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Biomedical subjects

J C Stoclet

Publications and source records attributed to J C Stoclet.

At least 163 records · Page 9Linked to original sources
PubMed1978

Variations in endogenous phosphodiesterase activator content of rat aorta.

The variations with age and blood pressure in the cyclic nucleotide phosphodiesterase activator content of rat aorta were studied. Activator content increased with age and was less in mineralocorticoid-hypertensive than in control rats. These variations were more pronounced in the particulate than in the soluble fraction of aorta. The data do not demonstrate any relationship between the activator level and blood pressure, but they suggest that the activator may modulate cyclic nucleotide metabolism in rat aorta.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1978

Flavonoid compounds are potent inhibitors of cyclic AMP phosphodiesterase.

The inhibitory activity of 19 flavonoid molecules on cyclic AMP breakdown by a commercial beef heart phosphodiesterase preparation is reported. 7 compounds are active in the micromolar range, 2 of which have a potency equivalent to that of papaverine. Some structure activity relationships are drawn.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1977

Effect of papaverine on cyclic nucleotide levels in the isolated rat aorta.

An increase in cAMP but no significant modification in cGMP content could be demonstrated in rat aorta strips after applying papaverine in concentrations which reduced contractile responses. Accumulation of cAMP was induced in noradrenaline-stimulated on K+-depolarized strips, under omission of external Ca2+. Thus the elevation of cAMP level preceded the reduction of contraction subsequently elicited by readdition of Ca2+. The effects could not be dissociated under the experimental conditions used here.

Animals↗
PubMed1975

Papaverine, cyclic AMP and the dependence of the rat aorta on extracellular calcium.

The spasmolytic effects of papaverine and dibutyryl cyclic AMP (db-cAMP) were compared on isometric contractile responses induced by addition of increasing amounts of external calcium to K+-depolarized or noradrenaline-stimulated rat aorta strips. Papaverine at a concentration active on depolarized strips (3 times 10(-5) moles/1) reduced the maximal contraction (Emax) elicited by Ca2+ in these preparations, while db-cAMP did not. Contrary to what was observed on depolarized aortae, the degree of inhibition of noradrenaline-stimulated strips did not decrease with increasing extracellular calcium concentration (Ca)e. Both db-cAMP and papaverine at a concentration which did not depress Emax (5 times 10(-6) moles/1) potentiated the relaxing effect of high (Ca)e on contractions elicited by noradrenaline. In conclusion, cyclic AMP is probably implicated in the mode of action of papaverine on the noradrenaline-stimulated rat aorta. At a concentration active on depolarized strips, papaverine is also able to impair contractility directly.

Animals↗
PubMedDate not supplied

Effect of lipopolysaccharide treatment on neurogenic contraction and noradrenaline release in rat arteries.

In the present study, contractile responses and [3H]-noradrenaline overflow evoked by electrical field stimulation were assessed, respectively, in the small mesenteric artery and in tail artery removed from rats pre-treated with either saline or lipopolysaccharide (LPS). In small mesenteric arteries, LPS treatment did not significantly modify the contractile responses elicited by electrical stimulation, in the absence or in the presence of L-arginine. However, in arteries removed from rats treated with LPS, L-arginine addition produced relaxation of vessels pre-contracted with noradrenaline. The amplification of neurogenic contraction by the nitric oxide (NO) synthase inhibitor Nomega-nitro-L-arginine methyl ester (L-NAME) was similar in arteries removed from saline and LPS-infused rats. In mesenteric arteries, LPS treatment suppressed the potentiation of the neurogenic responses by the alpha2-adrenoceptor antagonist, yohimbine and by the inhibitor of neuronal uptake of noradrenaline, cocaine. In rat tail artery exposed to L-arginine, LPS treatment produced an increase in [3H]-noradrenaline overflow evoked by electrical stimulation. Altogether, these data suggest that an enhanced noradrenaline release from sympathetic nerves, probably resulting from inhibition of the modulatory effect of both prejunctional alpha2-adrenoceptors and neuronal uptake mechanism, may play a role in the preservation of neurogenic response after LPS treatment despite evidence of the induction of NO synthase.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

Neuropeptide Y increases force development through a mechanism that involves calcium entry in resistance arteries.

The hypothesis that neuropeptide Y (NPY) potentiates noradrenaline (NA)-induced vascular force development by increasing free intracellular Ca2+ ([Ca2+]i) was tested in rat mesenteric resistance arteries. NPY (100 nM) alone was not able to increase either the contraction or [Ca2+]i. However, pretreatment of mesenteric resistance arteries with 100 nM NPY potentiated both [Ca2+]i and active stress induced by 1.5 microM NA. Addition of 100 nM NPY to vessels that had been precontracted with NA (1.5 microM) elicited a large increase in [Ca2+]i and an increase in active stress development. In Ca(2+)-free medium containing 2 mM ethylene glycol-bis(beta-aminoethyl ether) N,N,N',N'-tetraacetic acid, the potentiating effect of NPY on the NA-induced contraction was prevented, and readdition of Ca2+ resulted in a large increase in both [Ca2+]i and active stress development. It is concluded that NPY potentiates NA-induced contraction in the isolated mesenteric resistance artery by inducing a rise in [Ca2+]i through an influx of Ca2 from the extracellular source.

Animals↗