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Biomedical subjects

V VARAGIC

Publications and source records attributed to V VARAGIC.

At least 19 recordsLinked to original sources
PubMed1962

Effect of guanethidine, hemicholinium and mebutamate on the hypertensive response to eserine and catechol amines.

Guanethidine, hemicholinium and mebutamate were used to study the site and mechanism of the hypertensive response to eserine in the rat. Guanethidine was found to block very effectively the hypertensive effect of eserine and to produce at the same time a very strong potentiation of the response to catechol amines. Hemicholinium, after a certain latent period, also blocked the effect of eserine, at the same time leaving the response to adrenaline and noradrenaline intact. Mebutamate was also found to block the effect of eserine. The results of the present experiments suggest that eserine produces a central adrenergic activation in the rat.

Amines↗
PubMed1961

Factors influencing the hypertensive effect of eserine in the rat.

Several factors influencing the hypertensive effect of eserine in the rat were investigated. Pretreatment with reserpine regularly depressed or abolished the hypertensive response to eserine. The slow intravenous infusion of either noradrenaline, dihydroxyphenylalanine or 5-hydroxytryptamine only occasionally restored the hypertensive effect of eserine in reserpine-treated rats. Bretylium and choline 2,6-xylyl ether bromide significantly depressed or even abolished the hypertensive effect of eserine. The effect of bretylium was stronger than that of choline 2,6-xylyl ether bromide. Cocaine was found to antagonize the action of bretylium on the response to eserine. In doses which significantly depressed the action of eserine bretylium did not inhibit the hypertension due to excitation of medullary centres induced by clamping the common carotid arteries. Lowering of body temperature abolished the hypertensive effect of eserine. Pretreatment with isopropylisoniazid did not antagonize the inhibitory action of reserpine on the hypertensive response to eserine. It is concluded that the present experiments indicate that the hypertensive effect of eserine in the rat is due to central activation of adrenergic nervous elements. Liberation of noradrenaline (and adrenaline) from the adrenals and from the blood vessels by eserine is an insignificant factor in producing the hypertensive response to eserine.

Adrenal Glands↗
PubMed1961

Effect of noradrenaline, bretylium and cocaine on the blood pressure response to tyramine in the rat.

Tyramine is mainly a pressor agent in the rat under urethane, although the hypertensive effect of tyramine in some experiments is followed by a prolonged increase or depression of blood pressure. Bretylium, in doses up to 10 mg/kg, prolonged the response to tyramine, whereas larger doses depressed or blocked its effect. When the hypertensive effect of tyramine was blocked by bretylium, both noradrenaline and dihydroxyphenylalanine, when slowly infused, were found to restore it. The well-known block by cocaine of the hypertensive response to tyramine could also be reversed by intravenous infusion of noradrenaline and dihydroxyphenylalanine. It is concluded that the infusion of noradrenaline and dihydroxyphenylalanine makes available noradrenaline in the postganglionic adrenergic nerves which is necessary for the action of tyramine.

Animals↗
PubMed1960

The effect of substance P on the superior cervical ganglion of the cat.

Intra-arterial injections of substance p in doses from 10 to 30 units potentiated the response of the nictitating membrane to submaximal stimulation of the preganglionic sympathetic nerve, while higher doses (30 to 100 units) usually depressed the response. The stimulating action of acetylcholine on the superior cervical ganglion (as judged by the response of the nictitating membrane) was also potentiated by substance P. The responses of the nictitating membrane to adrenaline, noradrenaline and tyramine were potentiated by substance P as well. It is concluded that the potentiating effect of substance P on the response of the nictitating membrane to submaximal stimulation of the preganglionic sympathetic nerve is probably due to sensitization of acetylcholine receptors in the postsynaptic neurone. The present experiments do not explain how substance P potentiated the response to sympathomimetic amines.

Acetylcholine↗