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At least 1,531 records · Page 85Linked to original sources
PubMed1974

Effect of sympathomimetic amines on the histamine forming capacity of human leucocytes.

1 The effects of alpha- and beta-adrenoceptor stimulants on the histamine-forming capacity (HFC) of human isolated leucocytes have been studied, in vitro.2 It was confirmed that antigen significantly stimulates the HFC of human leucocytes.3 beta-Adrenoceptor stimulants, such as isoprenaline and salbutamol (10(-6)-10(-3)M) significantly inhibited the HFC of human leucocytes in the presence and absence of antigen. At concentrations lower than 10(-6)M, this effect was not observed. In general the degree of inhibition of HFC by beta-adrenoceptor stimulants followed their potency as beta-adrenoceptor stimulants.4 alpha-Adrenoceptor stimulants significantly stimulated leucocyte HFC; noradrenaline within a limited concentration of 10(-6)M, while stimulation was seen consistently with phenylephrine at concentrations of 10(-7)-10(-4)M. Adrenaline, which stimulates both alpha- and beta-adrenoceptors, produced small inhibition, no effect, or a degree of stimulation.5 Phentolamine, an alpha-adrenoceptor blocking agent, produced an effect opposite to that of the alpha-adrenoceptor stimulants, i.e. a significant inhibition of the HFC of human isolated leucocytes.

Adrenergic alpha-Agonists↗
PubMed1978

The effects of isoprenaline and a new beta-sympathomimetic amine upon spontaneous activity, diastolic depolarization and plateau height in cardiac Purkinje fibres.

1 In spontaneously active Purkinje fibres of young cows the dose-response curves of the action of isoprenaline upon different electrophysiological parameters were measured.2 The increase in slope of diastolic depolarization could roughly be described by a one-for-one binding curve with a half maximum effect near 10(-8) M and the increase in the height of the plateau level by a two-for-one binding curve with a half maximum effect near 10(-7) M (-)-isoprenaline.3 These dose-response curves were similar to those of two parameters measured under voltage clamp conditions by other authors. The increase in slope of diastolic depolarization behaved like the shift of the activation curve for the pacemaker potassium current towards positive potentials and the growth in plateau height like the increase in the slow inward current mainly carried by Ca ions. From this conformity we propose that the parameters evaluated by us from action potential records could be used for a qualitative analysis of the action of catecholamines on pacemaker potassium current and Ca influx.4 The effects of the isomers of a new drug, 1-isopropylamino-3(4'hydroxyphenoxy)-propan-2-ol (IHP), were evaluated in the same way as those of isoprenaline. The (-)-isomer was at optimal concentrations (10(-5) M) nearly half as effective as isoprenaline in increasing frequency and slope of diastolic depolarization but caused no increase in plateau height. An identical relationship, but at 5 to 10 times higher concentrations, was obtained with the (+)-isomer.5 When 10(-4) M(-)-IHP was added to a preparation equilibrated with a maximum dose of (-)-isoprenaline (10(-6) M), frequency and plateau height declined. This result together with the observation that the effects of IHP could be blocked by the specific beta-antagonist propranolol, revealed the beta-agonistic nature of the new drug. Its inefficiency in increasing the plateau height and thus the slow (Ca) inward current was explained by its relatively low potency and intrinsic activity.

Action Potentials↗
PubMed1975

Evidence for a central alpha-sympathomimetic action of clonidine in the rat.

The antihypertensive effects of clonidine (0.15 mg kg-1, i.p.) were studied in conscious DOCA/saline hypertensive rats having chronically implanted arterial cannulae. The response to clonidine was markedly reduced by simultaneously administered desipramine (3 mg kg-1, i.p.), antagonized dose-dependently by piperoxan (2-10 mg kg-1, i.v.) and prevented by pretreatment with phentolamine (0.2 mg, i.c.v.). Pretreatment with 6-hydroxydopamine (3 x 250 mu-g, i.c.v.), haloperidol (1 mg kg-1, i.p.), p-chloro-N-methylamphetamine (3.5 mg kg-1, i.p.) or 5,6-dihydroxytryptamine (50 mu-g and 25 mu-g, i.c.v.) did not significantly modify the antihypertensive response. It is concluded that the antihypertensive response to clonidine is mediated via stimulation of central alpha-adrenoceptors and is independent of central dopaminergic receptors and intact central serotoninergic neurons. The necessity for intact central noradrenergic neurons remains uncertain.

Adrenergic alpha-Agonists↗