beta-adrenergic receptor modulation of the LPS-mediated depression in CYPIA activity in astrocytes. Biochem Pharmacol 69 741-750. 

Xiang Y, Devic E, Kobilka B. The PDZ binding motif of the Pj adrenergic receptor modulates receptor trafficking and signaling in cardiac myocytes. J Biol Chem 2002 277 33,783-33,790. 

Chu CP, Kunitake T, Kato K, et al. The a1D-adrenergic receptor modulates cardiovascular and drinking responses to central salt loading in mice. Neurosci Lett 2004 356 33-36. 

Marx SO, Kurokawa J, Reiken S, Motoike H, D Armiento J, et al. 2002. Requirement of a macromolecular signaling complex for beta adrenergic receptor modulation of the KCNQ1-KCNE1 potassium channel. Science 295 496-99... 

Adrenergic receptor 2 Amino acid variants appear to be associated with receptor function and agonist induced down regulation. Some variants may predispose to some types of asthma and modulate action of (3-2-adrenergic drugs. 

Danner S, Lohse MJ (1999) Regulation of p-adrenergic receptor responsiveness modulation of receptor gene expression. Rev Physiol Biochem Pharmacol 136 183- 223... 

McGraw DW, Mihlbachler KA, Schwarb MR, et al. Airway smooth muscle prostaglandin-EPl receptors directly modulate beta2-adrenergic receptors within a unique heterodimeric complex. J Clin Invest 2006 116 1400-1409. 

Wilson AL, Womble SW, Prakash C, Cragoe EJ Jr, Blair IA, Limbird LE. Novel amiloride analog allosterically modulates the alpha 2-adrenergic receptor but does not inhibit Na+ /H exchange. Mol Pharmacol 1992 42 175-179. 

Because cardiac muscle is myogenic, nervous stimulation is not necessary to elicit the heart beat. However, the heart rate is modulated by input from the autonomic nervous system. The sympathetic and parasympathetic systems innervate the SA node. Sympathetic stimulation causes an increase in heart rate or an increased number of beats/min. Norepinephrine, which stimulates ( -adrenergic receptors, increases the rate of pacemaker depolarization by increasing the permeability to Na+ and Ca++ ions. If the heart beat is generated more rapidly, then the result is more beats per minute. 

Ramer-Quinn, D.S., Baker, R.A., and Sanders, V.M., Activated T helper 1 and T helper 2 cells differentially express the P-2-adrenergic receptor A mechanism for selective modulation of T helper 1 cell cytokine production, J. Immunol., 159, 4857,1997. 

Sallinen J, Haapalinna A, Viitamaa T, Kobilka BK, Scheinin M (1998) Adrenergic Ojc-receptors modulate the acoustic startle reflex, prepulse inhibition, and aggression in mice. J. Neuroscience 18 3035-3042 Sallinen J, Haapalinna A, Viitamaa T, Kobilka BK, Scheinin M (1998) D-amphetamine and L-5-hydroxytryptophan-induced behaviours in mice with genetically-altered expression of the a2c-adrenergic receptor subtype. Neuroscience 86 959-965... 

However, the posterior cortical areas may be aided by P and aj-adrenergic receptor stimulation and by dopaminergic stimulation, and thus stimulants may promote the attentional processing abilities of these areas. It is important to note that there has been no direct animal research on catecholamine modulation of posterior cortical function thus this idea remains speculative. 

The clinical effects of a2-adrenergic receptor agonists may also derive from the action of postsynaptic tt2A adrenoceptors, which modulate the excitability of target neurons in select noradrenergic terminal fields in... 

As mentioned in section 4.3.3, there are two kinds of a receptor in brain and peripheral tissues. The crucial experiments have shown that brain tissue prelabeled with pH]NE will release neurotransmitter upon electrical stimulation or exposure to K+. The release is reduced by the a agonist clonidine (4.42) and stimulated by the a antagonist yohimbine (4.43). Since the adrenoreceptor involved in this latter experiment plays a vital role in modulating neurotransmitter release, it must be presynaptic and located on the nerve-ending membrane. A similar selectivity has also been shown by peripheral tissues (heart, uterus), leading to the distinction of aj (postsynaptic) and (presynaptic) adrenergic receptors. There are also presynaptic [3 receptors, which show a feedback regulation opposite to that of the ttj receptors that is, their excitation by a neurotransmitter increases NE release. 

The interaction of the Pycomplex with G-protein coupled receptor kinases (see 5.3.4, P-adrenergic receptor kinase, PARK) appears to be of special regulatory importance. The function of the Py-complex in this system is shown in Fig. 5.9. The Py-complex binds specifically to the PARK and translocates this to the cell membrane. The translocation of PARK is necessary to switch off and modulate signal transmission via adrenaline. 

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