Effects of acute stress on the day of proestrus on sexual behavior and ovulation in female rats: Participation of the angiotensinergic system
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 AT(1) receptors, participates in the effects of acute stress in the morning of proestrus.
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- "Although a variety of stressors have been reported to influence female rat sexual behavior, the direction of change is not always consistent (Cecconello et al., 2009; Donadio et al., 2007; Gorzalka et al., 1998; Hulse and Coleman, 1983; Uphouse et al., 2008; Uphouse et al., 2005; White and Uphouse, 2004). It is possible that some of this inconsistency may arise from behavioral assessment at different phases of an inhibition/recovery process that is initiated by the stressor. "
ABSTRACT: Ovariectomized Fischer inbred rats were hormonally primed with 10μg estradiol benzoate and sesame seed oil (EO rats) or with estradiol benzoate and 500μg progesterone (EP rats). Four to six hours after progesterone or oil, rats were pretested for sexual behavior and then infused bilaterally into the ventromedial nucleus of the hypothalamus with 0, 50, 100 or 200ng of the 5-HT(1B) receptor agonist, 1,4-dihydro-3-(1,2,3,6-tetrahydro-4-pyridinyl)-5H-pyrrol[3,2-bi]pyridin-5-one-dihydrochloride (CP 93129). Sexual receptivity was monitored by the lordosis to mount (L/M) ratio. EO rats showed a transient decline in lordosis behavior following infusion with the saline vehicle and this was amplified by CP 93129. There were no effects of any infusion in EP rats. These findings are discussed in terms of the possible stress effect of the intracranial infusion in EO rats and their implications for a role of 5-HT(1B) receptors in the response to a mild stress.Pharmacology Biochemistry and Behavior 12/2010; 97(2):317-24. DOI:10.1016/j.pbb.2010.08.017 · 2.82 Impact Factor
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- "The present findings demonstrate that AT 1 receptor antagonists with dual peripheral and central effects inhibit the stress-induced increase in central and peripheral sympathetic activity. The anti-stress properties of candesartan are shared by other AT 1 receptor antagonists such as losartan (Vinícius et al. 2007). These observations indicate that AT 1 receptor blockers may be considered as effective anti-stress agents. "
ABSTRACT: Spontaneously hypertensive rats, a stress-sensitive strain, were pretreated orally for 14 days with the AT(1) receptor antagonist candesartan before submission to 2 h of cold-restraint stress. In non-treated rats, stress decreased AT(1) receptor binding in the median eminence and basolateral amygdala, increased AT(2) receptor binding in the medial subnucleus of the inferior olive, decreased AT(2) binding in the ventrolateral thalamic nucleus and increased tyrosine hydroxylase mRNA level in the locus coeruleus. In non-stressed rats, AT(1) receptor blockade reduced AT(1) receptor binding in all areas studied and enhanced AT(2) receptor binding in the medial subnucleus of the inferior olive. Candesartan pretreatment produced a similar decrease in brain AT(1) binding after stress, and prevented the stress-induced AT(2) receptor binding decrease in the ventrolateral thalamic nucleus. In the locus coeruleus and adrenal medulla, AT(1) blockade abolished the stress-induced increase in tyrosine hydroxylase mRNA level. Our results demonstrate that oral administration of candesartan effectively blocked brain AT(1) receptors, selectively increased central AT(2) receptor expression and prevented the stress-induced central stimulation of tyrosine hydroxylase transcription. The present results support a role of brain AT(1) and AT(2) receptors in the regulation of the stress response, and the hypothesis that AT(1) receptor antagonists may be considered as potential therapeutic compounds in stress related disorders in addition to their anti-hypertensive properties.Stress (Amsterdam, Netherlands) 07/2008; 11(6):457-66. DOI:10.1080/10253890801892040 · 3.46 Impact Factor