Biomedical subjects

R Tricoche

Publications and source records attributed to R Tricoche.

At least 19 recordsLinked to original sources

PubMed1998

Receptors involved in the positive inotropic action induced by dopamine on the ventricle of a 7-day-old chick embryo heart.

Earlier experiments only revealed involvement of sympathetic pre-synaptic dopaminergic receptors in dopamine induced inotropism in myocardium. We therefore used electrically stimulated (1 Hz) isolated 7-day-old chick embryo heart ventricles, thought to be devoid of functional sympathetic nerves, to re-investigate post-synaptic receptors involvement and particularly that of dopaminergic receptors in the positive inotropic effect of dopamine. The results showed that noradrenaline, isoprenaline and dopamine produced a positive inotropic effect with a similar efficacy and with an order of potency as follows: Isoprenaline = Noradrenaline > Dopamine. Tyramine induced no significant modification of the "initial tension" indicating that functional sympathetic innervation and/or releasable endogenous catecholamines were not demonstrable in the 7-day-old chick embryo heart ventricle. Propranolol (1 microM) competitively antagonized the positive inotropic response to isoprenaline, noradrenaline and dopamine, meanwhile phentolamine (3 microM) failed to significantly modify the effects of both noradrenaline and dopamine, indicating that these catecholamines induced their positive inotropic effects via stimulation of beta-adrenoceptors; involvement of alpha-adrenergic receptors stimulation was not demonstrable in these effects. Moreover, haloperidol (2 microM) antagonized the positive inotropic response to dopamine but had not any significant effect on the response to isoprenaline. The combined application of both propranolol and haloperidol antagonized the positive inotropic response to dopamine to a greater extent than when these two antagonists were given alone. Consequently, post-synaptic dopaminergic receptors were also involved in the positive inotropic effect of dopamine. Furthermore, in preparations in which sodium channels were inactivated by high potassium physiological salt solution, high concentrations of dopamine (0.1 mM to 1 mM) induced a slow developing electrical and positive inotropic responses which were also inhibited by propranolol and haloperidol, but not by phentolamine. These latter results indicated that like beta-adrenergic stimulation, the slow inward calcium current activated by stimulation of adenylate cyclase, was at least in part involved in the positive inotropic response to dopamine. In conclusion, dopamine induced its positive inotropism via stimulation of post-synaptic beta-adrenergic and dopaminergic receptors. The contribution of dopaminergic receptors in this positive inotropic effect might be of the DA-2 receptors since haloperidol used had been reported to be more DA-2 than DA-1 antagonist. These DA-2 receptors subtypes would mediate activation of adenylate cyclase.

Adrenergic alpha-Agonists↗

PubMed1997

[Inotropic effect of isoprenaline and noradrenaline on chick embryo heart].

Isolated ventricles of developing chick embryo heart, paced at 1 Hz, were used to assess the positive inotropic responses to isoprenaline and noradrenaline in order to characterize the adrenergic receptors involved in these effects. In 7 day-old-chick embryo heart ventricle, isoprenaline and noradrenaline exhibited similar potencies and efficacies. Moreover, propranolol (1 microM) inhibited the positive inotropic effect of isoprenaline and noradrenaline, while pentholamine (3 microM) failed to affect the latter response; in addition, phenylephrine (1 microM-1 mM) had no positive inotropic effect. It was therefore concluded that isoprenaline and noradrenaline induce their effect via stimulation of beta-adrenergic receptors. The efficacy of isoprenaline and noradrenaline and the potency of isoprenaline increased from the 7th to 10th day while the potency of noradrenaline decreased. The decrease in noradrenaline potency with age was attributed to its uptake, while the increase in isoprenaline potency was attributed to the increase in beta-adrenergic receptors. However, the increase in efficacy of both isoprenaline and noradrenaline with age might be due to the higher density and/or higher maturity of contractile proteins.

Age Factors↗

PubMed1992

Contractions induced by phenylephrine and noradrenaline are differently affected by endothelium-dependent relaxation in rat aorta.

In rings of rat aorta precontracted with phenylephrine (10 microM) or noradrenaline (10 microM), addition of carbachol (10 microM) produced an endothelium-dependent relaxation. However, regardless of the concentration of agonist tested, both the intensity and duration of the relaxation were significantly less when noradrenaline, rather than phenylephrine, was used as the precontracting agent. The different responses observed do not appear to be related to destruction of endothelium-derived relaxing factor by autoxidation of noradrenaline since neither EDTA (30 microM) nor superoxide dismutase (30 units mL-1) improved the relaxation to carbachol. In addition, in endothelium-free rings, the noradrenaline (1 microM)-induced contraction was less sensitive than the phenylephrine (1 microM)-induced contraction to sodium nitroprusside (0.1 microM) or to 8-Br-cGMP (300 microM). With phenylephrine-, but not noradrenaline-, induced contraction, the relaxation triggered by carbachol was significantly reduced by pretreatment of the aortic rings with chloroethylclonidine (50 microM), which inactivates a subpopulation of alpha 1-adrenoceptors. Thus, the results confirm that both alkylation sensitive and resistant alpha 1-adrenoceptors exist in rat aorta and indicate that EDRF may discriminate between these two alpha 1-adrenoceptor subtypes which are differently affected by phenylephrine and noradrenaline.

Animals↗

PubMed1991

The uterotonic action of the aqueous extract of Bridelia atroviridis in the rat.

The effects of the aqueous extract of leaves of Bridelia atroviridis (Bridelia), a small African tree, on the mechanical activity of rat uterus were studied. The aqueous extract of leaves of B atroviridis administered in a concentration-dependent manner (5 x 10(-6)-1.2 x 10(-3) g/ml) induced contractions that were antagonized by various calcium entry blockers (nifedipine, diltiazem, manganese chloride). In absence of external calcium ions, repeated applications of a supramaximal concentration of Bridelia (1.2 x 10(-3) g/ml) evoked sustained and repeated contractions the amplitude of which was congruent to 20% of those obtained in the physiological external calcium concentration. Bridelia-induced contractions in calcium-free medium were inhibited by isoprenaline (8 x 10(-7) M), caffeine (15 x 10(-3) M) and trifluoperazine (10(-5) M). Contractile responses induced by Bridelia in both calcium-containing and calcium-free media were antagonized by prior incubation of uterus with phorbol 12, 13-dibutyrate (6 x 10(-7) M), cholera toxin (6 x 10(-8) M) or pertussis toxin (5 x 10(-7) g/ml). These results show that Bridelia has a potent uterotonic action in the rat. The cellular basis of this action appears to be complex, and involves various mechanisms including calcium mobilization from both intra and extracellular compartments and activation of phospholipase C through a G-protein.

Animals↗

PubMed1987

Prejunctional alpha 2-adrenergic properties of S-3341 (dicyclopropylmethyl)amino-2-delta-2-oxazoline: a comparison with clonidine.

The prejunctional activities of S-3341 and clonidine have been studied in the transmural field-stimulated epididymal part of the rat vas deferens. Both S-3341 and clonidine inhibited these neuronally induced contractions. At high concentrations, these agonists induced spontaneous contractions in the preparation, which were abolished by 10(-7) M prazosin. The inhibitory effects of S-3341 and clonidine were antagonized in a competitive manner by rauwolscine and were found not to be modified in a statistically significant manner by 10(-7) M prazosin. The pA2 values of rauwolscine against S-3341 and clonidine were the same, indicating the receptors influenced by these drugs were the same also. However, the efficacy of S-3341 is lower than that of clonidine (by a factor of approximately 100). This lower efficacy of S-3341 at the prejunctional level could be linked to the lack of a sedative effect of this compound at therapeutic concentrations.

Adrenergic alpha-Agonists↗

PubMed1986

Source of calcium and cholinergic contraction of the rat portal vein and the sheep coronary artery.

To demonstrate the heterogeneity in behavior of the rat portal vein and the sheep coronary artery, we studied the effect of cholinergic stimulation and its dependence upon extracellular ions. Since acetylcholine produces a contraction antagonized by atropine (pA2 9.5), these effects must be mediated by muscarinic receptors. alpha- and beta-adrenergic blocking agents or a drug which destroys noradrenergic nerve endings (6-hydroxydopamine) do not modify the effects of acetylcholine. In a calcium-free medium (EGTA 10(-4) M), the portal vein, unlike the coronary artery, doses not contract to acetylcholine or caffeine. In the coronary artery only the phasic component of the cholinergic contraction is maintained in a calcium-free medium. Verapamil and cobalt abolish the cholinergic contraction of the portal vein, but inhibit only the tonic component in the coronary artery. In a calcium-free medium, hyperosmotic solutions (290 mM sucrose) produce a moderate contraction which occurs slowly in both vessels. In the coronary artery, a sodium-calcium exchange does not appear to participate in the sustained tonic component of the cholinergic contraction. Electron microscopy demonstrates differences between the two blood vessels regarding the size of the sarcoplasmic reticulum. The coronary artery uses calcium both from extra- and intracellular sources. Portal vein is extremely dependent of the extracellular calcium but we were unable to give direct evidence of the utilization of calcium from intracellular pools during the cholinergic contraction of the rat portal vein.

Acetylcholine↗

PubMed1974