Adrenergic receptors stimulation

Of the following structures, which does not respond to i-adrenergic receptor stimulation ... 

The answer is e. (Hardman, p 215 J Ritodrine hydrochloride is a selective [ -adrenergic agonist that relaxes uterine smooth muscle. It also has the other effects attributable to J3-adrenergic receptor stimulants, such as b rone hod il at ion, cardiac stimulation, enhanced renin secretion, and hyperglycemia. 

The short-acting / -agonists (Table 80-1) are the most effective broncho-dilators available. /J2-Adrenergic receptor stimulation activates adenyl cyclase, which produces an increase in intracellular cyclic adenosine monophosphate. This results in smooth muscle relaxation, mast cell membrane stabilization, and skeletal muscle stimulation. 

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 molecular basis of this synergy may be manifest at the level of genetic expression. Thus, beta-adrenergic receptor stimulation by NE results in gene expression, as discussed previously and shown in Figure 7—4. However, in the presence of... 

Prinz M, Hausler KG, Kettenmann H, Hanisch U (2001) beta-adrenergic receptor stimulation selectively inhibits IL-12p40 release in microglia. Brain Res. 899 264-270. 

Figure 8. Representation of the interaction between CRF, -adrenergic, and dopaminergic (DA.) receptors in the control of pars intermedia cell activity. The CRF and / -adrenergic receptors stimulate adenylate cyclase activity through interaction with the Ns-GTP-binding component. Dopamine, on the other hand, interacts with the Ni-GTP-binding component, causing inhibition of basal as well as CRF- and f3-adrenergic-induced adenylate cyclase activity.

Bogoyevitch MA, Andersson MB, Gillespie BJ, Clerk A, Glennon PE, Fuller SJ, Sugden PH. 1996. Adrenergic receptor stimulation of the mitogen-activated protein kinase cascade and cardiac hypertrophy. Biochem J 314 115-121. 

The putative role of PKA activation after beta-1 adrenergic receptor stimulation with xamoterol was further confirmed by the finding that both atenolol and H89 completely abolished protection (Robinet et al. 2005). These workers also showed that, besides PKA, transduction mechanisms following beta-1-adrenergic receptor stimulation, also involved PI-3K and PKC, with PKA activation occurring prior to PKC. 

Hool, L. C., Middleton, L. M., and Harvey, R. D. 1998. Genistein increases the sensitivity of cardiac ion channels to p-adrenergic receptor stimulation. Circ. Res. 83 33—42. 

There is ample evidence indicating that Ca2+ channels are regulated by phospho-rylation/dephosphorylation cycles involving cAMP-dependent protein kinase and cAMP levels. Indeed this is currently the principal mode by which ventricular contractile force is thought to be modulated positively by /3-adrenergic receptors stimulating adenylyl cyclase and by M2-type muscarinic receptors inhibiting adenylyl cyclase [138,139,145,229,230],... 

Figure 6.10. Calcium-dependent signalling by adrenergic receptors. a p-Adrenergic receptors activate adenylate cyclase. cAMP activates protein kinase A (PKA). In heart muscle, PKA phospho-rylates several Ca transporters and charmels, so that the amount of Ca available for contraction is increased. PL Phospholam-ban SERCA SR/ER Ca transporter, b In smooth muscle, myosin activation in works by way of phosphorylation, which is performed by myosin light chain kinase (MLCK). Inactivation is accomplished by myosin light chain phosphatase (MLCP). c aj-Adrenergic receptors stimulate phospholipase C, which releases inositoltriphosphate (IP3). IP3 binds to a cognate ligand-gated Ca chaimel in the ER and releases Ca, which with calmodulin activates MLCK.

Kohm AP, Sanders VM (2001) Norepinephrine and beta 2-adrenergic receptor stimulation regulate Cd4+ T and B lymphocyte func-tiorr in vitro and in vivo. Pharmacol Rev 53 487—525. 

Le Blanc P H, Eberhart S W, Robinson N E 1993 In vitro effects of aj-adrenergic receptor stimulation on cholinergic contractions of equine distal airways. American Journal of Veterinary Research 54 788-792 Lehner A F, Almeida P, Jacobs J et al 2000 Remifentanil in the horse identification and detection of its major urinary metabolite. Journal of Analytical Toxicology 24 309-315... 

Ruan Y, Kan H, Parmentier JH, Fatima S, Allen LF, Malik KU. a1A adrenergic receptor stimulation with phenylephrine promotes arachidonic acid release by activation of phospholipase D in rat-1 fibroblasts inhibition by protein kinase A. J Pharmacol Exp Therl998 284 576-585. 

Michel MC, Brass LF, Williams A, Bokoch GM, Lamorte VJ, Motulsky HJ. a2-Adrenergic receptor stimulation mobilizes intracellular Ca2+ in human erythroleu-kemia-cells. J Biol Chem 1989 264 4986-4991. 

Zhong H, Murphy TJ, Minneman KP. Activation of signal transducers and activators of transcription by ala-adrenergic receptor stimulation in PC 12 cells. Mol Pharmacol 2000 57 961-967. 

Hu ZW, Shi XY, Lin RZ, Chen J, Hoffman BB. ar Adrenergic receptor stimulation of mitogenesis in human vascular smooth muscle cells role of tyrosine protein kinases and calcium in activation of mitogen-activated protein kinase. J Pharmacol Exp Ther 1999 290 28-37. 

Dulfano MJ, Glass P. Evaluation of a new B 2 adrenergic receptor stimulant, terbutaline, in bronchial asthma. II. Oral comparison with ephedrine. Curr Ther Res Clin Exp 1973 15(4) 150-157. 

A quinolone ethanolamine derivative is one of the most selective Pp adrenergic receptor stimulants described to date.The compound, like salbutMol, is a partial agonist on Pj cardiac adrenergic receptors. 

Mediators other than catecholamines (e.g., circulating cytokines) may be responsible for these distal alterations. Macrophage-derived interleukin-1 (IL-1) and TNF-a produce impaired coupling of /3-adrenergic receptors to adenylate cyclase. Septic shock patients have exhibited impaired /8-adrenergic receptor stimulation of cAMP... 

Reinelt H, Radermacher P, Kiefer P, et al. Impact of exogenous beta-adrenergic receptor stimulation on hepatosplanchnic oxygen kinetics and metabolic activity in septic shock. Crit Care Med 1999 27 325-331. 

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