scholarly journals The regulation by ovarian steroids of prostaglandin synthesis and prostaglandin-induced contractility in non-pregnant rat myometrium. Modulating effects of isoproterenol

2001 ◽  
Vol 169 (1) ◽  
pp. 33-41 ◽  
Author(s):  
T Engstrom

The objectives of the present study were to investigate the effects of the reproductive steroids oestradiol and progesterone on myometrial levels of cyclooxygenase-2 (COX-2) mRNA and PGF(2alpha) induced myometrial contractility and to study whether the effect of beta(2)-adrenoceptor stimulation by isoproterenol on the myometrium alters these parameters. Oestrogen treatment of ovariectomized rats increased myometrial COX-2 mRNA whereas PGF(2alpha) receptor (PGF(2alpha)-R) mRNA was unchanged following this treatment and maximal contractility (E(max)) of isolated uterine strips challenged with PGF(2alpha) was unaltered. Progesterone treatment alone decreased COX-2 mRNA in comparison with values obtained from oestrogen-treated animals, and in combination with oestrogen the enhancing effect of progesterone on COX-2 mRNA was curbed. EC(50) of uterine strips challenged with PGF(2alpha) increased following oestrogen treatment whereas this parameter was substantially decreased following progesterone treatment. When oestrogen was combined with isoproterenol infusion mRNA values of both COX-2 and PGF(2alpha)-R were reduced. Finally, when isoproterenol infusions were given in combination with both oestrogen and progesterone, PGF(2alpha)-R mRNA and E(max )were enhanced as compared with similar rats not having received isoproterenol. We conclude that oestrogen increases COX-2 mRNA production and subsequent prostaglandin synthesis in non-pregnant rat myometrium. We further conclude that in the oestrogen-dominated rat myometrium the relaxing effect of beta(2)-adrenoceptor stimulation involves attenuation of both prostaglandin synthesis and PGF(2alpha)-R expression. We finally conclude that in the presence of both oestrogen and progesterone this effect of beta(2)-adrenoceptor stimulation is restrained.

1974 ◽  
Vol 63 (1) ◽  
pp. 13-20 ◽  
Author(s):  
NELIA T. VERMOUTH ◽  
R. P. DEIS

SUMMARY Ovariectomy of rats on day 19 of pregnancy induced a rapid rise in serum prolactin. Levels were significantly increased 4 h after removal of the ovaries and continued to rise up to 24 h. A transient fall occurred at 32 h, but serum prolactin concentration was still raised after 36, 48 and 58 h. Similar increases of serum prolactin occurred after ovariectomy on days 17 and 18 of pregnancy. Lactogenesis occurred 24·8 or 28·2 h after ovariectomy on days 19 or 17–18 of pregnancy respectively. Rats ovariectomized on day 17 or 18 delivered on day 21 and rats ovariectomized on day 19 delivered on day 22 of pregnancy. Ovariectomy impaired parturition in all groups. Treatment with oestrogen immediately after the operation did not prevent the rise in serum prolactin levels 4, 8 and 12 h after ovariectomy, but 24 h after ovariectomy, prolactin values were not significantly different from those in sham-operated control rats. When oestrogen was injected 12 h after ovariectomy, serum prolactin was markedly increased 12 h later. Lactogenesis occurred about 22·9 h after oestrogen treatment and all animals delivered on day 21 of pregnancy. Progesterone treatment prevented the rise in prolactin levels observed 4 and 8 h after ovariectomy, but at 12 h levels had risen and were similar to those observed in untreated ovariectomized rats. Progesterone prevented lactogenesis for 14 h (around 37.5 h after ovariectomy) and induced a delay in the onset of parturition. The results indicate that the decrease of progesterone in the blood after ovariectomy in pregnant rats may induce a release of prolactin and lactogenesis. Oestrogen seems to be effective in raising prolactin levels at low blood concentrations of progesterone.


1992 ◽  
Vol 267 (12) ◽  
pp. 7975-7978
Author(s):  
V Vivat ◽  
J Cohen-Tannoudji ◽  
J.P. Revelli ◽  
P Muzzin ◽  
J.P. Giacobino ◽  
...  

1982 ◽  
Vol 94 (2) ◽  
pp. 177-182 ◽  
Author(s):  
Takashi Higuchi ◽  
Masazumi Kawakami

Changes in the characteristics of LH secretory pulses in female rats were determined in different hormonal conditions; during the oestrous cycle and after ovariectomy and oestrogen treatment. The frequency and amplitude of the LH pulses were stable during the oestrous cycle except at oestrus when a pattern could not be discerned because of low LH concentrations. These were significantly lower than those measured during other stages of the cycle. Mean LH concentrations and LH pulse amplitudes increased with time up to 30 days after ovariectomy. The frequency of the LH pulse was unchanged 4 days after ovariectomy when mean LH levels had already increased. The frequency increased 10 days after ovariectomy and then remained stable in spite of a further increase in mean serum LH concentrations. Oestradiol-17β injected into ovariectomized rats caused a decrease in LH pulse amplitude but no change in pulse frequency. One day after treatment with oestradiol benzoate no LH pulse was detectable, probably because the amplitude was too small. A generator of pulsatile LH release is postulated and an oestrogen effect on its function is discussed.


1970 ◽  
Vol 46 (3) ◽  
pp. 341-346 ◽  
Author(s):  
K. P. MEYERS

SUMMARY Ovariectomized rats treated with 2·5 or 5·0 mg. progesterone daily received a single subcutaneous injection of 0·2 μg. oestradiol on the third day of the progesterone treatment. The deciduomal response to trauma by endometrial scratching was used to determine the degree of uterine sensitivity at various times after oestradiol. Uterine sensitivity was partially and then completely lost 36 and 48 hr. after oestradiol administration. The inhibition of uterine sensitivity persisted until 9 and 11 days after oestradiol when the animals received 2·5 and 5·0 mg. progesterone daily. Uterine sensitivity was completely inhibited on day 11 with doses of oestradiol from 0·2 to 0·05 μg. Withdrawal of progesterone treatment for 48 or 72 hr., but not for 24 hr., after oestradiol treatment restored uterine sensitivity. These results show that the oestradiol-induced inhibition of uterine sensitivity in the progestational endometrium is maintained by continuous progesterone treatment and that the duration of this effect is dependent on the dose of progesterone given.


1972 ◽  
Vol 54 (1) ◽  
pp. 39-45 ◽  
Author(s):  
Z. DICKMANN

SUMMARY The effects of progesterone, medroxyprogesterone acetate (MPA), and oestrone on shedding and dissolution of the zona pellucida were studied in intact pregnant rats, ovariectomized pregnant, and ovariectomized pseudopregnant rats into whose uteri blastocysts had been transferred. Treatment with progesterone, MPA and oestrone delayed shedding of the zona. The highest percentage of blastocysts delaying, and with the longest delay period, occurred in ovariectomized, progesterone-treated rats. Ovariectomy of pregnant rats, and treatment of ovariectomized rats with progesterone, MPA or oestrone, delayed dissolution of the zona. Oestrone together with progesterone caused both shedding and dissolution of the zona within 24 h. It is deduced that in the intact pregnant rat, the synergistic action of oestrogen superimposed on progesterone synchronizes shedding and dissolution of the zona so that they occur together at a specified time.


1990 ◽  
Vol 258 (1) ◽  
pp. E191-E202 ◽  
Author(s):  
L. J. Van Tits ◽  
M. C. Michel ◽  
H. Grosse-Wilde ◽  
M. Happel ◽  
F. W. Eigler ◽  
...  

We investigated the mechanisms underlying the increase in mononuclear leukocyte (MNL) beta 2-adrenergic receptor (AR) number and responsiveness after acute infusion of catecholamines. Infusion of isoproterenol and epinephrine, but not of norepinephrine, acutely increased MNL beta-AR density, and this was blocked by the beta 2-selective antagonist ICI 118,551 but not by the beta 1-selective antagonist bisoprolol, suggesting a beta 2-AR-mediated effect. Infusion of isoproterenol but not of norepinephrine also induced a lymphocytosis, with an increase in the number of circulating suppressor/cytolytic T (Ts/c)- and natural killer (NK)-cells but a decrease in helper T (Th)-cells, leading to a decreased Th-Ts/c-cell ratio. beta-AR density was higher in Ts/c-cells than in Th-cells. After isoproterenol infusion, beta-AR density was elevated in all lymphocyte subsets but not in monocytes or platelets, suggesting a lymphocyte-specific phenomenon. Infusion of isoproterenol in splenectomized patients did not alter lymphocyte subset composition and only slightly increased beta 2-AR density. In healthy subjects lymphocyte proliferation in response to various mitogens was attenuated after infusion of isoproterenol but not of norepinephrine; this effect was abolished in splenectomized patients. We conclude that the elevated MNL beta-AR density after acute exposure to beta-adrenergic agonists is caused by a release of lymphocyte subsets from the spleen into the circulation and/or by an exchange of lymphocyte subsets between the spleen and the circulation, whereby freshly released splenic lymphocytes appear to carry more beta-AR than those found in the circulation. This appears to impair immune responsiveness in a dual manner, by decreasing the Th-/Ts/c-cell ratio and by rendering lymphocytes more sensitive to the antiproliferative effects of catecholamines via a higher beta-AR density.


1993 ◽  
Vol 139 (2) ◽  
pp. 253-258 ◽  
Author(s):  
A. M. Salicioni ◽  
R. W. Carón ◽  
R. P. Deis

ABSTRACT There is evidence that the adrenals play a role in the regulation of the synthesis and release of gonadotrophins in various vertebrates. The aim of this study was to determine the part played by adrenal steroids, with special reference to progesterone, on the concentration of LH in ovariectomized (OVX) and oestrogen-primed rats. OVX rats received a single s.c. injection of vehicle or oestradiol benzoate (OB, 20 μg/rat). This day was designated as day 0. Three or four days later (day 3–day 4), the rats were treated with mifepristone (10 mg/kg) or with two doses of progesterone antiserum and blood samples were obtained at 13.00 and 18.00 h. OB treatment of OVX rats reduced serum LH at 13.00 h and 18.00 h on day 3 but only at 13.00 h on day 4. The administration of mifepristone at 08.00 h to OVX and oestrogen-treated rats induced a significant increase in serum LH at 18.00 h on days 3 and 4, without modifying the values at 13.00 h. When mifepristone was given at 13.00 h a much larger increase in serum LH was obtained at 18.00 h. In OVX and oestrogen-treated rats, adrenalectomy on day 2 (08.00–09.00 h) induced an increase in serum LH at 18.00 h similar to that observed in the OVX and oestrogen-primed rats after mifepristone treatment. In order to determine the specificity of the effect of mifepristone, a group of OVX and oestrogentreated rats was injected with progesterone antiserum at 08.00 and 13.00 h on day 3. Serum LH concentrations at 13.00 and 18.00 h on day 3 were similar to values obtained in OVX rats treated with oestrogen and mifepristone. Serum progesterone was measured at 08.00 and 13.00 h in OVX and OVX and oestrogenprimed rats. At both times, values were similar in OVX rats but oestrogen treatment significantly increased serum progesterone levels. The important role of adrenal progesterone on the regulation of LH secretion in OVX and oestrogen-primed rats is evident from these results. Blocking progesterone action at the receptor level, we showed that OB significantly increased LH values at 18.00 h. On the basis of these studies it is tempting to speculate on the possibility of an inhibitory or stimulatory effect of oestrogen on serum LH concentration in OVX rats, according to the presence or absence of adrenal progesterone action. Journal of Endocrinology (1993) 139, 253–258


1966 ◽  
Vol 51 (2) ◽  
pp. 231-244 ◽  
Author(s):  
Andrew B. Kaufman ◽  
I. Rothchild

ABSTRACT The effect of progesterone on pituitary gonadotrophin release has been studied in the rat. Castrated female rats bearing ovarian autotransplants, or unilaterally ovariectomized rats, were given 1 to 5 mg of progesterone daily for intervals from 7 to 28 days, and then killed. The ovaries, uteri, and vaginas were examined grossly and microscopically, and the pituitary glands were assayed for total gonadotrophin content by the mouse uterine weight method. Although treatment with 5 mg of progesterone for 28 days inhibited ovulation, it did not prevent Graafian follicle development (determined histologically) or secretory function (evaluated by the presence of vaginal mucification) in either of the animal preparations. Progesterone treatment was associated with a significant elevation of pituitary gonadotrophic potency in the castrated rats bearing ovarian autotransplants, but not in the unilaterally ovariectomized rats. These findings suggest that the tonic rate of gonadotrophin secretion is unaffected by treatment with 5 mg of progesterone daily. The acute discharge of the ovulation inducing hormone complex (probably primarily LH) is, however, inhibited by such a dose of progesterone, and probably accounts for the inhibition of ovulation. The findings also suggest that the amount of progesterone secreted by the functioning corpora lutea during pseudopregnancy in the rat is equivalent in effect to between 2 and 5 mg of progesterone injected once daily.


1993 ◽  
Vol 137 (3) ◽  
pp. 505-510 ◽  
Author(s):  
R. S. Weisinger ◽  
P. Burns ◽  
L. W. Eddie ◽  
E. M. Wintour

ABSTRACT During pregnancy, in women and the rat, there is a resetting of the plasma osmolality–arginine vasopressin relationship (Posmol/PAVP) such that a decrease in Posmol is maintained without suppression of PAVP. This occurs at a time when relaxin is detectable in plasma. The hypothesis tested here was that relaxin could alter the Posmol/PAVP in the non-pregnant rat. One group of ovariectomized rats (n = 15) was treated for 7 days with intravenous synthetic human relaxin (10 μg/h) in 10 pi 0·9% (w/v) NaCl. Controls were two groups of rats either with no treatment (n = 15) or treated with vehicle alone (n = 15). One-third of each group received hypertonic saline (0·4 mol NaCl/l, 2 ml/100 g body weight i.p.) on day 7, and one-third were deprived of water for the final 24 h. All rats were killed by decapitation and blood was collected rapidly (<40 s) for hormone and osmolality assays. The Posmol in all relaxin-treated rats was significantly (P < 0·001) lower than that in both control groups, but the PAVP was unchanged. The log PAVP/Posmol regression line was significantly shifted in elevation (P <0·001) but not in slope. Thus treatment of ovariectomized rats with relaxin caused changes in fluid balance which mimic those occurring in normal pregnancy. Journal of Endocrinology (1993) 137, 505–510


Sign in / Sign up

Export Citation Format

Share Document