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At least 1,369 records · Page 76Linked to original sources
PubMed1984

Comparison of sympathomimetic amines with collagen, calcium ionophor and adenosine diphosphate in their effects on thromboxane formation of human platelet rich plasma.

Platelet rich plasma (PRP) was stimulated by addition of epinephrine, norepinephrine, dopamine, dobutamine, ADP, collagen or A 23187 in various concentrations. Before, during and after aggregation the levels of thromboxane B2 (TxB2) were measured by radioimmunoassay. After addition of collagen or A 23187 a strong stimulation of thromboxane synthesis was observed, beginning with the early aggregation phase. TxB2 values after complete aggregation amounted to 110-220 ng/ml and up to 500 ng/ml, respectively. After ADP, epinephrine and norepinephrine the thromboxane formation took place mainly in the late aggregation phase and reached levels of 37-51 ng TxB2/ml PRP. Dopamine and dobutamine in concentrations up to 50 microM failed to stimulate platelet's thromboxane synthesis and induced only small changes of optical density of PRP.

Adenosine Diphosphate↗
PubMed1980

[Therapy of orthostatic dysregulation. Comparative studies on anti-hypotensive sympathomimetics with a tilt-table test].

In 7 patients suffering from orthostatic hypotension the early behaviour of arterial mean blood pressure was studied in the tilting table experiment under influence of etilefrine, norfenefrine, gepefrine (D-(+)-1-(3-hydroxyphenyl)-2-aminopropan-(2R, 3R)-hydrogentartrat) and of its I-isomere. Significant improvement of early orthostatic disregulation of the arterial pressure could be only observed under gepefrine. Amelioration seems to be induced by sensitization of the pressoreceptors.

Adult↗
PubMed1983

On the antihypertensive mechanisms of beta-adrenoceptor antagonists in relation to intrinsic sympathomimetic activity, cardioselectivity and hydrophilicity.

A review of the relevant literature indicates that the effects of beta-blockers on cardiac output and plasma renin or penetration of these drugs into the brain and cerebrospinal fluid are not essential for their antihypertensive effect. Reduction in blood pressure during long-term beta-blocker therapy is always associated with reduction of total peripheral resistance. Evidence is presented which suggests that blockade of presynaptic beta-receptors underlies this vasodilator effect of beta-blockers.

Adrenergic beta-Antagonists↗