| 1. |
- Ahrén, K, et al.
(författare)
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Histamine stimulates progesterone synthesis and cyclic adenosine 3',5'-monophosphate accumulation in isolated preovulatory rat follicles
- 1987
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Ingår i: Neuroendocrinology. - : S. Karger AG. - 0028-3835 .- 1423-0194. ; 46:1, s. 69-74
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Tidskriftsartikel (refereegranskat)abstract
- The effect of histamine on progesterone synthesis and cyclic adenosine 3',5'-monophosphate (cAMP) accumulation was studied in superfused and incubated follicles dissected free from immature rats treated with pregnant mare serum gonadotrophin (PMSG). Histamine, like LH, increased the progesterone synthesis, but to a smaller extent. The H2-antagonist, cimetidine, inhibited completely the histamine-induced progesterone increase while the H1-antagonist, pyrilamine, as well as propranolol and atropine did not affect the initial response but modified its duration. The specific H2-agonist, 4-methylhistamine, but not the H1-agonist, 2-methylhistamine, mimicked the effect of histamine on progesterone synthesis. In the presence of the phosphodiesterase inhibitor, IBMX, histamine increased tissue levels of cAMP. These results suggest that histamine stimulates progesterone synthesis via the H2-receptor with cAMP acting as secondary intracellular messenger.
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| 2. |
- Kannisto, P, et al.
(författare)
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Characterization of presynaptic 5-HT receptors on adrenergic nerves supplying the bovine ovarian follicle
- 1987
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Ingår i: British Journal of Pharmacology. - : Wiley. - 0007-1188. ; 92:3, s. 97-487
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Tidskriftsartikel (refereegranskat)abstract
- 1. The effects of 5-hydroxytryptamine (5-HT) on contraction and release of [3H]-noradrenaline were investigated in vitro in bovine ovarian follicle strips. Using available selective agonists and antagonists, an effort was made to characterize the type of receptor mediating the inhibitory effect of 5-HT on neurogenic contraction and release of [3H]-noradrenaline by electrical field stimulation. 2. 5-Hydroxytryptamine inhibited the neurogenic contraction and release of [3H]-noradrenaline evoked by electrical field stimulation in a concentration-dependent manner. Like 5-HT, 5-carboxamidotryptamine (5-CT) and methysergide reduced the transmitter release as well as the neurogenic contraction, whereas 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) failed to inhibit both responses in concentrations up to 0.1 microM. 3. The 5-HT (1 microM)-induced inhibition of contractile responses was more evident during stimulation at low frequencies (4 and 8 Hz) than during high frequency electrical stimulation (16 and 32 Hz). 4. Methiothepin (1 microM) and methysergide (10 microM) significantly antagonized the inhibitory effect of 5-HT on the electrically evoked release of tritium, whereas cyanopindolol, MDL 72222 and ketanserin (all 0.1 microM) were without effect. In addition, ketanserin, MDL 72222, cimetidine, pyrilamine, atropine, propranolol and indomethacin were without effect on the 5-HT-induced inhibition of the neurogenic contraction. 5. It is suggested that 5-HT inhibits the electrically evoked transmitter release from adrenergic nerves in the bovine ovarian follicle wall via prejunctional 5-HT1-like receptors. This was based on the findings that 5-CT was a potent agonist, methiothepin an antagonist and the lack of effect of MDL 72222, cyanopindolol and ketanserin.
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| 3. |
- Kannisto, P, et al.
(författare)
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Evidence for prejunctional GABAB receptors mediating inhibition of ovarian follicle contraction induced by nerve stimulation
- 1986
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Ingår i: European Journal of Pharmacology. - : Elsevier BV. - 0014-2999. ; 122:1, s. 9-123
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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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| 4. |
- Schmidt, Gunther, et al.
(författare)
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Alteration by histamine of the sympathetic nerve-mediated contractions in the bovine ovarian follicle wall in vitro
- 1987
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Ingår i: European Journal of Pharmacology. - : Elsevier BV. - 0014-2999. ; 135:1, s. 11-22
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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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