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Träfflista för sökning "L773:1879 0712 OR L773:0014 2999 srt2:(1985-1989)"

Sökning: L773:1879 0712 OR L773:0014 2999 > (1985-1989)

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1.
  • Wallengren, Joanna, et al. (författare)
  • Effects of substance P, neurokinin A and calcitonin gene-related peptide in human skin and their involvement in sensory mediated responses.
  • 1987
  • Ingår i: European Journal of Pharmacology. - : Elsevier BV. - 1879-0712 .- 0014-2999. ; 143:2, s. 267-273
  • Tidskriftsartikel (refereegranskat)abstract
    • The effects evoked by intradermal injections of substance P (SP), neurokinin A (NKA) or calcitonin gene-related peptide (CGRP) were studied in 51 non-atopic subjects. SP and NKA produced flare and weal, and CGRP produced an indurated erythema. The reactions to SP were strong, the flare being maximal 3–5 min after injection and the weal after 10–15 min. NKA evoked a much weaker flare and a slightly weaker weal than did SP. CGRP produced a prominent long-lasting, indurated erythema with pseudopodia surrounded by a pallor edge. The mode of action of the three peptides was studied by pretreatment of the skin with the histamine-releasing compound 48/80, the H1-antagonist mepyramine or the local anesthetic xylocaine. The results suggest that mast-cell histamine and an intact sensory nerve supply are essential for the flare response to both SP and NKA. The weal response to SP was somewhat reduced by pretreatment with either 48/80 or xylocaine. The weal response to NKA, however, did not seem to depend upon either mast cells or sensory nerve fibres. The erythema evoked by CGRP was not suppressed by pretreatment with xylocaine, compound 48/80 or mepyramine, suggesting a direct action of CGRP on the blood vessels. The interaction between SP and CGRP was studied in subjects receiving a low dose of CGRP and increasing doses of SP or a low dose of SP and increasing doses of CGRP. CGRP did not potentiate the SP-evoked flare and weal and SP did not seem to enhance the response to CGRP.
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2.
  • Kannisto, P, et al. (författare)
  • Evidence for prejunctional GABAB receptors mediating inhibition of ovarian follicle contraction induced by nerve stimulation
  • 1986
  • Ingår i: European Journal of Pharmacology. - : Elsevier BV. - 0014-2999. ; 122:1, s. 9-123
  • Tidskriftsartikel (refereegranskat)abstract
    • The motor effects of gamma-aminobutyric acid (GABA) on the bovine ovarian follicle were studied in vitro using strips from follicle walls. Electrical field stimulation of nerves in the preparation, secured by tetrodotoxin blockade, caused a contraction that was almost totally abolished by phentolamine and only slightly affected by atropine. This mainly adrenergic neurogenic response was inhibited by GABA in a dose-dependent way. The GABAA-receptor antagonists, bicuculline and picrotoxin, did not affect the GABA action whereas the GABAB-receptor antagonist, homotaurine, significantly inhibited the GABA effect. The GABAA-receptor agonist, muscimol, did not affect the contractile response while the GABAB-receptor agonist, baclofen, imitated the action of GABA. On the other hand, GABA had no direct contractile or relaxing effect on the follicle strips nor did it interfere with the contractile response induced by noradrenaline or acetylcholine. The findings suggest that activation of prejunctional GABAB receptors inhibits transmitter release from mainly adrenergic nerves associated with the follicle, thereby affecting nerve-mediated tension in the follicle wall.
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3.
  • Kannisto, Päivi, et al. (författare)
  • Extracellular and intracellular calcium sources mediating contractile responses of smooth muscle in bovine ovarian follicle and ovarian artery
  • 1987
  • Ingår i: European Journal of Pharmacology. - : Elsevier BV. - 0014-2999. ; 144:3, s. 299-308
  • Tidskriftsartikel (refereegranskat)abstract
    • The relative importance of extracellular and intracellular calcium sources mediating smooth muscle contraction in ovarian follicle and ovarian artery was assessed in experiments on the influence of nifedipine, D-600, amrinone, diethylstilbestrol (DES), lanthanum and/or calcium removal on contractions induced by K+ depolarization, by noradrenaline, histamine and acetylcholine. The K+-induced response was biphasic in the ovarian artery but not in the ovarian follicle. The K+-induced contraction in both preparations was greatly inhibited by nifedipine (1 μM), D-600 (10 μM) and lanthanum (2 mM). Although both phases of the responses in the ovarian artery appeared to be completely dependent on extracellular calcium, phase I was significantly more sensitive to nifedipine than phase II. Incubation in calcium-free medium for 15 min almost abolished the K+-induced contraction. Noradrenaline- and histamine-induced contractions of ovarian follicle were essentially unaffected by nifedipine (1 μM) and D-600 (10 μM) whereas the noradrenaline-induced contraction in ovarian artery was inhibited significantly by D-600 (1 and 10 μM) but not nifedipine (1 μM). In calcium-free medium containing EGTA (1 mM) the responses of ovarian follicle to noradrenaline and histamine were reduced by 26 and 22% respectively. When preparations were stimulated with noradrenaline more than one in calcium-free medium, the contraction decreased progressively compared to time-matched controls. The response was 34% of the control after 50 min in calcium-free medium containing EGTA. In the ovarian artery the response obtained (6% of control) was significantly smaller (P < 0.05) than that in the follicle. Amrinone (100 μM) inhibited both noradrenaline- and K+-induced contractions to a similar degree (about 40%) in the follicle wall. The results indicate that agonist-induced responses of ovarian follicle and artery are mediated by the release of calcium from intracellular stores in addition to influx of extracellular calcium. In contrast, the K+-induced contraction seems to be totally dependent on extracellular calcium. The difference in sensitivity to nifedipine of the two phases of the K+ response in ovarian artery strongly suggests the presence of two different types of K+-activated calcium channels in this smooth muscle.
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4.
  • Schmidt, Gunther, et al. (författare)
  • Alteration by histamine of the sympathetic nerve-mediated contractions in the bovine ovarian follicle wall in vitro
  • 1987
  • Ingår i: European Journal of Pharmacology. - : Elsevier BV. - 0014-2999. ; 135:1, s. 11-22
  • Tidskriftsartikel (refereegranskat)abstract
    • The histaminergic effect on electrically induced contractions and tritium release was studied in vitro, using strips from the wall of mature bovine ovarian follicles. Follicular fluid and blood plasma from the animals were analysed for electrolyte, bicarbonate, glucose and total protein concentrations in order to compare them with the concentrations of these components in the Krebs-Ringer solution used in the experiments. Electrical field stimulation (EFS) of the follicle strip caused a contraction which was completely blocked by tetrodotoxin and was predominantly of adrenergic origin since phentolamine, in contrast to atropine, blocked the response. The neurogenic response was inhibited by histamine in a concentration-dependent way via the H1-receptor since the H1-antagonist, pyrilamine, counteracted the inhibitory effect of histamine while the H2-antagonist, cimetidine, potentiated the effect. This histaminergic response of EFS-induced contractions could be reproduced in experiments where the H1-agonist, 2-methylhistamine, was inhibitory while the H2-agonist, 4-methylhistamine, had no obvious influence on the twitch response. Histamine reduced the contractile response to exogenous noradrenaline via the H1-receptor, because pyrilamine counteracted, and cimetidine potentiated the effect. The histamine-induced depression of the motor response to EFS and exogenous noradrenaline was probably due to a postjunctional effect mediated by the H1-receptor. Experiments utilizing [3H]noradrenaline release during EFS did not suggest prejunctional effects of histamine. Chemical determinations on follicle fluid and plasma showed that the artificial follicular fluid imitated well the environmental conditions the follicle wall is exposed to in situ.
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