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Adrenergic receptor stimulation, effects

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. [Pg.187]

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. [Pg.922]

Mechanism of Action A sympathomimetic (adrenergic agonist) that stimulates betai-adrenergic receptors. Therapeutic Effect Increases myocardial contractility, stroke volume, cardiac output. [Pg.652]

MecHanism of Action A sympathomimetic that directly stimulates alpha-adrenergic and beta-adrenergic receptors. Therapeutic Effect Produces vasoconstriction of respiratory tract mucosa shrinks nasal mucous membranes reduces edema and nasal congestion. [Pg.1052]

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... [Pg.305]

Ephedrine is a sympathomimetic or central nervous system stimulant. It is a potent stimulator of a, pi and p2 adrenergic receptors. The effects include vasoconstriction, raised blood pressure and pulse, bronchodilation and diuresis. Ephedrine-based drugs are used as nasal decongestants, bronchodilators and in anaphylactic shock. In excess they cause insomnia, tachycardia and dizziness. [Pg.153]

Relatively selective stimulation of Pi-adrenergic receptors can be achieved with dobutamine. This is a racemic drug of which both isomers activate the Pi-receptor, and in addition the (-) isomer activates ( -receptors whereas the (+) isomer activates p2-receptors the simultaneous activation of ai- and p2-receptors results in no major net effect on peripheral resistance, and thus the overall cardiovascular effects are mediated by Pi-stimulation leading to increases in cardiac contractility and output. Dobutamine is used for the short-term treatment of acute cardiac failure and for diagnostic purposes in stress echocardiography. [Pg.49]

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... [Pg.563]

Antagonism of several characteristic effects of amphetamine and cocaine by the alpha adrenergic receptor antagonist prazosin is a most recent example of noradrenergic mechanisms in the actions of psychomotor stimulants (Tessel and Barrett 1986). We investigated whether or not prazosin may attenuate the disruptive effects of amphetamine on social and aggressive behavior in mice and squirrel monkeys (Miczek, unpublished observations). Pretreatment with prazosin (0.4 mg/kg) attenuated the disruption of attack... [Pg.85]

Epinephrine and norepinephrine have equal affinity for Pj-receptors, the predominant adrenergic receptors on the heart. However, the human heart also contains a small percentage of P2-receptors that, like Pj-receptors, are excitatory. Therefore, epinephrine is capable of stimulating a greater number of receptors and causing a greater stimulatory effect on the myocardium. [Pg.108]

Sympathetic stimulation increases heart rate. Norepinephrine, the neurotransmitter released from sympathetic nerves, binds to the (3-adrenergic receptors in the heart and causes the following effects ... [Pg.183]

The major circulating hormones that influence vascular smooth muscle tone are the catecholamines epinephrine and norepinephrine. These hormones are released from the adrenal medulla in response to sympathetic nervous stimulation. In humans, 80% of catecholamine secretion is epinephrine and 20% is norepinephrine. Stimulation of cy-adrenergic receptors causes vasoconstriction. The selective a,-adrenergic receptor antagonist, prazosin, is effective in management of hypertension because it causes arterial and venous smooth muscle to relax. [Pg.209]


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See also in sourсe #XX -- [ Pg.148 ]




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