scholarly journals Actions of angiotensin II and dopamine in the medial preoptic area on prolactin secretion

2008 ◽  
pp. 109-118
Author(s):  
CM Leite ◽  
GJR Machado ◽  
RCM Dornelles ◽  
CR Franci
Keyword(s):  
Angiotensin Ii ◽  
Inhibitory Action ◽  
Preoptic Area ◽  
Medial Preoptic Area ◽  
Prolactin Secretion ◽  
Ovariectomized Rats ◽  
Ang Ii ◽  
Stimulatory Action ◽  
D 2 Receptors ◽  
Plasma Prl

Dopamine (DA) is known as a primary regulator of prolactin secretion (PRL) and angiotensin II (Ang II) has been recognized as one brain inhibitory factor of this secretion. In this work, estrogen-primed or unprimed ovariectomized rats were submitted to the microinjection of saline or Ang II after previous microinjection of saline or of DA antagonist (haloperidol, sulpiride or SCH) both in the medial preoptic area (MPOA). Our study of these interactions has shown that 1) estrogen-induced PRL secretion is mediated by Ang II and DA actions in the MPOA, i.e. very high plasma PRL would be prevented by inhibitory action of Ang II, while very low levels would be prevented in part by stimulatory action of DA through D(2) receptors, 2) the inhibitory action of Ang II depends on estrogen and is mediated in part by inhibitory action of DA through D(1) receptors and in other part by inhibition of stimulatory action of DA through D(2) receptors.

scholarly journals Alpha- but not beta-adrenergic receptors mediate the effect of angiotensin II in the medial preoptic area on gonadotropin and prolactin secretion

1998 ◽  
pp. 583-586 ◽  
Author(s):  
RC Dornelles ◽  
CR Franci
Keyword(s):  
Angiotensin Ii ◽  
Adrenergic Receptors ◽  
Preoptic Area ◽  
Medial Preoptic Area ◽  
Prolactin Secretion ◽  
Beta Adrenergic Receptors ◽  
Beta Adrenergic ◽  
Alpha Adrenergic Receptors ◽  
Ovx Rats ◽  
Plasma Prl

The aim of this work was to study the participation of alpha- and beta-adrenergic receptors on the effect of microinjection of angiotensin II (A II) into the medial preoptic area (MPOA) on the secretion of luteinizing hormone (LH), follicle-stimulating hormone (FSH) and prolactin (PRL) in estrogen-primed ovariectomized (OVX) rats. Microinjection of A II into the MPOA increased plasma LH. This effect was reduced by previous microinjection of an alpha- (phentolamine), but not a beta- (propranolol) adrenergic blocker into the MPOA. Plasma PRL decreased after microinjection of A II into the MPOA, but this effect was unchanged by phentolamine or propranolol. There was no change in plasma FSH in any condition. These results indicate that A II in the MPOA stimulates LH secretion and inhibits PRL secretion in estrogen-primed OVX rats. The effect on secretion of LH, but not of PRL, is mediated by alpha-adrenergic receptors in the MPOA.

scholarly journals High-Dose Estradiol-Replacement Therapy Enhances the Renal Vascular Response to Angiotensin II via an AT2-Receptor Dependent Mechanism

2015 ◽  
Vol 2015 ◽  
pp. 1-7
Author(s):  
Tahereh Safari ◽  
Mehdi Nematbakhsh ◽  
Roger G. Evans ◽  
Kate M. Denton
Keyword(s):  
Angiotensin Ii ◽  
Replacement Therapy ◽  
Hormone Replacement ◽  
Renal Perfusion ◽  
Ovariectomized Rats ◽  
High Dose ◽  
Ang Ii ◽  
Renal Vasoconstriction ◽  
Increased Risk ◽  
Angiotensin Type 2 Receptor

Physiological levels of estrogen appear to enhance angiotensin type 2 receptor- (AT2R-) mediated vasodilatation. However, the effects of supraphysiological levels of estrogen, analogous to those achieved with high-dose estrogen replacement therapy in postmenopausal women, remain unknown. Therefore, we pretreated ovariectomized rats with a relatively high dose of estrogen (0.5 mg/kg/week) for two weeks. Subsequently, renal hemodynamic responses to intravenous angiotensin II (Ang II, 30–300 ng/kg/min) were tested under anesthesia, while renal perfusion pressure was held constant. The role of AT2R was examined by pretreating groups of rats with PD123319 or its vehicle. Renal blood flow (RBF) decreased in a dose-related manner in response to Ang II. Responses to Ang II were enhanced by pretreatment with estradiol. For example, at 300 ng kg−1 min−1, Ang II reduced RBF by45.7±1.9% in estradiol-treated rats but only by27.3±5.1% in vehicle-treated rats. Pretreatment with PD123319 blunted the response of RBF to Ang II in estradiol-treated rats, so that reductions in RBF were similar to those in rats not treated with estradiol. We conclude that supraphysiological levels of estrogen promote AT2R-mediated renal vasoconstriction. This mechanism could potentially contribute to the increased risk of cardiovascular disease associated with hormone replacement therapy using high-dose estrogen.

scholarly journals Renal Vascular Response to Angiotensin II Administration in Two Kidneys-One Clip Hypertensive Rats Treated with High Dose of Estradiol: The Role of Mas Receptor

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Samira Choopani ◽  
Mehdi Nematbakhsh
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Ovariectomized Rats ◽  
Ang Ii ◽  
Vascular Response ◽  
Hypertensive Rats ◽  
Vascular Responses ◽  
Mas Receptor ◽  
Renal Vascular

Backgrounds. High blood pressure is one of the most important causes of death around the world. The renin-angiotensin system (RAS) and estradiol are two important items that regulate arterial blood pressure in women. However, hypertension, RAS, and sex hormone estradiol may influence renal vascular responses. This study was designed to determine the role of Mas receptor (MasR) on renal vascular response to angiotensin II (Ang II) administration in two kidneys-one clip (2K1C) hypertensive rats treated with estradiol. Method. The ovariectomized rats were subjected to 2K1C or non-2K1C and simultaneously treated with estradiol (500 μg/kg/weekly) or placebo for a period of 4 weeks. Subsequently, under anesthesia, renal vascular responses to graded doses of Ang II administration with MasR blockade (A779) or its vehicle were determined. Results. A779 or its vehicle did not alter mean arterial pressure (MAP), renal perfusion pressure (RPP), and renal blood flow (RBF). However, in non-2K1C rats, Ang II infusion decreased RBF and increased renal vascular resistance (RVR) responses in a dose-related manner ( P treat < 0.0001 ). The greatest responses were found in ovariectomized estradiol-treated rats that received A779 ( P group < 0.05 ) in non-2K1C rats. Such findings were not detected in 2K1C hypertensive rats. For example, in estradiol-treated rats that received A779, at 1000 ng/kg/min of Ang II infusion, RBF reduced from 1.6 ± 0.2 to 0.89 ± 0.19  ml/min in non-2K1C rats, and it reduced from 1.6 ± 0.2 to 1.2 ± 0.2  ml/min in 2K1C rats. Conclusion. Hypertension induced by 2K1C may attenuate the role of A779 and estradiol in renal vascular responses to Ang II infusion. Perhaps, this response can be explained by the reduction of Ang II type 1 receptor (AT1R) expression in the 2K1C hypertensive rats.

Varying sensitivity to the negative oestrogen feedback during the ovarian cycle of female rats: evidence for the involvement of oestrogen and the medial preoptic area

1984 ◽  
Vol 102 (3) ◽  
pp. 287-294 ◽  
Author(s):  
F. Döcke ◽  
W. Rohde ◽  
P. Gerber ◽  
R. Chaoui ◽  
G. Dörner
Keyword(s):  
Preoptic Area ◽  
Medial Preoptic Area ◽  
Ovarian Cycle ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Adult Rats ◽  
Gonadotrophin Secretion ◽  
Arcuate Region ◽  
Lh Secretion ◽  
Follicle Maturation

ABSTRACT The gonadotrophic response to a single injection of oestradiol benzoate (OB) was studied in acutely ovariectomized adult rats during the different stages of a 4-day ovarian cycle. The results showed a sudden decline of the sensitivity to the gonadotrophin-inhibiting effect of OB between metoestrus and dioestrus. This desensitization to the negative oestrogen feedback was probably caused by an oestrogen action on the medial preoptic area (MPOA). In rats ovariectomized and implanted with OB in the MPOA in metoestrus, an s.c. injection of OB on the presumptive day of pro-oestrus did not lower the circulating LH and FSH levels, whereas a clear suppression of gonadotrophin secretion was seen in females implanted with cholesterol in the MPOA or implanted with OB in the hypothalamic ventromedial–arcuate region. Similar findings were obtained in rats which had been ovariectomized 3–4 weeks before implantation. A final experiment demonstrated that bilateral lesioning of the MPOA also reduced the sensitivity to the negative feedback action of oestrogen in long-term ovariectomized rats. In all experiments performed, diminution of the oestrogen-induced inhibition of LH secretion was more marked than that of suppression of FSH secretion. It is proposed that desensitization to the negative oestrogen feedback, probably resulting from an inhibitory oestrogen action on medial preoptic neurones, is a prerequisite for adequate gonadotrophic support of preovulatory follicle maturation in the presence of a continuously rising oestrogen concentration in the blood. J. Endocr. (1984) 102, 287–294

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