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Biomedical subjects

J Velly

Publications and source records attributed to J Velly.

At least 37 records · Page 2Linked to original sources
PubMed1985

[3H]-tetracaine binding on rat synaptosomes and sodium channels.

[3H]-tetracaine binding was studied in a rat synaptosomal preparation. [3H]-tetracaine bound to a single class of binding sites with a mean KD of 188 +/- 28 nM and a mean maximal binding capacity of 13 +/- 0.7 pmol mg-1 protein. [3H]-tetracaine binding was inhibited by tetracaine, procaine and by beta-adrenoceptor blocking agents which possess local anaesthetic properties. [3H]-tetracaine binding was not modified by neurotoxins interacting specifically with the sodium channels.

Adrenergic beta-Antagonists↗
PubMed1985

Interference of sodium with [3H]-nitrendipine binding to cardiac membranes.

Interference of sodium with [3H]-nitrendipine binding was studied on membrane homogenates from guinea-pig skeletal muscle, cerebral cortex and left cardiac ventricle. [3H]-nitrendipine binding on homogenates from cerebral cortex and skeletal muscle was unaffected by Na+ (35 and 140 mEql(-1]. On the other hand, for the myocardial receptors, addition of Na+ resulted in an increase in IC50 of nitrendipine. Simultaneously, for the myocardial preparations, saturation curves showed a decrease in [3H]-nitrendipine affinity and an increase in the number of binding sites.

Animals↗
PubMed1983

Beta-adrenoceptors of the human myocardium: determination of beta 1 and beta 2 subtypes by radioligand binding.

beta-Adrenoceptors of the human myocardium were investigated with binding studies using 125iodocyanopindolol (ICYP) as ligand. Inhibition of ICYP-binding by betaxolol (a selective beta 1-antagonist) and ICI 118551 (a selective beta 2-blocking drug) resulted in non-linear Scatchard-plots suggesting that both beta-adrenoceptor subtypes are present in human left atrium and left ventricle. Computer analysis of the data gave a beta 1/beta 2-adrenoceptor ratio of approximately 65:35 both for left atrium and for left ventricle.

Binding, Competitive↗
PubMed1983

The beta-adrenoceptor of pig coronary arteries: determination of beta 1 and beta 2 subtypes by radioligand binding.

beta-Adrenoceptors of pig coronary arteries were investigated by the use of a new ligand, 125iodocyanopindolol (ICYP) in binding studies. Inhibition of ICYP binding by betaxolol (a selective beta 1-antagonist), zinterol (a selective beta 2-agonist) and ICI 118551 (a selective beta 2-blocking drug) resulted in non-linear Scatchard plots, suggesting that both beta-adrenoceptor subtypes are present in pig coronary arteries. Computer analysis of the data gave a beta 1:beta 2-adrenoceptor ratio of approximately 65:35.

Animals↗
PubMed1982

Effects of N-aralkyl substitution of beta-agonists on alpha- and beta-adrenoceptor subtypes: pharmacological studies and binding assays.

The pharmacological and binding properties of four beta-adrenomimetic drugs with N-alkyl substitutions (isoprenaline, terbutaline, salbutamol and soterenol) were compared with those of four corresponding drugs with N-aralkyl substitutions (protokylol, ME 506, salmefamol and zinterol). BD-40 A, a very powerful beta 2-agonist with a related chemical structure, was also included in this study. The beta 1- and beta 2-activities of these drugs were determined on guinea-pig atria and trachea, their alpha-adrenolytic activity was measured on rat aorta and their affinities (Ki) for alpha 1- and alpha 2-adrenoceptors on rat cortical membranes were assessed using [3H]prazosin and [3H]yohimbine. In this group of beta-agonists, substitution of the N-alkyl by an N-aralkyl group had a variable effect on the beta 2-selectivity whereas alpha-adrenolytic properties were always enhanced. An increase of the affinities (Ki) for both alpha 1- and alpha 2-adrenoceptors was found but the effect was much more pronounced for alpha 1-adrenoceptors. These results indicated that the alpha-adrenolytic activity observed with the N-aralkyl beta-agonists was selective for alpha 1-adrenoceptors.

Adrenergic beta-Agonists↗
PubMed1980

Studies on some para-substituted clonidine derivatives that exhibit an alpha-adrenoceptor stimulant activity.

1 alpha-Adrenoceptor stimulant activity was determined for noradrenaline (NA), clonidine and a series of para-substituted derivatives of clonidine on rat aortic strips, a rat brain synaptosome preparation, and anaesthetized pithed rats. The effects on the blood pressure of intraventricular (i.c.v.) injections of para-aminoclonidine were also determined in anaesthetized rats. 2 Para-substituted derivatives of clonidine (amino-, diethylamino-, ethylamino-, acetamido-, bromoacetamido-, N-chloroethyl-N-methyl-amino and N-beta-chloroethyl-N-methylaminomethyl-) retain alpha-adrenoceptor stimulant activity. 3 pD2 values determined on rat aortic strips were 11.2, 7.67 and 9.05 respectively for para-aminoclonidine, clonidine and noradrenaline. The Ki values of these agents, determined on a rat brain synaptosomal preparation with a radioreceptor assay using [3H]-clonidine as ligand, were 1.3, 8.0 and 23 nM respectively for para-aminoclonidine, clonidine and NA. When given by i.c.v. injection in rats, para-aminoclonidine lowered the blood pressure. 4 N-beta-chloroethyl-N-methylaminomethylclonidine is an alkylating agent with an unusual agonist activity. It elicits contractions of the rat aorta that persist despite repeated washing. 5 alpha-Adrenoceptor affinities are discussed in relation to their structural features.

Adrenergic alpha-Agonists↗
PubMed1980

Comparison of pharmacological and binding assays for ten beta-adrenoceptor blocking agents and two beta-adrenoceptor agonists.

1 The inhibition constants evaluated by binding assays for ten beta-adrenoceptor blocking agents and two beta-adrenoceptor agonists, were compared with the pA2 and pD2 values determined in vitro and in vivo. 2 There was only a limited correlation between beta 1 or beta 2 selectivities observed with the different methods. 3 Selectivity is generally less pronounced in binding assays than for in vivo and in vitro experiments.

Adrenergic beta-Agonists↗
PubMed1977

Comparison of the effect of two groups of diuretics on renin secretion in the anaesthetized dog.

1. The effects of two groups of diuretics on renin secretion have been compared in dogs anaesthetized with pentobarbital. 2. Frusemide, ethacrynic acid and bumetanide cause an immediate rise in renin secretion which is not inhibited either by DL-propranolol or by a bilateral ureterovenous anastomosis which prevents salt and water loss. 3. Clopamide, metolazone and indapamide do not cause an immediate rise in renin secretion. Renin hypersecretion is induced only 1 h after intravenous injection of these diuretics. 4. Renin secretion was studied for 6 h after frusemide injection: the immediate rise was followed by a later increase in renin secretion. This later rise was inhibited by propranolol and by ureterovenous anastomosis. 5. These results allow us to distinguish between a direct renal mechanism responsible for early renin hypersecretion, which appears to be connected with the action of the diuretic on the ascending limb of Henle's loop, and an indirect mechanism responsible for late renin hypersecretion, which appears to be connected with salt and water loss.

Animals↗
PubMed1977

A potent new beta2-adrenoceptor blocking agent.

1 (t-Butyl-amino-3-ol-2-propyl) oximino-9 fluorene is a new beta2-adrenoceptor blocking agent with a pA2 of 9.23+/-0.25 on isolated trachea. 2 It provokes hypertension in normotensive rats and does not prevent arterial hypertension in SHR rats, although it does prevent the renin secretion normally induced by isoprenaline infusion.

Adrenergic beta-Antagonists↗
PubMed1976

Effects of apomorphine and of pimozide on renin secretion in the anaesthetized dog.

This paper presents the results of a study of the receptors involved in renin hypersecretion induced by dopamine. Apomorphine induces renin hypersecretion without significantly modifying the renal blood flow. This renin hypersecretion is inhibited by haloperidol. However, pimozide, a selective dopaminolytic agent, is incapable of inhibiting the renin hypersecretion induced by dopamine. These results provide supplementary evidence for the existence of renal dopaminergic receptors which would appear to differ from the central dopaminergic receptors.

Animals↗
PubMed1975

Role of the ventral surface of the brain stem in the hypotensive action of clonidine.

The areas S of the ventral surface of the brain stem and the immediately surrounding zone were superficially destroyed by the means of electro-coagulation, in 14 cats. This destruction produced a drop in blood pressure, which was transient in 9 and definitive in 4 animals; in one cat only the arterial pressure did not change after the destruction. In 6 animals which have been sham-operated, clonidine (15 mug/kg, i.v.) always induced a marked fall in blood pressure whereas in 10 animals which had maintained or recovered a normal blood pressure after the destruction of the area S, clonidine (15 mug/kg) injected intravenously no longer produced any decrease of the arterial pressure. These results suggest that the integrity of the areas S is necessary for the development of the hypotensive action of clonidine. This hypotensive drug may act, at least at the level of the ventral surface of the brain stem, through inhibition of a vasopressive structure.

Animals↗
PubMed1975

Effect of catecholamines on renin release in vitro.

Beta receptor activation by isoproterenol stimulates renin release by kidney slices "in vitro". This effect is dose-dependent and blocked by propranolol. High norepinephrine concentration has an inhibitory effect on renin secretion which is reversed by phentolamine: activation of alpha receptors probably decreases renin release.

Animals↗
PubMed1975

[Role of ventral surface of brain stem in control of arterial pressure and in hypotensive action of clonidine].

Superficial destructions of the brain stem have been performed in cats at the level of the chemosensitive areas "S". These destructions produced a drop in blood pressure, which was transient in 9 and definitive in 4 animals. In 6 sham-operated animals, clonidine (15 mug/kg), injected intravenously, always induced a marked fall in blood pressure, whereas in the 10 animals which have maintained or regained normal blood pressure after the destruction of the areas S, clonidine no longer induced any decrease in blood pressure. These results suggest that the integrity of the areas S is necessary for the development of the hypotensive action of clonidine. This hypotensive drug may act, at least at that level of the ventral surface of the brain stem, through an inhibition of a vasopressive structure.

Animals↗