Mechanisms regulating hormone release and the duration of dioestrus in the lactating rat

1983 ◽  
Vol 99 (2) ◽  
pp. 173-180 ◽  
Author(s):  
S. Hansen ◽  
P. Södersten ◽  
P. Eneroth
Keyword(s):  
Dopamine Receptor ◽  
Post Partum ◽  
Prolactin Secretion ◽  
Dopamine Receptor Agonist ◽  
Hormone Release ◽  
Serum Progesterone ◽  
Dopamine Receptor Antagonist ◽  
Lh Secretion ◽  
Cross Fostering ◽  
Prolactin Suppression

Lactation in rats nursing seven pups was associated with a period of dioestrus lasting for 3 weeks, reduced LH secretion, hyperprolactinaemia and increased serum progesterone levels. Removal of the litter resulted in increased LH secretion, a prompt return of oestrus and termination of the prolactin-dependent luteal phase. Administration of domperidone (2·5 mg/day), a dopamine receptor antagonist, to rats deprived of their litters on day 1 or 9 post partum maintained hyperprolactinaemia and delayed the reappearance of oestrus. Administration of bromocriptine (0·5 mg/day), a dopamine receptor agonist, to lactating rats with suckling pups suppressed prolactin secretion and advanced oestrus, females in the middle of lactation being considerably more sensitive to prolactin suppression than those in the early post-partum period. Cross-fostering experiments revealed that the greater sensitivity to bromocriptine of mothers in late lactation was due to their lactational age rather than to the age of the offspring. Similarly, the length of lactational dioestrus was not affected either by giving newborn pups to females in the middle of lactation or by giving 9-day-old pups to newly parturient females.

Inhibition of sexual behaviour in lactating rats

1983 ◽  
Vol 99 (2) ◽  
pp. 189-197 ◽  
Author(s):  
P. Södersten ◽  
S. Hansen ◽  
P. Eneroth
Keyword(s):  
Dopamine Receptor ◽  
Sexual Behaviour ◽  
Inhibitory Effect ◽  
Daily Treatment ◽  
Female Rats ◽  
Serum Prolactin ◽  
Dopamine Receptor Agonist ◽  
Serum Progesterone ◽  
Behavioural Effects

Treatment with oestradiol benzoate (OB; 2–250 μg) and progesterone (0·5–25 mg) failed to induce sexual behaviour in lactating rats 6 days after parturition. Removal of pups permitted the induction of sexual behaviour by OB and progesterone and the inhibitory effect of the presence of pups was proportional to the number present. Ovariectomy of lactating rats or reduction of serum prolactin levels in intact lactating rats by daily treatment with the dopamine receptor agonist bromocriptine (0·5 mg/day) permitted the induction of sexual behaviour despite the presence of suckling pups. Removal of pups from lactating rats and subsequent maintenance of high prolactin levels by daily treatment with the dopamine receptor antagonist domperidone (2·5 mg/day) maintained the state of refractoriness to the behavioural effects of OB and progesterone provided that the ovaries remained in situ. Inhibition of sexual behaviour in lactating rats could be maintained after ovariectomy by implantation of progesterone-filled, but not androgen-filled implants at the time of ovariectomy. Removal of the pups or reduction of prolactin levels by bromocriptine treatment permitted the induction of sexual behaviour by OB in ovariectomized progesterone-implanted lactating rats. Inhibition of the behaviour in ovariectomized progesterone-implanted lactating rats could be maintained after pup removal by daily domperidone treatment. Continuously raised serum progesterone or prolactin levels have no effect on the induction of sexual behaviour in female rats but the present data suggest that during lactation progesterone and prolactin act in synergy to inhibit the behaviour.

Role of Na+/K+-stimulated adenosine triphosphatase in the action of dopaminergic-D2 receptors of the liver in rats

1987 ◽  
Vol 7 (11) ◽  
pp. 839-842 ◽  
Author(s):  
Abdulrahim Abu-Jayyab ◽  
Ahmed Mahgoub
Keyword(s):  
Atpase Activity ◽  
Receptor Antagonist ◽  
Dopamine Receptor ◽  
Inhibitory Activity ◽  
Receptor Agonist ◽  
Adenosine Triphosphatase ◽  
D2 Receptors ◽  
Dopamine Receptor Agonist ◽  
Dopamine Receptor Antagonist

The dopamine receptor agonist, bromocriptine, in a dose of 10 mg/kg i.p. for 14 days, in rats caused a significant increase in liver Na+/K+-ATPase activity, whereas sulpiride, a dopamine receptor antagonist, in a dose of 10 mg/kg, i.p. for 14 days, in rats, caused a significant decrease in liver Na+/K+-ATPase activity. Injection of bromocriptine and sulpiride simultaneously in a group of rats, under the same conditions and using the same doses caused a complete block of both stimulatory activity of bromocriptine and inhibitory activity of sulpiride on liver Na+/K+-ATPase activity. It is suggested that Na+/K+-ATPase may have a role in the action of dopaminergic-D2 receptors.

Hormonal Effects of Apomorphine in Schizophrenia

1984 ◽  
Vol 144 (4) ◽  
pp. 349-357 ◽  
Author(s):  
I. N. Ferrier ◽  
E. C. Johnstone ◽  
T. J. Crow
Keyword(s):  
Dopamine Receptor ◽  
Negative Symptoms ◽  
Dopamine Receptor Agonist ◽  
Positive Symptoms ◽  
Hormonal Effects ◽  
Dopamine Receptor Antagonists ◽  
Chronic Schizophrenics ◽  
Schizophrenic Patients ◽  
Direct Acting ◽  
Prolactin Suppression

SummaryThe hormonal effects of apomorphine, a direct-acting dopamine receptor agonist, in schizophrenic patients are of interest in view of the therapeutic efficacy of dopamine receptor antagonists. In this study, apomorphine (0.75 mg s.c.) and placebo were administered to unmedicated acute and chronic schizophrenics and controls. Apomorphine-induced prolactin suppression did not discriminate between the groups. However, an inverse relationship between basal prolactin levels and the severity of positive symptoms was detected in the patients with acute schizophrenia, consistent with a role for dopamine in the genesis of these symptoms. Growth hormone increments after apomorphine administration were blunted in the chronic schizophrenic patients, particularly those with ‘negative’ symptoms. It is argued that this blunting is not due to previous neuroleptic therapy and may represent evidence of structural change in the hypothalamus in this group of patients.

A modulatory role of endogenous opioids on prolactin secretion at the end of pregnancy in the rat

1994 ◽  
Vol 140 (1) ◽  
pp. 97-102 ◽  
Author(s):  
M Soaje ◽  
R P Deis
Keyword(s):  
Time Course ◽  
Prolactin Secretion ◽  
Endogenous Opioids ◽  
Opioid Antagonist ◽  
Serum Prolactin ◽  
Serum Progesterone ◽  
Pregnant Rats ◽  
Pregnant Rat ◽  
Ru 486 ◽  
Prolactin Suppression

Abstract It is well known that the fall in serum progesterone concentrations during late pregnancy induces prolactin secretion in rats. On day 19 of pregnancy, administration of 10 mg of the antiprogesterone RU-486/kg induced a small but significant increase in serum prolactin. A lower dose (2 mg/kg) was not effective. Administration of naloxone (2 mg/kg) to pregnant rats on day 19 of pregnancy did not modify circulating prolactin but, after RU-486 treatment, a notable increase in serum prolactin was obtained 30 min after naloxone was given. The lack of effect of naloxone-methobromide in pregnant rats pretreated with RU-486 may indicate that the opioid-induced prolactin suppression acts centrally, most probably at the hypothalamic level. During day 21 of pregnancy, the time-course of prolactin secretion, measured at 0900, 1400, 1900 and 2200 h, was inversely correlated with circulating progesterone levels. At 0900 h, serum prolactin was very low with high serum progesterone concentrations but a significant increase in serum prolactin occurred at 2200 h; this was coincident with a significant decrease in the steroid. The stimulatory effect of naloxone on prolactin secretion was clearly dependent on the circulating progesterone level. Thus, at 1900 h of day 21, naloxone induced a significant increase in serum prolactin but, at 2200 h, the opioid antagonist dramatically enhanced the circulating level of prolactin. The serum prolactin increase induced by naloxone at 1900 h was prevented by the s.c. administration of 5 mg progesterone given 7 h earlier. Similarly, the large increase in serum prolactin levels at 1800 h on day 19 of pregnancy, after administration of RU-486 plus naloxone, was completely abolished by treatment with CB154. The lack of effect of RU-486 and naloxone on serum prolactin levels in virgin rats on the day of pro-oestrus demonstrates that the effect of naloxone on prolactin in pregnant rat is peculiar to the end of pregnancy. In conclusion, the attenuation of the central inhibitory action of progesterone facilitates the release of prolactin which is dramatically enhanced by naloxone treatment. These results provide an important new insight into the existence of a neuromodulatory regulation of prolactin secretion by the opioid system showing a paradoxical opioid-induced prolactin suppression at the end of pregnancy. Journal of Endocrinology (1994) 140, 97–102

Parkinson Disease Treated With a Suspected Dopamine Receptor Agonist

1974 ◽  
Vol 30 (5) ◽  
pp. 383-386 ◽  
Author(s):  
T. N. Chase ◽  
A. C. Woods ◽  
G. A. Glaubiger
Keyword(s):  
Parkinson Disease ◽  
Dopamine Receptor ◽  
Receptor Agonist ◽  
Dopamine Receptor Agonist

scholarly journals Effects of costimulation of dopamine D1- and D2-like receptors on renal function

1998 ◽  
Vol 275 (4) ◽  
pp. R986-R994 ◽  
Author(s):  
Pedro A. Jose ◽  
Laureano D. Asico ◽  
Gilbert M. Eisner ◽  
Felice Pocchiari ◽  
Claudio Semeraro ◽  
...  
Keyword(s):  
Dopamine Receptor ◽  
Sodium Transport ◽  
Sodium Excretion ◽  
Rank Order ◽  
Sch 23390 ◽  
Urine Flow ◽  
Dopamine Receptor Agonist ◽  
Vasodilatory Effect

In vitro studies have suggested that dopamine D1- and D2-like receptors interact to inhibit renal sodium transport. We used Z-1046, a dopamine receptor agonist with the rank-order potency D3 ≥ D4 > D2 > D5 > D1, to test the hypothesis that D1- and D2-like receptors interact to inhibit renal sodium transport in vivo in anesthetized rats. Increasing doses of Z-1046, administered via the right renal artery, increased renal blood flow (RBF), urine flow, and absolute and fractional sodium excretion without affecting glomerular filtration rate. For determination of the dopamine receptor involved in the renal functional effects of Z-1046, another group of rats received Z-1046 at 2 μg ⋅ kg−1 ⋅ min−1( n = 10) in the presence or absence of the D2-like receptor antagonist domperidone and/or the D1-like antagonist SCH-23390. Domperidone alone had no effect but blocked the Z-1046-mediated increase in urine flow and sodium excretion; it enhanced the increase in RBF after Z-1046. SCH-23390 by itself decreased urine flow and sodium excretion without affecting RBF and blocked the diuretic, natriuretic, and renal vasodilatory effect of Z-1046. We conclude that the renal vasodilatory effect of Z-1046 is D1-like receptor dependent, whereas the diuretic and natriuretic effects are both D1- and D2-like receptor dependent.

Sign in / Sign up

Export Citation Format

Share Document