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A-Adrenergic stimulation

MISCELLANEOUS ANTIDEPRESSANTS. An uncommon but potentially serious adverse reaction of trazodone is priapism (a persistent erection of die penis). If not treated within a few hours, priapism can result in impotence The nurse instructs the patient to report any prolonged or inappropriate penile erection. Use of the drug is discontinued immediately and the primary care provider notified. Injection of a-adrenergic stimulants (eg, norepinephrine) may be helpful in treating priapism. In some cases, surgical intervention may be required. Venlafaxine may cause an increase in die blood pressure. A sustained increase in die blood pressure may indicate that die dosage of venlafaxine needs to be decreased. [Pg.291]

Symptomatic carotid sinus hypersensitivity also should be treated with permanent pacemaker therapy. Patients who remain symptomatic may benefit from adding an a-adrenergic stimulant such as midodrine. [Pg.85]

Decreased HR, contractility, and blood pressure reduce MVo2 and oxygen demand in patients with effort-induced angina. j3-Blockers do not improve oxygen supply and, in certain instances, unopposed a-adrenergic stimulation may lead to coronary vasoconstriction. [Pg.147]

H. Pittner, H. Stormann, R. Enzenhofer, Pharmacodynamic Actions of Midodrine, a New a-Adrenergic Stimulating Agent, and Its Main Metabolite, ST 1059 , Arzneim.-Forsch. 1976, 26, 2145 - 2154. [Pg.370]

Do not use OTC products containing a-adrenergic stimulants (nasal decongestants, cold remedies) unless directed by physician... [Pg.198]

Estes, K.S. and J.W. Simpkins (1982). Resumption of pulsatile luteinizing hormone release after a-adrenergic stimulation in aging constant estrous rats. Endocrinology. Ill 1776-1784. [Pg.409]

One matter that has been very much debated in recent years is that of the response of the mitochondrial Ca pool in liver to a-adrenergic stimulation. Whereas some authors [117,118] maintain that the documented increase in cytosolic Ca ", consequent upon a-adrenergic stimulation of various liver preparations, is due to mobilization of Ca " from mitochondria, others have concluded that the main source of the mobilized Ca " is elsewhere, possibly in the plasma membrane [119,120]. [Pg.283]

Recent interesting information on this problem has come from work by Crompton and his associates [121,122] who found that a-adrenergic stimulation of rats increased the velocity of Ca influx via the electrophoretic uniporter in isolated... [Pg.283]

Pharmacological antagonism. Sympathomimetics, e.g. amphetamine, phentolamine (present in anorectics and cold and cough remedies) may lead to loss of antihypertensive effect, and indeed to a hypertensive reaction when taken by a patient already on a P-adrenoceptor blocker, due to xmopposed a-adrenergic stimulation. [Pg.492]

Lamorte VJ, Thorburn J, Absher D, et al. Gq-Dependent and Ras-dependent pathways mediate hypertrophy of neonatal rat ventricular myocytes following a,-adrenergic stimulation. J Biol Chem 1994 269 13,490-13,496. [Pg.80]

Nakaki, T., Nakayama, M., Yamamoto, S., and Kato, R. (1990b). a-Adrenergic stimulation and -adrenergic inhibition of DNA synthesis in vascular smooth muscle cells. Mol. Pharmacol. 37, 30-36. [Pg.321]

Clonidine hydrochloride is an antihypertensive agent, whose mechanism of action appears to be central a-adrenergic stimulation. This result in the inhibition of bulbar sympathetic cardioaccelarator and sympathetic vasoconstrictor centers, therapy causing a decrease in sympathetic outflow from the brain. Initially drug stimulates pheripheral a-adrenergic receptors producing transient vasoconstriction (5). [Pg.115]

Intravenously in cats, V (SIP 15 68) caused a brief rise in blood pressure followed by hypotension of long duration during which responses to norepinephrine were potentiated and those to carotid occlusion were reduced. Heart rate was slowed. It was ooncluded that negative ciironotropic and inotropic effects predominated over an a-adrenergic stimulation to produce hypotensiont ... [Pg.50]

In isolated rat hepatocytes, a-adrenergic stimulation of glycogen-olysis depends on the activation of phosphorylase by calcium (Assi-macopoulos-Jeannet et al., 1977). The primary action of calcium is on phosphorylase b kinase. [Pg.587]


See other pages where A-Adrenergic stimulation is mentioned: [Pg.71]    [Pg.264]    [Pg.60]    [Pg.116]    [Pg.477]    [Pg.60]    [Pg.116]    [Pg.566]    [Pg.419]    [Pg.284]    [Pg.566]    [Pg.207]    [Pg.757]    [Pg.178]    [Pg.280]    [Pg.351]    [Pg.350]    [Pg.574]    [Pg.590]    [Pg.60]    [Pg.116]    [Pg.75]    [Pg.437]    [Pg.437]    [Pg.436]    [Pg.322]    [Pg.42]    [Pg.214]    [Pg.538]    [Pg.68]   
See also in sourсe #XX -- [ Pg.283 , Pg.295 ]




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