Alteration in the reactivity of hamster cheek pouch arterioles to prostaglandin E2 and noradrenaline during pregnancy or sex steroid treatment

Orosz, M; Csapó, István; Varga, B

doi:10.1016/0090-6980(83)90085-0

Prostaglandins

1983

DOI: 10.1016/0090-6980(83)90085-0

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Alteration in the reactivity of hamster cheek pouch arterioles to prostaglandin E2 and noradrenaline during pregnancy or sex steroid treatment

M Orosz

István Csapó

B Varga

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1985

1990

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Cited by 3 publications

(1 citation statement)

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“…Kalsner [ 17] has reported that sex steroids potentiate catechola mine action on the isolated rabbit aortic strips by inhibiting a major mechanism for the inactivation. Progesterone has also been reported to decrease tissue catecholamine content [3] and to blunt the vascular effect of both prostaglandin E: and nor adrenaline [28]. Recently, Fischer and Swain [9] have found that testosterone treatment of castrated male rats resulted in a signif icantly higher arterial blood pressure than that found in ca strated male rats treated with oil vehicle.…”

mentioning

confidence: 99%

Loss of the Effects of Clonidine on the Growth Hormone Release and Hypotensive Action in Long-Term Castrated Rats: The Possible Role of Testosterone on Alpha-2-Adrenergic Mechanisms of Clonidine

Kiem

Stark

1990

Neuroendocrinology

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The effect of testosterone on the growth hormone (GH)-releasing and hypotensive actions of clonidine was evaluated in vivo using male Wistar rats. Clonidine at various doses and by various routes (5 µg/kg, Lev.; 15 µg/kg, i.v., and 7, 15, 31, 125 and 250 µg/kg, i.p.) induced a significant increase in plasma GH levels in rats. Intracerebroventricular (5 µg/kg) injection of clonidine significantly decreased blood pressure. The effects of clonidine on the GH release and blood pressure were lost in long-term castrated rats, but were restored by testosterone replacement in the castrates. In addition, the hypotensive response to clonidine in testosterone-replaced castrated rats lasted longer than in the sham-operated rats. The injection of yohimbine (3 mg/kg, i.p.) strongly inhibited the secretion of GH induced by clonidine treatment in sham-operated animals, and its inhibitory action was significantly attenuated in castrates. In long-term castrated rats, basal blood pressure decreased significantly compared with that of sham-operated rats. This was also restored after testosterone administration to castrates. The results of the present study indicate that the α₂-adrenergic receptor-mediated effects of clonidine on the GH release and blood pressure might be dependent on the endogenous testosterone secretion.

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mentioning

confidence: 99%

Loss of the Effects of Clonidine on the Growth Hormone Release and Hypotensive Action in Long-Term Castrated Rats: The Possible Role of Testosterone on Alpha-2-Adrenergic Mechanisms of Clonidine

Kiem

Stark

1990

Neuroendocrinology

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Vascular catecholamine sensitivity during pregnancy in the ewe

McLaughlin

Keve

Cooke

1989

American Journal of Obstetrics and Gynecology

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Study of the Luteinizing Hormone-Induced Increase of Ovarian Blood Flow During the Estrous Cycle in the Rat

Varga

Horvath

Folly

et al. 1985

Biology of Reproduction

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CYF rats were anesthetized on various days of the 4-day cycle and blood samples were collected at 5-min interals from the ovarian vein before and after i.v. administration of 5 micrograms/100 g BW of luteinizing hormone (LH). Ovarian venous outflow, blood pressure and hematocrit were continuously recorded, and from the blood samples progesterone (P) and 17 beta-estradiol (E2) were determined by radioimmunoassay (RIA). Ovarian blood flow and P secretion showed a parallel increase on Day 1 (estrus), on Day 2, and on the afternoon of Day 4 (proestrous). LH increased ovarian blood flow each day of the cycle together with P and E2 secretion; however, no relationship was seen between the initial value of hormone secretion and the LH-induced increase of ovarian blood flow. Inhibition of hormone secretion by cycloheximide prevented the LH-induced increase of ovarian blood flow; moreover, a decrease in ovarian blood flow parallel with the diminution of hormone secretion was observed. Indomethacin pretreatment abolished the hyperemic effect of LH and partially inhibited the LH-induced increase of hormone secretion. Propranolol blocked the LH-induced increase of ovarian blood flow and blunted the effect of LH on hormone secretion. It was concluded that in LH-induced hyperemia, cAMP, prostaglandins and other vasoactive metabolites released during the process of hormone synthesis, and also a beta-adrenergic mechanism, are involved in the regulation of ovarian blood flow.

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Alteration in the reactivity of hamster cheek pouch arterioles to prostaglandin E2 and noradrenaline during pregnancy or sex steroid treatment

Cited by 3 publications

References 20 publications

Loss of the Effects of Clonidine on the Growth Hormone Release and Hypotensive Action in Long-Term Castrated Rats: The Possible Role of Testosterone on Alpha-2-Adrenergic Mechanisms of Clonidine

Loss of the Effects of Clonidine on the Growth Hormone Release and Hypotensive Action in Long-Term Castrated Rats: The Possible Role of Testosterone on Alpha-2-Adrenergic Mechanisms of Clonidine

Vascular catecholamine sensitivity during pregnancy in the ewe

Study of the Luteinizing Hormone-Induced Increase of Ovarian Blood Flow During the Estrous Cycle in the Rat

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