Adrenergic beta-receptor stimulating

The catecholamines produce their action by direct combination with receptors located on the cell membrane. In 1948, Ahlquist divided the adrenergic receptors into two main groups - alpha and beta. The alpha receptor stimulation produces excitatory effect and beta receptor stimulation usually produces inhibitory effect. 

Epinephrine administered intramuscularly and by venous infusion lowers plasmatic kininogen in man and in rabbit, whilst nor-epinephrine is inactive in this sense. Decrease of kininogen (that is, release ofiki-nins) is perhaps another metabolic feature of epinephrine, and is appears to be correlated to stimulation of adrenergic beta-receptors. As an indirect evidence of this, we can consider the results of researches by means of isoproterenol and beta-adrenergic blocking agents. 

Adrenergic Beta 1 receptor ADRBl Agonism May stimulate cardiac muscle (increase heart rate and force of contraction) and contributes to the relaxation of blood vessels. Antagonism May stress cardiovascular performance. 

These are the agents which block the action of sympathetic nerve stimulation and circulating sympathomimetic amines on the beta adrenergic receptors. At the cellular level, they inhibit the activity of the membrane cAMP. The main effect is to reduce cardiac activity by diminishing (3 receptor stimulation in the heart. This decreases the rate and force of myocardial contraction of the heart, and decreases the rate of conduction of impulses through the conduction system. They are classified as in table 3.3.2. 

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. 

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. 

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. 

Ahlquist has attempted to explain the actions of the catecholamines in terms of two different types of adrenergic receptors. According to Ahlquist s nomenclature, alpha receptors generally mediate vasoconstriction and excitatory functions, while stimulation of the beta receptors produces vasodilation and other responses associated with smooth muscle relaxation Beta receptors are believed to mediate the chronotropic and inotropic action of catecholamines. Epinephrine is active on both alpha and beta receptors while the action of norepinephrine is primarily on the alpha sites. Isoproterenol has little action on alpha sites, being a potent stimulator of beta receptors. 

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. 

Two different kinases are involved in phosphorylating beta-adrenergic receptors. Protein kinase A is positively regulated by cyclic AMP and is stimulated by substances that activate adenylate cyclase. Beta-adrenergic receptor kinase (BARK) is related functionally to rhodopsin kinase and may be important for regulating neural transmission (see Figure 52). A cytosolic protein, beta-arrestin, interacts with the BARK-phosphorylated receptors and disrupts the activation of Gs by the beta receptor. 

Pike, L.J. and Lefkowitz, R.J. (1981) Correlation of beta-adrenergic receptor-stimulated [3H]GDP release and adenylate cyclase activation. /. Biol. Chem. 256 2207-2212. 

A study in 30 patients being evaluated for chest pain found that 2 mg/kg of a 10% intranasal solution of cocaine reduced coronary sinus flow hy about 14% and coronary artery diameter by 6 to 9%. The coronary vascular resistance increased by 22%. The addition of propranolol 400 micrograms/minute by intracoronary infusion, (to a total of 2 mg) reduced coronary sinus flow by a further 15% and increased the coronary vascular resistance by 17%. The probable reason is that the cocaine stimulates the alpha-receptors of the coronary blood vessels causing vasoconstriction. When the beta-receptors are blocked by propranolol, the resultant unopposed alpha-adrenergic stimulation may lead to enhanced coronary vasoconstriction (see also Beta blockers + Inotropes and Vasopressors , p.848). The clinical importance of these frndings is uncertain but the authors of the report suggest that beta blockers should be avoided in patients with myocardial ischaemia or infarction associated with the use of cocaine. ... 

The adrenergic receptors of the sympathetic system are not identical but can be subdivided into two main types, namely alpha and beta receptors, which can then be further subdivided. The sympatiiomimetics are categorised in Table 24.1 , (p.879), and a brief summary of the principal effects of stimulation of these receptors is listed below ... 

Beta Blocker Glass of drugs that compete with beta-adrenergic receptor-stimulating agents. 

Class II antiarrhythmic drugs include beta (( -adrenergic blocking drugs, such as acebutolol (Sectral), esmolol (Brevibloc), and propranolol (Inderal). These drugp also decrease myocardial response to epinephrine and norepinephrine (adrenergic neurohormones) because of their ability to block stimulation of p receptors of the... 

Ritodrine has an effect on beta (p)2-adrenergic receptors, principally those that innervate the uterus. Stimulation of these p2-adrenergic receptors inhibits uterine smooth muscle contractions. The pradrenergic receptors are located in the heart and are not stimulated by ritodrine when administered as prescribed. Ritodrine is used to... 

One of the few examples of decreased susceptibility among elderly is the effect of catecholamines on the heart. There is a down-regulation of beta-adrenergic receptors and a reduced response to beta-adrenergic stimulation (Turnheim 1998). This results in decreased effect of betablockers on heart rate and stroke volume. In the elderly betablockers may be less effective than other drugs against hypertension and they should not be considered appropriate for first-line therapy of uncomplicated hypertension in the elderly (Grossman and Messerli 2002). 

Atenolol stimulation of arteriolar contraction Beta-adrenergic receptor anatagonist, reduces cardiac output... 

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