Effects of LHRH and ANG II on prolactin stimulation are mediated by hypophysial AT1 receptor subtype

1994 ◽  
Vol 266 (2) ◽  
pp. E274-E278 ◽  
Author(s):  
D. Becu-Villalobos ◽  
I. M. Lacau-Mengido ◽  
S. M. Thyssen ◽  
G. S. Diaz-Torga ◽  
C. Libertun
Keyword(s):  
Luteinizing Hormone ◽  
Follicle Stimulating Hormone ◽  
Female Rats ◽  
Receptor Subtype ◽  
Receptor Subtypes ◽  
Ang Ii ◽  
Prolactin Release ◽  
Luteinizing Hormone Releasing Hormone ◽  
Prolactin Response

We have used the nonpeptide angiotensin II (ANG II) receptor antagonists losartan (receptor subtype AT1) and PD-123319 (AT2) to determine the participation of ANG II receptor subtypes in luteinizing hormone-releasing hormone (LHRH)-induced prolactin release in a perifusion study using intact pituitaries in vitro. LHRH (1.85 x 10(-7) M) released prolactin consistently, whereas losartan (10(-5) M) abolished prolactin response without modifying basal prolactin or luteinizing hormone (LH) and follicle-stimulating hormone (FSH) release. PD-123319 (10(-5) M) had no effect on basal or LHRH-induced prolactin, LH, or FSH release. We also determined that the effect of ANG II on prolactin release was mediated by the same receptor subtype. In adenohypophysial cells dispersed in vitro ANG II (10(-8) M) released prolactin. Losartan (10(-7) and 10(-6) M), but not PD-123319, inhibited this effect. We conclude that in intact hypophyses of 15-day-old female rats the effect of LHRH on prolactin release is readily demonstrated. LHRH-induced prolactin release appears to be mediated by ANG II acting in a paracrine manner on AT1 receptors located on lactotrophs.

Modulation of pituitary responsiveness to LHRH by androgens in ovariectomized female rats

1977 ◽  
Vol 55 (2) ◽  
pp. 188-192
Author(s):  
Padmaja N. Kulkarni ◽  
Alan A. Simpson ◽  
William H. Moger
Keyword(s):  
Luteinizing Hormone ◽  
Follicle Stimulating Hormone ◽  
Estradiol Benzoate ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Luteinizing Hormone Releasing Hormone ◽  
Daily Dose ◽  
17Β Estradiol ◽  
High Doses ◽  
Pronounced Inhibition

The effect of androgens on pituitary response to luteinizing-hormone-releasing hormone (LHRH) and their ability to modify effects of 17β-estradiol (E2) on pituitary responsiveness to LHRH were tested in ovariectomized rats maintained on a daily dose of 0.25 μg estradiol benzoate per rat for 6 d before androgen administration.Testosterone propionate (TP) (4, 40, 400, or 4000 μg per rat), administered 24 h before LHRH (500 ng per rat), had no significant effect on luteinizing hormone (LH) or follicle-stimulating hormone (FSH) response. Similar doses of dihydrotestosterone (DHT) did not significantly alter the LH response but significantly suppressed the FSH response. Even the lowest dose completely blocked the FSH response to LHRH. TP in combination with 4 or 400 μg of E2 suppressed the stimulatory effect of E2 on both LH and FSH response to LHRH in a dose-related manner. DHT and E2 in combination affected LH response inconsistently, whereas their ratio determined FSH response; there was pronounced inhibition of FSH response in rats given high doses of DHT combined with low doses of E2; DHT inhibition of FSH response in animals receiving 4 μg of DHT with 400 μg E2 was partially overcome by the stimulatory effect of E2. Our results indicate that TP and DHT affect LH and FSH response to LHRH differently. The ratio of androgen to estrogen is important in determining the response to LHRH.

EFFECT OF OVINE LUTEINIZING HORMONE ON THE SECRETION OF PROGESTERONE IN VITRO BY OVARIAN FOLLICLES FROM HYPOPHYSECTOMIZED RATS TREATED WITH FOLLICLE-STIMULATING HORMONE

1978 ◽  
Vol 77 (3) ◽  
pp. 419-420
Author(s):  
A. R. LABARBERA ◽  
MERO R. NOCENTI
Keyword(s):  
New York ◽  
Luteinizing Hormone ◽  
Corn Oil ◽  
Follicle Stimulating Hormone ◽  
Virgin Female ◽  
Ovarian Follicles ◽  
Female Rats ◽  
Hypophysectomized Rats ◽  
Stimulating Hormone

Department of Physiology, College of Physicians and Surgeons, Columbia University, New York 10032, U.S.A. (Received 14 November 1977) Ovarian follicles from oestrous, pro-oestrous and hypophysectomized rats have the capacity to secrete progestins in vitro and to respond to luteinizing hormone (LH) by increasing this secretion (Stoklosowa & Nalbandov, 1972; LaBarbera, Nocenti & Castellano, 1974; Lindner, Tsafriri, Lieberman, Zor, Koch, Bauminger & Barnea, 1974). Follicles from hypophysectomized rats, untreated or treated with follicle-stimulating hormone (FSH), were therefore studied in experiments in vitro to investigate further the gonadotrophic control of progesterone secretion. Mature virgin female rats (200–250 g) were hypophysectomized and, beginning on day 4 after the operation, received a total of 360 μg ovine FSH (NIH-FSH-S9)/100 g body weight, injected s.c. in corn oil as six divided doses, one every 12 h for 3 days. Untreated controls received corn oil only. On day 7 after hypophysectomy, the ovaries were excised and

scholarly journals Orphanin FQ/Nociceptin Is a Physiological Regulator of Prolactin Secretion in Female Rats

Endocrinology ◽  
2006 ◽  
Vol 147 (11) ◽  
pp. 5087-5093 ◽  
Author(s):  
Matthew Chesterfield ◽  
James Janik ◽  
Emily Murphree ◽  
Courtney Lynn ◽  
Erin Schmidt ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Prolactin Secretion ◽  
Secretory Response ◽  
Female Rats ◽  
Receptor Subtype ◽  
Orphanin Fq ◽  
Prolactin Release ◽  
Endogenous Opioid Peptide ◽  
Male And Female Rats ◽  
Prolactin Response

Orphanin FQ/nociceptin (OFQ/N), the most recently identified endogenous opioid peptide, stimulates prolactin secretion in both male and female rats. OFQ/N, however, did not elicit this stimulatory effect through the μ-, δ-, or κ-opiate receptor subtype. The role OFQ/N plays in prolactin regulation under physiological conditions and its mechanism of action are not known. The purpose of these studies was to determine the physiological significance and pharmacological specificity of the prolactin secretory response to OFQ/N. In addition, the role of the tuberoinfundibular dopaminergic (TIDA) neurons in mediating this response was examined. Opioid receptor-like-1 (ORL-1) receptors were blocked by pretreatment with compound B (Comp B), a purported OFQ/N antagonist, or receptor synthesis was disrupted by pretreatment with ORL-1 receptor antisense oligonucleotides. The prolactin secretory response to OFQ/N administration in diestrous females was measured. Furthermore, the suckling-induced prolactin response was also determined after Comp B pretreatment. TIDA neuronal activity was quantified in diestrous female rats to determine whether OFQ/N stimulates prolactin release by inhibiting TIDA neurons. OFQ/N significantly inhibited the TIDA neurons by 1 min, preceding the prolactin secretory response. Both Comp B and antisense pretreatment blocked the stimulatory effects of OFQ/N on prolactin release, and Comp B abolished the suckling-induced prolactin response. These studies indicate that OFQ/N is a potent stimulus for prolactin secretion in female rats and that it mediates this effect by rapid and transient inhibition of TIDA neuronal activity. Furthermore, OFQ/N plays a physiologically significant role in the regulation of prolactin secretion during lactation, and it mediates its effects via actions at the ORL-1 receptor subtype.

Hypothalamic catecholaminergic effects on prolactin release in vitro

1978 ◽  
Vol 56 (2) ◽  
pp. 304-309 ◽  
Author(s):  
W. C. Friend ◽  
G. M. Brown ◽  
S. Kirpalani ◽  
D. Wilson
Keyword(s):  
Luteinizing Hormone ◽  
Thyrotropin Releasing Hormone ◽  
Prolactin Release ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Release In Vitro ◽  
Lh Rh ◽  
Hypothalamic Mechanism

Hypothalamic catecholaminergic influences on prolactin release were investigated in vitro. Both dopamine and norepinephrine caused long lasting inhibition of prolactin release from either an isolated hemipituitary or a hemipituitary coincubated with a hypothalamus. Epinephrine also inhibited prolactin release. L-Dihydroxyphenylalanine (L-dopa) inhibited prolactin release from pituitaries in the presence of a hypothalamus but not in isolated pituitaries. DL-Threodihydroxyphenylserine (threodops), serotonin, 5-hydroxy-L-tryptophan (5-HTP), tyramine, octopamine, synephrine, thyrotropin-releasing hormone (TRH), luteinizing hormone releasing hormone (LH-RH), and somatostatin all failed to alter prolactin release. Results confirm that dopamine and norepinephrine directly inhibit prolactin release from pituitary and suggest that the hypothalamic mechanism inhibiting prolactin involves dopamine but not norepinephrine.

In vivo studies on paracrine actions of pituitary angiotensin II in stimulating prolactin release in rats

1990 ◽  
Vol 258 (4) ◽  
pp. E619-E624 ◽  
Author(s):  
M. K. Steele ◽  
L. S. Myers
Keyword(s):  
Angiotensin Ii ◽  
Luteinizing Hormone ◽  
Intravenous Administration ◽  
Female Rats ◽  
In Vivo Studies ◽  
Ovariectomized Rats ◽  
Ang Ii ◽  
Prolactin Release ◽  
Paracrine Actions

The present experiments were performed to test the hypothesis that, in vivo, intrapituitary angiotensin II (ANG II) mediates the effect of luteinizing hormone-releasing hormone (LHRH) on prolactin release. After intravenous administration of LHRH (100 ng/100 microliters saline), plasma levels of both luteinizing hormone (LH) and prolactin were increased in ovariectomized rats pretreated with estradiol and progesterone. Intravenous administration of saralasin or sarthran (ANG II receptor blockers) reduced or abolished, respectively, the LHRH-induced increase in prolactin without affecting the rise in LH. In other ovariectomized steroid-treated rats, saralasin did not affect the increase in LH or prolactin induced by 10 min of restraint stress. Finally, in intact female rats on the day of proestrus, neither saralasin nor sarthran affected the mid-cycle prolactin surge. Taken together, these results show that in vivo exogenous LHRH stimulates prolactin release via a paracrine action of pituitary ANG II. However, under other conditions in which both LH and prolactin (and presumably endogenous LHRH) are elevated, pituitary ANG II does not appear to be involved in the prolactin rise.

REFRACTORINESS OF THE PITUITARY GLAND AFTER CONTINUOUS EXPOSURE TO LUTEINIZING HORMONE RELEASING HORMONE

1978 ◽  
Vol 79 (3) ◽  
pp. 311-318 ◽  
Author(s):  
J. DE KONING ◽  
J. A. M. J. VAN DIETEN ◽  
G. P. VAN REES
Keyword(s):  
Luteinizing Hormone ◽  
Cyclic Amp ◽  
Female Rats ◽  
Continuous Exposure ◽  
High Concentration ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Lh Rh ◽  
Depressed Response

The refractoriness of LH release by pituitary glands from intact female rats was studied during stimulation by luteinizing hormone releasing hormone (LH-RH), monobutyryl cyclic AMP+theophylline or potassium in vitro. Various concentrations of LH-RH (0·1, 0·3 and 10 ng/ml) all caused refractoriness within 24 h. Subsequent exposure to a supramaximally active concentration of LH-RH for 6 h also resulted in a depressed response; the degree of inhibition depended on the concentration of LH-RH to which the glands had been exposed previously. Glands made refractory to LH-RH also showed a depressed response to monobutyryl cyclic AMP+theophylline, although these agents by themselves were unable to induce refractoriness. Incubation in medium containing a high concentration of potassium also resulted in the release of LH, which in all respects was similar to that caused by LH-RH. Glands made refractory to LH-RH showed a decreased response to potassium and, conversely, the release of LH in response to LH-RH was reduced after exposure of glands to potassium. It is concluded that the LH releasing activity of LH-RH, which is mimicked by potassium, deteriorates during continuous exposure to the secretagogue.

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