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PubMed1983

Studies of catecholamine effect on cyclic AMP in human cultured thyroid cells: their interaction with thyrotrophin receptor.

Even though adrenergic nerve terminals between and around thyroid follicles and catecholamine stimulation of thyroid adenylate cyclase have been reported, there is no uniform concept on catecholamine interaction with thyrotrophin (TSH) receptors. Therefore, the effect of catecholamines on TSH-stimulated cyclic AMP (cAMP) accumulation in human follicular thyroid cells has been investigated, to thus eliminating the extrathyroidal actions of catecholamines. Epinephrine, norepinephrine and isoproterenol appeared to be rapid and potent stimulators of intracellular cAMP accumulation, the half maximum increase doses being 4 X 10(-7)M, 1 X 10(-5)M and 5 X 10(-7)M, respectively. While propranolol (1 X 10(-5)M) prevented the stimulatory effect of catecholamines and failed to inhibit the effect of bovine TSH, phentolamine (1 X 10(-5)M) enhanced the potency of norepinephrine and bovine TSH, leaving that of epinephrine unchanged. The effects of epinephrine (2 X 10(-8)M) and isoproterenol (2 X 10(-8)M) were additive to that of bovine TSH (0.5 mU/ml), but the effect of simultaneous stimulation with norepinephrine (5 X 10(-7)M) and bovine TSH (0.5 mU/ml) was lower than expected. Prenalterol, a selective beta 1-agonist, did not stimulate cAMP accumulation, while terbutaline, a selective beta 2-agonist, exerted a potent stimulation. Metoprolol, a selective beta 1-adrenergic blocker, did not affect the response of thyroid follicular cells to isoproterenol. These results demonstrate the existence of beta-adrenergic receptors in human thyroid follicular cells, mainly of the type beta 2, apparently not correlated with TSH receptor. The existence of alpha-adrenergic receptors which counter-regulate TSH functional responses in human thyroid follicular cells is suggested.

Adrenergic beta-Agonists↗
PubMed1982

Characterization of the beta-adrenoceptors in coronary vasculature of the dog heart.

In the present study an attempt has been made to characterize the beta-adrenoceptors of coronary vasculature in dog. Blockade of beta 1-adrenoceptors with ICI 50172 or beta 2-adrenoceptors with RB2 showed only partial antagonism of isoprenaline-induced decrease in coronary resistance. However, combined treatment with ICI 50172 and RB2 completely blocked the isoprenaline-induced fall in coronary resistance. Essentially similar results were observed in controlled heart rate experiments where the drugs were administered locally into the coronary circulation. These results demonstrate the involvement of both beta 1 and beta 2 adrenoceptors in isoprenaline-induced coronary vasodilation.

Animals↗
PubMed1976

Adverse drug reactions during treatment of hypertension.

Adverse drug reactions (ADRs) can be broadly classified as either "a nuisance" or "life-threatening". Voluntary reporting systems gradually accumulate a quite impressive list of suspected ADRs with antihypertensive drugs as their use becomes widespread. Such data gives no clue to true or relative incidence. The absolute and comparative incidence of ADRs can only be determined fairly by a system of unbiased general data collection of ADRs from which the data for antihypertensive drugs is then selected. The Boston Collaborative Drug Surveillance Program provides such a source of information. Data from the Boston Program reveals that most of the listed ADRs with antihypertensive drugs occur very infrequently, that "nuisance" ADRs occur in 10 to 29% of patients in whom they are used, and that "life-threatening" ADRs occur in less than 1%. ADRs tend to discourage patient compliance with medication aims. In selecting specific antihypertensive therapy the clinician should be mindful not only of the severity of the hypertension to be treated, but also of the nature, type, and severity of potential ADRs, the personality and likely complicance of the patient, and the need for patient education regarding drug effects, possible unwanted effects, and what measures should be taken when ADRs occur.

Adrenergic beta-Antagonists↗