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S St-Pierre

Publications and source records attributed to S St-Pierre.

At least 145 records · Page 8Linked to original sources
PubMed1983

Structure-activity studies on neurobehavioral effects of bombesin (BB) and gastrin releasing peptide (GRP).

In the present study, we evaluated and compared effects of BB, GRP and related C-terminal fragments on body temperature and grooming. Peptides were administered into the left cerebral ventricle of rats. Body temperature and grooming behavior were assessed over a 2 hr period following injections. All peptides significantly decreased body temperature and increased grooming behavior of animals. However, important differences in potency, efficacy and duration of action were found between BB, GRP and their fragments.

Amino Acid Sequence↗
PubMed1983

Evaluation of the contribution of mast cell mediators to the hypotensive activity of various peptides in rats.

We have tested the effects of intravenous injections of substance P (SP), bradykinin (BK), somatostatin (SS) and vasoactive intestinal peptide (VIP) on the blood pressure, histaminemia and hematocrit in pentobarbital-anesthetized rats. The four peptides elicited a decrease of the mean arterial blood pressure which varied both in amplitude and in duration depending both on the peptide and on the doses utilized. The hypotensive effects of SP and VIP were more persistent than those caused by BK or SS. Only SP evoked an increase of histaminemia. Both SP and BK caused an increase of hematocrit. The change of hematocrit was more prominent and of longer duration after Sp than after BK. Pretreatment of rats with the antiinflammatory drug dexamethasone inhibited markedly the changes of blood pressure, histaminemia and hematocrit caused by SP. The hypotensive effects of BK, SS and VIP as well as the transient change of hematocrit evoked by BK were not affected by dexamethasone. The results suggest that part of the hypotensive activity and changes of hematocrit evoked by SP in rats is due to the release and action of histamine and possibly of other vasoactive substances, of mast cell origin. The results also indicate that mast cell mediators, particularly histamine, are unlikely to be instrumental in the hypotensive activity of BK, SS or VIP in rats.

Animals↗
PubMed1983

Partial blockade of neurotensin-induced hypotension in rats by nephrectomy captopril and saralasin. Possible mechanisms.

We have assessed the influence of acute bilateral nephrectomy, of captopril and saralasin, on the hypotensive activity of neurotensin (NT) and of various hypotensive drugs in pentobarbital-anesthetized rats. The results show that the hypotensive activity of NT and of compound 48/80 (C48/80), in contrast to that of histamine, of 5-hydroxytryptamine and of hexamethonium, is markedly reduced, especially for NT, in nephrectomized as compared to sham operated rats. The pretreatment of rats with captopril (10 mg kg-1, i.v.) or with saralasin (20 micrograms kg-1 min-1, i.v.) was found to inhibit significantly the hypotensive activity of NT and of C48/80. Adrenalectomy restored partially the hypotensive activity of NT in nephrectomized rats. The potent vasopressin antagonist [d(CH2)5 Tyr(Me)AVP] did not alter the refractoriness of nephrectomized rats to the hypotensive activity of NT. Neither nephrectomy nor saralasin were found to interfere with the ability of NT or of C48/80 to evoke an increase of plasma histamine level or of the hematocrit. The results were interpreted as an indication that NT produces part of its hypotensive effect in anesthetized rats by reducing the activity of the renin angiotensin system. The results also suggest that part of the refractoriness of nephrectomized rats to the hypotensive activity of NT could be due to the release of catecholamines from adrenal glands by NT. Endogenous vasopressin does not appear to contribute to the refractoriness of nephrectomized rats to the hypotensive action of NT.

Angiotensin II↗
PubMed1983

Neurotensin affects hyperactivity but not stereotypy induced by pre and post synaptic dopaminergic stimulation.

The effects of intraventricular administration of neurotensin (0.9, 3.75 and 15.0 micrograms) on hyperactivity and stereotypy induced by either amphetamine (1 mg/kg), nomifensine (20 mg/kg), apomorphine (0.5 mg/kg) or N-n-propylnorapomorphine (0.5 mg/kg) were examined. Results indicate that for each drug treatment, the effects of neurotensin were identical: hyperactivity was significantly reduced while stereotypy remained unaffected. Results also revealed that neurotensin significantly increased the hypothermia induced by apomorphine and N-n-propylnorapomorphine. Possible mechanisms which could underly neurotensin's selective inhibitory action on hyperactivity produced by both pre and post synaptic dopaminergic stimulation are discussed.

Amphetamine↗
PubMed1983

Response of urethral smooth muscles to pharmacological agents. II. Noncholinergic, nonadrenergic agonists and antagonists.

We studied the effects of a variety of noncholinergic, nonadrenergic agents on the smooth muscles of the cat urethra. Prostaglandin F2 alpha contracted both urethral muscle layers to a similar extent. Prostaglandin E2 contracted the longitudinal and relaxed the circular muscle layers. The effects of the prostaglandins seem to be directly myogenic since cholinergic and adrenergic blockers and tetrodotoxin did not affect them. Bradykinin and substance P contracted both urethral muscle layers. Other tested agonists (neurotensin, vasoactive intestinal peptide, cyclic 3,5 adenosine monophosphate, adenosine diphosphate sodium, cyclic 3,5 guanosine monophosphate sodium, bombesin) had no effect on the cat urethral smooth muscles.

Animals↗
PubMed1983

Primary structure determination of Escherichia coli heat-stable enterotoxin of porcine origin.

The chemical characterization of Escherichia coli heat-stable enterotoxin (ST) is described. The toxin was isolated and purified to homogeneity from the E. coli strain F11 (PI55) of porcine origin. Following quantitative amino acid analysis, the enterotoxin was found to contain 18 amino acids including 6 cysteines, but was devoid of Ser, Val, Met, Ile, Lys, His, and Arg residues. All cysteine residues were found to be involved in disulfide bridges, even though their positions could not be localized. The enterotoxin thus has a molecular weight of 1979 and was shown to be an octadecapeptide with the following sequence: H2N-Asn-Thr-Phe-Tyr-Cys-Cys-Glu-Leu-Cys-Cys-Asn-Pro-Ala-Cys-Ala-Gly-Cys-Tyr- COOH. Its relationship to other known enterotoxins is discussed.

Amino Acid Sequence↗
PubMed1983

[Amanita virosa peptides: viroidin and viroisin are more effective than phalloidin for the in vitro protection of actin against the effects of osmic acid].

Virotoxins are a group of monocyclic peptides recently identified in the deadly mushroom Amanita virosa by Faulstich and coll. We found that two of these peptides, which have a methyl sulfonyl group, namely viroidin and viroisin are very effective to protect F-actin against oxidative degradation by osmium tetroxide in vitro. Their desoxo analogs, which have a methyl sulfoxyde group instead of methyl sulfonyl are less active, therefore there exists a relationship between the chemistry of the sulfur group and the activity of the peptides.

Actins↗
PubMed1982

Characterization of substance P and somatostatin receptors on adrenal chromaffin cells using structural analogues.

Substance P (SP) and somatostatin (SRIF) are known to inhibit the nicotine-induced release of catecholamines (CAs) from isolated adrenal chromaffin cells in culture22,24. In order to characterize the receptors mediating this action, we have tested several SP and SRIF analogues for their effects on release of [3H]L-norepinephrine ([3H]NE) from chromaffin cell cultures. SP-free acid and a series of 11 SP analogues, in which each amino acid of SP is replaced in turn by L-alanine, all inhibited the nicotine-induced release of [3H]NE from these cultures. The rank order of potency of the analogues for this action was similar to their reported order of potency in other SP-responsive tissues. The least potent were SP-free acid, [Ala7]-SP, [Ala10]-SP, [Ala8]-SP and [Ala11]-SP, while the potencies of the Ala 1 to 6 analogues and [Ala9]-SP were closer to that of SP. [Leu7]- and [Leu7,8]-SP had potencies similar to that of SP. SP itself had no effect on basal [3H]NE release and only the highest concentrations of some of the analogues tested had an effect (enhancement) on basal [3H]NE release. The results suggest that adrenal chromaffin cells possess a specific SP receptor mediating inhibition of agonist-induced CA release and that the binding site of this receptor shares similar structural requirements with the binding site of the SP receptor on other tissues. Several SRIF analogues, which have been previously shown to be more potent than native SRIF at selective SRIF receptors2,3,31, 35, were compared to SRIF for effects on [3H]NE release from chromaffin cell cultures. These analogues were found to be active but less potent than SRIF in inhibiting nicotine-induced [3H]NE release from these cultures, suggesting that the site mediating this action differs in its structural requirements from the SRIF receptor found in some other tissues.

Adrenal Medulla↗
PubMed1982

Kininases and vascular responses to kinins.

We have utilized several inhibitors to assess the effects of kininases on the contractile activity of bradykinin (BK), kallidin (KD), des-Arg9-BK and des-Arg10-KD on two isolated blood vessels, the rabbit aorta and mesenteric vein. The response of the two vessels to kinins are mediated by B1-receptors, implying that fragments of kinins without the C-terminal arginine are much more active on these tissues than the whole kinin sequences. Blockers of carboxypeptidase B-like enzymes, such as SQ24798 and pivalyl-L-arginine decrease the apparent affinity of BK and KD on the two vessels, while not changing those of des-Arg9-BK and des-Arg10-KD; this suggests that a major part of the contractile activities of BK and KD are mediated by des-Arg metabolites formed in situ at the tissue level by a kininase I. The block of kininase II by captopril or desacetylated MK-421 bring about a complex pattern of activity changes that include the potentiation of BK and KD and the depression of des-Arg10-KD. These results, in conjunction with those obtained with the non-specific inhibitors of metallopeptidases, thioglycolic acid and EDTA, suggest that the relative contribution of kininase I and kininase II to the degradation of kinins in arterial and venous vessels may be different. The implications of these findings on the pharmacology of B1-receptors are discussed.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1982

Influence of various drugs on the variations of blood pressure, hematocrit and plasma histamine caused by neurotensin and compound 48/80 in rats.

Intravenous injections of neurotensin (NT) (0.5, 1 and 2 nmoles kg-1) evoked dose-dependent increases in histaminemia and hematocrit, and marked hypotensive effect, in anesthetized rats. The increase of plasma histamine was rapid in onset (within sec), peak plasma histamine being reached in less than 2 min. The decline of plasma histamine was gradual and almost complete 15 min after injection of NT. The hematocrit increased slowly, maximum values being obtained 5-10 min after injection of NT, and it persisted throughout the period of observation. The hypotensive effect of NT was rapid in onset and of prolonged duration. Compound 48/80, a well known histamine liberator and mast cell depletor, produced variations of blood pressure, of hematocrit and of plasma histamine very similar to those elicited by NT. Pretreatment of rats with cromoglycate, a well known mast cell stabilizer, or with dexamethasone, inhibited markedly the changes of histaminemia, of hematocrit and of blood pressure evoked by NT and compound 48/80. The results clearly suggest that the effects of NT on blood pressure and on vascular permeability in rats are mediated to some extent by mast cell histamine. Hexamethonium, a ganglion blocker, inhibited slightly the effect of NT on histaminemia but it did not block NT-induced changes of hematocrit. However, the hypotensive effect of NT was severely blocked in hexamethonium-treated rats. These results were interpretated as an indication that hexamethonium prevents NT-induced hypotension not merely by reducing the mobilization of mast cell histamine by NT but most likely by interfering with the mechanism by which NT and/or its mast cell mediators produce their effects on blood pressure.

Animals↗
PubMed1982

Synthesis of peptides by the solid-phase method. 7. Substance P and analogues.

Substance P and 21 related peptides containing isosteric or isofunctional groups were prepared by the solid-phase method. After purification by gel filtration and ion-exchange chromatography, the compounds were characterized by thin-layer chromatography, paper electrophoresis, and amino acid and elemental analysis. The biological activities of the peptides were evaluated in vitro on the guinea pig ileum, the rabbit mesenteric vein, and the dog common carotid artery and in vivo on the rat blood pressure. It is shown that the replacement of some residues in the undecapeptide substance P causes variable losses of apparent affinity with a little or no change in the intrinsic activity. All the analogues used in the present study were found to be inactive as antagonists.

Animals↗
PubMed1982

Dynorphin in bovine adrenal medulla. I. Detection in glandular and cellular extracts and secretion from isolated chromaffin cells.

The presence and secretion of immunoreactive dynorphin in bovine adrenal medulla and isolated adrenal chromaffin cells were examined and compared with those of immunoreactive leucine-enkephalin. Using an antiserum raised against dynorphin-(1-13), a sensitive and highly specific radioimmunoassay was developed. A nearly intact antigen was required for recognition by the antiserum since it did not react with leucine-enkephalin and reacted poorly with dynorphin-(1-12) (cross-reactivity 0.5%) and other fragments of dynorphin-(1-13). On the other hand, the antibody used for detection of leucine-enkephalin did not cross-react with dynorphin(1-13). Adrenal medulla acid extracts contained 195 times more immunoreactive leucine-enkephalin than dynorphin. However, the concentration of immunoreactive dynorphin in acid extract of freshly isolated adrenal chromaffin cells was only 1.4 times smaller than that of leucine-enkephalin. Incubation of the isolated chromaffin cells in the presence of acetylcholine, nicotine, high potassium, but not muscarine, induced a concomitant release of immunoreactive dynorphin (3.5-9% of total cell content) and leucine-enkephalin (6.5-11.4% of total cell content).

Acetylcholine↗