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Physical or emotional stress can affect the female reproductive physiology and angiotensin II (Ang II) is a hormone that participates in the stress response and also in the control of reproductive hormones. The present study aimed at evaluating the effects of acute stress in the morning and afternoon of proestrus on sexual behavior and ovulation and the participation of Ang II in the stress-induced effects. Female rats with regular estrous cycles were used. Several different stress protocols were tested in the morning and in the afternoon of proestrus: restraint stress 10 min; restraint stress 1 h and ether stress, respectively. The participation of Ang II was evaluated by injecting Ang II receptor antagonists (losartan and PD123319) 15 min before stress. The lordosis quotient was recorded and the number of oocytes was counted. Plasma levels of luteinizing hormone, progesterone, prolactin and corticosterone were measured. All types of stress in the morning of proestrus induced a reduction in the number of oocytes. Restraint stress (1 h) in the afternoon of proestrus induced a significant reduction in the lordosis quotient. Peripheral and central losartan, but not PD123319, injections partly reverted the effects of stress on ovulation in the morning of proestrus. Acute stress in the morning of proestrus also reduced luteinizing hormone, progesterone and prolactin surges later on the same day. In conclusion, acute stress on the day of proestrus can affect female reproductive physiology. Moreover, the angiotensinergic system, through AT(1) receptors, participates in the effects of acute stress in the morning of proestrus.

Abstract: There is an association between hypertension and reproductive dysfunction. Angiotensin II (Ang II) is involved in the pathogenesis of hypertension and the regulation of reproduction. The present study aimed to determine whether the angiotensinergic system mediates the effects of hypertension on reproductive function in male rats subjected to a two-kidney, one-clip (2K1C) model. Sexual behavior parameters, gametogenesis and plasma concentrations of Ang II, testosterone, prolactin and corticosterone were evaluated in male rats 28days after 2K1C or sham surgery and losartan (Los) treatment (a type 1 angiotensin II (AT1) receptor antagonist) or vehicle (V) treatment. The animals were divided into Sham+V, 2K1C+V, Sham+Los and 2K1C+Los groups. The 2K1C+V group showed a hypertensive response, inhibition of sexual behavior, spermatogenesis dysfunction, and increases in plasma Ang II and prolactin. Conversely, plasma testosterone decreased, and plasma corticosterone remained constant. Losartan treatment normalized blood pressure and prevented the changes in plasma testosterone and prolactin, sexual behavior and spermatogenesis in the 2K1C+Los group. In addition, losartan treatment caused an additional increase in circulating Ang ll in both groups (Sham+Los and 2K1C+Los). Together, these results suggest that Ang ll, acting through the AT1 receptor, modulates behavioral and endocrine parameters of reproductive function during renovascular hypertension. In addition, the effects of circulating Ang II on plasma testosterone and prolactin seem to contribute to the spermatogenic and sexual dysfunctions in hypertensive rats. [Copyright &y& Elsevier]

Our objective was to study in which situations the median preoptic nucleus (MnPO) interferes with the control of oxytocin secretion and salt intake and the possible mediation of angiotensin II (AII) through their AT1 receptors. Lesion of the MnPO by ibotenic acid in male rats did not change water and NaCl intake in conditions of ad libitum offer, water deprivation or salt load, but it did cause significant decrease of NaCl intake in sodium depleted animals. These animals presented higher water intake or lower NaCl intake after microinjection of AII or losartan into the MnPO, respectively. They decreased plasma oxytocin after microinjection of losartan into the MnPO, but not of AII or isotonic saline. Oxytocin secretion induced by hypertonic saline i.p. was reduced by microinjection of AII, but not losartan into the MnPO. On the other hand, microinjection of losartan in this area, but not AII, reduced plasma oxytocin in animals submitted to the isotonic saline i.p. Thus, it seems that the sodium intake control is performed by MnPO neurons through the stimulatory action of angiotensin II on AT1 receptors under sodium depletion, but not water deprivation or salt overload neither of ad libitum water and salt intake condition. On the other hand, in the high-sodium condition, endogenous angiotensin did not act on MnPO neurons to the control of oxytocin secretion while exogenous angiotensin inhibited oxytocin secretion. These results indicate two possible angiotensinergic neural circuits: one is stimulating and the other is inhibiting oxytocin secretion, depending on sodium balance. [Copyright &y& Elsevier]

Angiotensin II (Ang II) is a peptide that exerts an inhibitory effect upon pituitary prolactin (PRL) release through the hypothalamic arcuate nucleus (ARC). Since both PRL and Ang II are known to be affected by stress, the experiments reported here were conducted to investigate the possible participation of Ang II in the stress-induced response of PRL in situations in which pre-stress PRL levels are high, as during the PRL surge induced by estradiol (E2) and progesterone (P) in ovariectomized rats (OVXE2P) and lactating females on day 7 post-partum. Adult female rats were stereotactically implanted with bilateral guide-cannulae in the ARC; 3 days later, they were microinjected with saline or losartan and, after a 15-min interval, they were submitted to stress by ether inhalation during 1 min. Five minutes after stress, trunk blood samples were collected. Plasma PRL was measured by radioimmunoassay (RIA). In OVXE2P and lactating rats, a significant reduction in PRL levels was detected after stress compared to non-stressed animals. The microinjection of losartan in the ARC before stress blocked the reduction of PRL in both OVXE2P and lactating females. In conclusion, the stress-induced reduction of plasma PRL in OVXE2P and lactating rats is mediated by Ang II through AT1 receptors in the ARC. [Copyright &y& Elsevier]

Abstract: Physical or emotional stress can affect the female reproductive physiology and angiotensin II (Ang II) is a hormone that participates in the stress response and also in the control of reproductive hormones. The present study aimed at evaluating the effects of acute stress in the morning and afternoon of proestrus on sexual behavior and ovulation and the participation of Ang II in the stress-induced effects. Female rats with regular estrous cycles were used. Several different stress protocols were tested in the morning and in the afternoon of proestrus: restraint stress 10 min; restraint stress 1 h and ether stress, respectively. The participation of Ang II was evaluated by injecting Ang II receptor antagonists (losartan and PD123319) 15 min before stress. The lordosis quotient was recorded and the number of oocytes was counted. Plasma levels of luteinizing hormone, progesterone, prolactin and corticosterone were measured. All types of stress in the morning of proestrus induced a reduction in the number of oocytes. Restraint stress (1 h) in the afternoon of proestrus induced a significant reduction in the lordosis quotient. Peripheral and central losartan, but not PD123319, injections partly reverted the effects of stress on ovulation in the morning of proestrus. Acute stress in the morning of proestrus also reduced luteinizing hormone, progesterone and prolactin surges later on the same day. In conclusion, acute stress on the day of proestrus can affect female reproductive physiology. Moreover, the angiotensinergic system, through AT1 receptors, participates in the effects of acute stress in the morning of proestrus. [Copyright &y& Elsevier]

Abstract: The expression of angiotensin II (Ang II) receptors in the brain is modulated by estradiol and progesterone. Considering that Ang II plays a critical role in controlling prolactin secretion and that neurons in the arcuate nucleus (ARC) are the main regulator of this function, the present study aimed to evaluate ARC Ang II receptor binding in 2 experimental models with different estradiol and progesterone plasma levels. Animals were divided into 4 groups: ovariectomy (OVX) plus oil vehicle, OVX plus estradiol and progesterone replacement, lactating rats on day 7 postpartum, and lactating rats on day 20. Animals were killed by decapitation, and the brains were removed. Ang II receptors were quantified by autoradiography in ARC. Trunk blood samples were collected, and plasma estradiol and progesterone were measured by radioimmunoassay. Treatment of OVX rats with estradiol and progesterone increased Ang II receptor binding when compared to OVX vehicle-treated animals. Plasma estradiol (r = +0.77) and progesterone (r = +0.87) were highly correlated with Ang II receptors in ovariectomized animals. Lactating rats (day 20) showed a significant decrease in Ang II receptor binding and plasma progesterone when compared to lactating rats (day 7), however, no difference was seen in plasma estradiol. Plasma levels of progesterone (r = +0.81), but not estradiol (r = +0.32), were highly correlated with Ang II receptors in lactating rats. In conclusion, present results show that ARC Ang II receptors decreases on day 20 of lactation compared to day 7 and are highly correlated with plasma progesterone, indicating a pivotal role for progesterone in this regulation. [Copyright &y& Elsevier]

Abstract: Neonatal handling alters the hypothalamic–pituitary–adrenal (HPA) axis and the hypothalamic–pituitary–gonads axis (HPG) in adult animals, and angiotensin II (Ang II) modulates the functions in these axes. We tested whether neonatal handling could change the density of Ang II receptors in some central areas in female rats. Results showed decreased density of the Ang II receptors in the medial preoptic area (MPOA) and hypothalamic paraventricular nucleus (PVN) of the neonatal handled group. [Copyright &y& Elsevier]