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Biomedical subjects

E Hong

Publications and source records attributed to E Hong.

At least 145 records · Page 8Linked to original sources
PubMed1982

Tryptophan analogues. 1. Synthesis and antihypertensive activity of positional isomers.

A series of tryptophan analogues having the carboxyl function at the beta-position was synthesized and tested for antihypertensive activity. The 5-methoxy analogue 46 exhibited antihypertensive activity in the rat via the oral route and was much more potent than the normal tryptophan analogue. The methyl ester was found to be a critical structural feature for activity.

Animals↗
PubMed1982

Correlation between phosphatidylinositol labeling and contraction in rabbit aorta: effect of alpha-1 adrenergic activation.

Activation of rabbit aortic strips with alpha adrenergic agonists increased the labeling (with [32P]Pi) of phosphatidylinositol (PI) and phosphatidic acid and contracted the vascular preparations in dose-related fashion. Epinephrine, norepinephrine and methoxamine produced maximal effects, whereas clonidine behaved as partial agonist and B-HT 933 (2-amino-6-ethyl-4,5,7,8-tetrahydro-6H-oxazole-[5,4-d] azepin dihydrochloride) was almost without activity in the two experimental models used. Phenylephrine was a full agonist in producing contraction, but failed to elicit the maximal increase in PI labeling. The EC50 values to produce contraction of aortic strips were lower for all agonists than those required to increase the incorporation of radioactive phosphate into PI, but there was a good correlation between the two sets of data. The increased PI labeling and contraction of aortic strips induced by epinephrine were antagonized by prazosin and yohimbine in dose-related fashion, but the first alpha blocker was about three orders of magnitude more potent than the second in antagonizing the two effects. The present results indicate that both stimulation of PI labeling and contraction are mediated through activation of alpha-1 adrenoceptors in rabbit aorta.

Adrenergic alpha-Agonists↗
PubMed1977

Influence of the route of administration of prostaglandin E1 on rat gastric secretion.

Changes in gastric secretion induced by the subcutaneous, intraduodenal or intragastric administration of prostaglandin E 1 (PGE1) were evaluated in pylorus-ligated rats. Subcutaneous and intraduodenal injections produced a dose-related inhibition in both total acid and volume of gastric secretion. Dose-response curves for inhibition obtained by these routes were parallel, although PGE1 was more potent when given subcutaneously. Gastric administration produced a dose-related decrease in acid and an increase in volume. The slope of the dose-response curve for acid inhibition with this route was flatter than with subcutaneous or intraduodenal administrations. The present results suggest that PGE1 inhibits gastric secretion by the same mechanism of action when given subcutaneously or into the duodenum, while the effects observed after gastric administration are consequences of local actions. The difference in potency of PGE1 given subcutaneously and in the duodenum would seem to be due to differences in absorption from the site of administration and/or to a greater metabolism of PGE1 during its absorption from the intestines.

Animals↗
PubMed1976

On the adrenergic neuron blocking activity of 1-methyl-3-keto-4-phenylquinuclidinium bromide (MA540) during acute and chronic administration.

The quaternary quinuclidine derivative 1-methyl-3-keto-4-phenylquinuclidinium bromide (MA540) antagonized rabbit ileum and cat nictitating membrane responses to postganglionic sympathetic stimulation in a manner similar to guanethidine, indicating adrenergic neuron blocking activity. The potency of MA540 in relation to guanethidine varied according to the experimental procedure employed for assay, being equal to, less and greater than that of the reference agent in the rabbit ileum, and the acute and chronic nictitating membrane, respectively. Preferential blockade of nictitating membrane responses to both lower and higher frequencies of sympathetic stimulation were found with MA540 and guanethidine, depending on the dose used in acute experiments, or on the number of daily administrations in chronic tests. Significant tolerance to the adrenergic impairment induced by MA540 and guanethidine was not apparent in membranes subjected to supramaximal sympathetic stimulation, but was evident in membranes under the influence of normal sympathetic tone in unanesthetized cats. This phenomenon appeared much earlier with guanethidine than with the quinuclidine derivative. Tolerance was correlated neither with norepinephrine supersensitivity nor with catecholamine depletion, which was evaluated indirectly through measurement of membrane responses to tyramine. The results of this study indicate that MA540 may be a useful antihypertensive agent, possessing some advantages over guanethidine.

Animals↗
PubMed1976

Cardiovascular and antihypertensive actions of 1-methyl-3-keto-4-phenylquinuclidinium bromide.

The sympatholytic and norepinephrine depleting drug 1-methyl-3-keto-4-phenylquinuclidinium bromide (MA540) possessed significant chronic antihypertensive activity in mecamylamine- and renal-hypertensive dogs. The compound was approximately four times more potent than guanethidine in the former model and three times as potent in the latter. MA540 reduced orthostatic blood pressure responses in unanesthetized rabbits, but was approximately ten times less potent than guanethidine. The quinuclidine derivative did not affect cardiac output, heart rate or stroke volume in anesthetized open chest dogs and moderately increased mean blood pressure and total peripheral resistance. It produced diuresis and saluresis in anesthetized dogs, but did not influence water or electrolyte urinary excretion in conscious rats. In the latter test, guanethidine produced antidiuresis and antisaluresis. It was concluded that MA540 is a potent, orally effective antihypertensive agent acting through adrenergic neuron blockade, that it lacks undesirable effects on cardiac and renal functions, and that compared with guanethidine, it is more potent in lowering blood pressure but less so in interfering with orthostatic cardiovascular reflexes.

Animals↗
PubMed1976

Vascular tone and reactivity to serotonin in the internal and external carotid vascular beds of the dog.

The effects of intra-arterial infusions of serotonin on internal and external carotid blood flow were determined in anesthetized dogs by electromagnetic flow measurements. Serotonin decreased flow in the internal carotid and increased it in the external carotid. Both responses were blocked by the serotonin antagonist methysergide. The alpha adrenergic antagonist zolertine, the ganglionic blocking agent chlorisondamine and the vasodilator diazoxide blocked external carotid dilator responses but did not modify constriction in the internal carotid. Blockade of external carotid responses by the three drugs was also demonstrated in experiments in which this bed was perfused at a constant rate. These results indicate that the internal and external carotid vascular beds of the dog react in opposite ways to serotonin, that both responses are mediated through the same type of serotonin receptors and that the dilator responses of the external carotid are dependent on vascular tone.

Animals↗