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Biomedical subjects

G Joly

Publications and source records attributed to G Joly.

29 records · Page 2Linked to original sources
PubMed1985

Stereoselectivity of central alpha-adrenoceptors involved in sleep induced by clonidine in chickens.

The stereoselectivity of central alpha 2-adrenoceptors involved in sleep induced in chicks by clonidine, suggested by the results observed with the stereoisomers of idazoxan, was further investigated with the stereoisomers of (imidazolinyl-2)-2-dihydro-2,3-benzofurane (S9871) and those of (imidazolinyl-2)-2-benzocyclobutane (S10089). As for the stereoisomers of idazoxan, there was not a good separation between the effects of the stereoisomers of S10089. In contrast, there was a clearcut separation between the effects of (+)S9871 (antagonist) and (-)S9871 (no effect against the action of clonidine). Therefore, these results strongly support the view that central alpha 2-adrenoceptors which mediate sedation are stereoselective for alpha 2-antagonists.

Adrenergic alpha-Antagonists↗
PubMed1985

[Partial agonist properties of a new derivative of dihydrobenzofuran, S 9871, and its stereoisomers in pithed rats].

In the pithed rat, (imidazolinyl-2)-2 dihydro 2,3 benzofuran or S 9871 and its stereoisomers were found to block alpha-adrenoceptors. In the present investigation the agonistic effect were studied in pithed rats. With (+/-) and (+) S 9871 this effect is compatible with a stimulation of alpha 1-adrenoceptors and the effect of (-) stereoisomer with a stimulation of alpha 1 and alpha 2 adrenoceptors.

Adrenergic alpha-Agonists↗
PubMed1985

Antagonistic effects of S9871 or (imidazolinyl-2)-2-dihydro 2,3 benzofurane and its stereoisomers on some central and peripheral actions of alpha 2-agonists.

(+/-) and (+), but not (-) S9871 are new alpha 2-adrenoceptor selective antagonists. The effect of the racemic mixture and of the stereoisomers on cardiovascular and sedative responses to clonidine have been studied in rats and chickens, respectively. Blockade of central alpha 2-adrenoceptors was also measured as a recovery of the sympathoinhibitory effect induced by intravenous administration of B-HT 933 (azepexole). The potency profiles of these agents established in the central nervous system were confirmed in studies using the vas deferens in situ in the pithed rat. (+/-) and (+) S9871 blocked and antagonized some centrally mediated effects of clonidine such as the depressor response to both intravenous and intracerebroventricular administration. However, the return of arterial pressure to the control value, after intravenous administration of (-) S9871, does not result from an antagonistic action on alpha 2-adrenoceptors, since the depressor effects of clonidine were not blocked, but could be explained by alpha-agonistic properties of (-) S9871. (+/-) and (+) S9871 also blocked and antagonized the hypotensive and bradycardic action induced by intravenous administration of B-HT 933. The loss of the righting reflex induced by clonidine in the chicken was prevented by (+/-) and (+) S9871, as shown by a shift of the dose-response curve to clonidine to the right by both agents; on the contrary, (-) S9871 potentiated the sedation induced by clonidine. In the pithed rat, intravenously administered (+/-) and (+) S9871 fully antagonized the inhibitory effects of clonidine on the electrically induced contractions of the vas deferens. These observations are consistent with a selective alpha 2-adrenoceptors antagonistic effect of (+/-) and (+) S9871 at central and peripheral alpha 2-adrenoceptors.

Adrenergic alpha-Agonists↗
PubMed1984

Pre- and postsynaptic alpha-adrenoceptor blocking properties of a new dihydrobenzofurane derivative (imidazolinyl-2)-2-dihydro 2,3 benzofurane (S 9871) and its stereoisomers in rats.

In the present investigation, the alpha-adrenoceptor blocking effect of (imidazolinyl-2)-2-dihydro 2,3 benzofurane or S 9871 and its stereoisomers was studied. In the pithed rat (+/-) and (+) S 9871 competitively antagonized the pressor effects of azepexole and clonidine more effectively than those of cirazoline and phenylephrine. (-) S 9871 only blocked the pressor response of the alpha 1-agonists used: phenylephrine and cirazoline. (+/-) and (+) S 9871 antagonized the inhibitory effects of clonidine on the increase in heart rate produced by stimulation of the sympathetic efferent fibres of the thoracic spinal cord. (-) S 9871 was twenty times less potent on the decrease in heart rate induced by clonidine. On the vas deferens of the rat, (+/-) and (+) S 9871 appeared to be more potent than (-) S 9871 in antagonizing the inhibitory effects of clonidine on the twitch response produced by electrical stimulation. Therefore, (+/-) and (+) S 9871 appear to be more preferential for alpha 2-adrenoceptors than for alpha 1-adrenoceptors; in contrast (-) S 9871 appears to be selective for alpha 1-adrenoceptors. (+/-) and (+) S 9871 appears to be one of the most selective agents for blocking alpha 2-adrenoceptors.

Adrenergic alpha-Antagonists↗
PubMed1984

[Effect of 2 new derivatives of imidazoline and their optical isomers on postsynaptic alpha adrenergic receptors in pithed rats].

The effects of the stereoisomers of two alpha adrenoceptor antagonists [S 10089 (Imidazolinyl-2)-2 benzocyclobutane and S 9871 (Imidazolinyl-2)-2 dihydro 2,3 benzofuran] were studied in pithed Rats. Vasoconstriction elicited via stimulation of alpha 1 adrenoceptors by cirazoline was antagonized, stimulation of alpha 2 adrenoceptors by azepexole was also antagonized by all these derivatives except (-) S 9871 which was ineffective on the pressor response of azepexole.

Adrenergic alpha-Antagonists↗
PubMed1984

Peripheral postsynaptic alpha-adrenoceptor blocking properties of some new dihydrobenzofurane and imidazoline derivatives in pithed rats.

Peripheral postsynaptic alpha-adrenoceptor blocking properties of six new dihydrobenzofurane and imidazoline derivatives have been investigated in pithed rat against the pressor effects of phenylephrine and cirazoline (alpha 1-agonists) and clonidine and azepexole (alpha 2-agonists). Except for (N-methylimidazolinyl-2)-2 dihydro-2,3 benzofurane (II) that acted neither on alpha 1- nor alpha 2-adrenoceptors, all the compounds revealed blocking effects - plus or minor - on both alpha 1- and alpha 2-adrenoceptors. (Imidazolinyl-2)-2-chloro-7 dihydro-2,3-benzofurane (IV) is equipotent in blocking both alpha 1- and alpha 2-adrenoceptors. 7-Methoxy-(imidazolinyl-2)-2 dihydro-2,3-benzofurane (III) and (imidazolinyl-2)-2-fluoro-7-dihydro-2,3-benzofurane (V) block more effectively alpha 1- than alpha 2-adrenoceptors whereas (imidazolinyl-2)-2-benzocyclobutane (VI) is more potent in blocking alpha 2- than alpha 1-adrenoceptors. (Imidazolinyl-2)-2-dihydro-2,3-benzofurane (I) is a preferential alpha 2-adrenoceptor blocking agent. The most effective agents on alpha 2-adrenoceptors are under further pharmacological investigations.

Adrenergic alpha-Agonists↗
PubMed1979

Hysteresis, oscillations, and pattern formation in realistic immobilized enzyme systems.

Hysteresis, oscillations, and pattern formation in realistic biochemical systems governed by P.D.E.s are considered from both numerical and mathematical points of view. Analysis of multiple steady states in the case of hysteresis, and bifurcation theory in the cases of oscillations and pattern formation, account for the observed numerical results. The possibility to realize these systems experimentally is their main interest, thus bringing further arguments in favor of theories explaining basic biological phenomena by diffusion and reaction.

Biochemical Phenomena↗
PubMed1975

The kinetic behavior of an artificial bienzyme membrane.

Artificial membranes bearing immobilized enzymes can be used to study some effects of membrane structure on enzyme kinetic behavior. The bienzyme system described is a mixture of beta-glucosidase and glucose oxidase. Gluconolactone, the product of thesecond enzyme, is an inhibitor of the first one. The resulting feedback effect has been compared using a mixed two-enzyme membrane, two separated one-enzyme membranes, and astirred bienzyme solution. The feedback effect is quicker and more efficient in the two-enzyme membrane than in solution; it is slower and less efficient in the case of the separated one-enzyme membranes. Effects of enzyme proximity in the structure are discussed. Conclusions are drawn concerning the efficiency of feedback mechanisms when enzymes are embedded within a single structure.

Anaerobiosis↗
PubMed1975

Kinetic studies dealing with an immobilized bienzyme system.

The binding of enzymes into artificial membranes makes possible a study of the interaction between membrane structure and enzyme kinetics within a simple context. Artificial protein membranes bearing a bienzyme system (xanthine oxidase, uricase) are produced by using a co-crosslinking method. The inhibition of uricase was shown to be dependent not only on the concentration of inhibitor in the bulk solution, but also on the kinetic properties of the membrane-bound enzymes. In the presence of xanthine oxidase inside the structure the uricase inhibition by xanthine is less important than in solution. Under defined conditions the activity was found to be higher in the presence of inhibitor than in its absence. Due to diffusion limitations this specific bienzyme system is more efficient when immobilized inside a membrane than when in solution.

Binding, Competitive↗
PubMedDate not supplied

[Interactions between alpha 1, alpha 2 and beta receptors in the blood pressure effects of adrenaline and noradrenaline in the dog].

In anaesthetized dog, the adrenaline induced hypertension is reversed by both alpha 1- and alpha 2-adrenoceptor blocking agents such as AR-C 239 and yohimbine. After alpha 1 or alpha 2 and beta-blockade, adrenaline induced again an increase in blood pressure. This hypertensive effect was suppressed by an alpha 2-adrenoceptor blocking agent when an alpha 1-adrenoceptor blocking was responsible for the reversal of adrenaline-induced hypertension, and conversely. After beta-blockade, both alpha 1- and alpha 2-adrenoceptor blockade is necessary for suppressing any tensional effect of adrenaline. On the other hand, alpha 1- and alpha 2-adrenoceptor blockade are both required to prevent beta-blockade from restoring adrenaline hypertensive effect. Similar effects were observed wih noradrenaline. In fact, only a significant decrease of the noradrenaline-induced hypertension was observed after each alpha-blocker. Both alpha 1- and alpha 2-adrenoceptor blocking agent also significantly inhibited the hypertension induced by noradrenaline. For completely suppressing the effect of noradrenaline on blood pressure, a combination of alpha 1, alpha 2 and beta-blockade is necessary. These results are compatible with a stimulation by adrenaline and noradrenaline of both alpha 1- and alpha 2-adrenoceptors to produce increase in blood pressure.

Adrenergic alpha-Antagonists↗