Physiologically Significant Inhibitory Hypothalamic Action of Substance P on Prolactin Release in the Male Rat

1990 ◽  
Vol 52 (1) ◽  
pp. 22-27 ◽  
Author(s):  
Masayoshi Arisawa ◽  
Gary D. Snyder ◽  
Wen H. Yu ◽  
Louis R. de Palatis ◽  
Raymond H. Ho ◽  
...  
Keyword(s):  
Substance P ◽  
Male Rat ◽  
Prolactin Release

scholarly journals Interaction between substance P and TRH in the control of prolactin release

2000 ◽  
Vol 166 (2) ◽  
pp. 373-380 ◽  
Author(s):  
BH Duvilanski ◽  
D Pisera ◽  
A Seilicovich ◽  
M del Carmen Diaz ◽  
M Lasaga ◽  
...  
Keyword(s):  
Substance P ◽  
Anterior Pituitary ◽  
Prolactin Secretion ◽  
Male Rat ◽  
Prolactin Release ◽  
Anterior Pituitary Function ◽  
Specific Antagonist ◽  
Autocrine Factor

Substance P (SP) may participate as a paracrine and/or autocrine factor in the regulation of anterior pituitary function. This project studied the effect of TRH on SP content and release from anterior pituitary and the role of SP in TRH-induced prolactin release. TRH (10(-7) M), but not vasoactive intestinal polypeptide (VIP), increased immunoreactive-SP (ir-SP) content and release from male rat anterior pituitary in vitro. An anti-prolactin serum also increased ir-SP release and content. In order to determine whether intrapituitary SP participates in TRH-induced prolactin release, anterior pituitaries were incubated with TRH (10(-7) M) and either WIN 62,577, a specific antagonist of the NK1 receptor, or a specific anti-SP serum. Both WIN 62,577 (10(-8) and 10(-7) M) and the anti-SP serum (1:250) blocked TRH-induced prolactin release. In order to study the interaction between TRH and SP on prolactin release, anterior pituitaries were incubated with either TRH (10(-7) M) or SP, or with both peptides. SP (10(-7) and 10(-6) M) by itself stimulated prolactin release. While 10(-7) M SP did not modify the TRH effect, 10(-6) M SP reduced TRH-stimulated prolactin release. SP (10(-5) M) alone failed to stimulate prolactin release and markedly decreased TRH-induced prolactin release. The present study shows that TRH stimulates ir-SP release and increases ir-SP content in the anterior pituitary. Our data also suggest that SP may act as a modulator of TRH effect on prolactin secretion by a paracrine mechanism.

2-HYDROXYOESTRADIOL INHIBITS PROLACTIN RELEASE FROM THE SUPERFUSED RAT PITUITARY GLAND

1981 ◽  
Vol 90 (3) ◽  
pp. 315-322 ◽  
Author(s):  
ELIZABETH A. LINTON ◽  
NICKI WHITE ◽  
OFELIA LIRA DE TINEO ◽  
S. L. JEFFCOATE
Keyword(s):  
Pituitary Gland ◽  
Prolactin Secretion ◽  
Male Rat ◽  
Prolactin Release ◽  
Rat Pituitary ◽  
Lh Release

The effects of 2-hydroxyoestradiol (2OH-OE2), dopamine, oestradiol-17β and 2OH-OE2 plus dopamine on prolactin and LH release from the male rat pituitary gland were examined in vitro. 2-Hydroxyoestradiol reduced prolactin secretion by 51% at 10−10 mol/l and by 34% at 10−7 mol/l, while oestradiol-17β had no effect at these doses. Dopamine alone (5 × 10−7 mol/l) decreased prolactin released by 58%, 2OH-OE2 plus dopamine produced a similar inhibition of 60%. No significant effect on LH release was observed throughout.

Effects of secretagogues on cytosolic Ca2+ levels in rat submandibular granular ducts and acini

1991 ◽  
Vol 261 (2) ◽  
pp. G359-G363 ◽  
Author(s):  
I. H. Valdez ◽  
R. J. Turner
Keyword(s):  
Substance P ◽  
Salivary Secretion ◽  
Male Rat ◽  
Primary Fluid ◽  
Epidermal Growth ◽  
Submandibular Acini ◽  
Stage Process ◽  
Granular Ducts ◽  
Substance P Receptors

Saliva is thought to be formed by a two-stage process, with the secretion of a "primary fluid" by the acinar cells followed by various ionic modifications in the salivary ducts. Both of these processes are under the control of autonomic stimuli. Although the role of the acini in salivary secretion has been studied in some detail, little is known about properties of ducts, particularly the intralobular ducts that make up the bulk of the ductal tissue. In the present study, microfluorometric methods were employed to examine the responses of intracellular Ca2+ concentration ([Ca2+]i) in individual male rat submandibular acini and intralobular (granular) ducts to various fluid secretory stimuli. We show that granular ducts respond to muscarinic (carbachol) and alpha-adrenergic (epinephrine) stimulation by increasing [Ca2+]i in a manner that is qualitatively similar to acini, but that in contrast to acini, these ducts do not respond to substance P. Because the transduction of a substance P peptidergic signal typically occurs via increased [Ca2+]i, this observation suggests that there are no substance P receptors on granular ducts. Ducts were also found to be somewhat more responsive to both carbachol and epinephrine than acini. Although muscarinic, alpha-adrenergic, and vasoactive intestinal peptide (VIP) stimulation are known to induce the secretion of epidermal growth factor from granular ducts, no significant increase in ductal [Ca2+]i in response to VIP (10(-9) to 10(-6) M) was observed.

Acute continuous exposure to cigarette smoke produces discrete changes in cholecystokinin and substance P levels in the hypothalamus and preoptic area of the male rat

1985 ◽  
Vol 125 (3) ◽  
pp. 437-443 ◽  
Author(s):  
KJELL FUXE ◽  
RICHARD A. SIEGEL ◽  
KURT ANDERSSON ◽  
PETER ENEROTH ◽  
FRANCO MASCAGNI ◽  
...  
Keyword(s):  
Substance P ◽  
Cigarette Smoke ◽  
Preoptic Area ◽  
Male Rat ◽  
Continuous Exposure

Influence of maternal pineal gland on the developmental pattern of neurokinin A (NKA) and substance P (SP) in male-rat-offspring: relationship to the season of the year

2004 ◽  
Vol 368 (3) ◽  
pp. 243-248 ◽  
Author(s):  
N. Vázquez Moreno ◽  
L. Debeljuk ◽  
E. Dı́az Rodrı́guez ◽  
C. Fernández Alvarez ◽  
B. Dı́az López
Keyword(s):  
Substance P ◽  
Pineal Gland ◽  
Developmental Pattern ◽  
Male Rat ◽  
Neurokinin A ◽  
Rat Offspring

Bovine neurophysin-II stimulates prolactin release without involvement of dopaminergic prolactin-release inhibiting factor receptor in the estradiol-primed male rat

1989 ◽  
Vol 121 (3) ◽  
pp. 411-416
Author(s):  
S. H. Shin ◽  
M. C. Obonsawin ◽  
R. Stirling
Keyword(s):  
Blocking Agent ◽  
Male Rats ◽  
Male Rat ◽  
Prolactin Release ◽  
Inhibiting Factor ◽  
Inert Carrier ◽  
A Chain ◽  
Neurophysin Ii ◽  
Factor Release ◽  
Stimulation Of

Abstract. Neurophysins have been considered to be physiologically inert carrier proteins for the neurohypophysial hormones, oxytocin and vasopressin. We have observed that bovine neurophysin-II indirectly stimulates prolactin release in estradiol-primed male rats. The release of prolactin is regulated by a dual hypothalamic control system, the prolactin-release-inhibiting factor and the prolactin-releasing factor. We have tried to clarify whether neurophysin-II is acting through stimulation of prolactin-releasing factor by eliminating the possibility of dopaminergic prolactin release-inhibiting factor release. Male rats were primed with estradiol and functional dopaminergic prolactin release-inhibiting factor receptors were completely blocked by pretreatment with a large dose of pimozide (3 mg/kg), a dopaminergic receptor blocking agent. The neurophysin-II stimulated prolactin release in the rats which did not have any functional dopaminergic prolactin release-inhibiting factor receptors suggesting that neurophysin-II likely initiates a chain of events which eventually stimulates prolactin-releasing factor release since the possibility of involvement of the dopaminergic prolactin release-inhibiting factor system is eliminated. Opioids are known to be one of a chain of events which transmit external stress into a stimulation of prolactin release. Naloxone, a μ-receptor antagonist, was injected 20 min before neurophysin-II administration into rats which were primed with estradiol and pretreated with pimozide (3 mg/kg), but the naloxone administration did not block the prolactin release stimulated by neurophysin-II injection. This result indicates that opioids are not one of the chain of events between initiation of stimulation by neurophysin-II and prolactin release.

Kallidin-induced stimulation of inositol phosphate production and prolactin release in rat anterior pituitary cells

1990 ◽  
Vol 123 (1) ◽  
pp. 37-42 ◽  
Author(s):  
T. Hugh Jones ◽  
Barry L. Brown ◽  
Pauline R. M. Dobson
Keyword(s):  
Anterior Pituitary ◽  
Inositol Phosphate ◽  
Prolactin Secretion ◽  
Male Rat ◽  
Pituitary Cells ◽  
Phosphoinositide Metabolism ◽  
Prolactin Release ◽  
Anterior Pituitary Cells ◽  
Inositol Phosphate Production ◽  
Stimulation Of

Abstract. The effect of the kinin, kallidin (lysyl-brady-kinin) on phosphoinositide metabolism and prolactin secretion was examined in male rat anterior pituitary cells in primary culture. Kallidin was found to stimulate both total inositol phosphate production and prolactin release. The stimulation of inositol phosphate was biphasic in nature, similar to that previously reported for bradykinin, although kallidin was approximately 10-fold more potent. Kallidin also stimulated prolactin secretion provoking a maximal stimulation of 193.0±11.1 (sem)% at 1 μmol/l. These findings suggest that kallidin-induced prolactin secretion may be mediated intracellularly by activation of phosphoinositide metabolism. The B2 receptor antagonists had no significant inhibitory effects on kallidin-stimulated phosphoinositide metabolism or prolactin release. The B1 agonist des-Arg9-bradykinin has previously been shown to have no effect on either parameter. As the effects of kinins on anterior pituitary cells do not appear to be mediated by either of the known kinin receptors, they may, therefore, act via a hitherto unrecognised kinin receptor.

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