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Estrogen Protects Female Rats Against The Nicotine‐Induced Attenuation Of Reflex Tachycardia: Role Of Central Estrogen Receptors
Author(s) -
ElMas Mahmoud M,
Elgowilly Sahar M,
Fouda Mohamed A,
Saad Evan I
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.961.3
Subject(s) - nicotine , endocrinology , medicine , baroreflex , estrogen , estrogen receptor , reflex , antagonist , chemistry , receptor , pharmacology , blood pressure , heart rate , cancer , breast cancer
Our preliminary studies showed that nicotine attenuates reflex tachycardia in male and not female rats. Here, the hypothesis was tested that the resistance of female rats to the nicotine effect is estrogen‐dependent. Baroreflex curves relating reflex tachycardic responses to decreases in blood pressure evoked by sodium nitroprusside (1–16 μg/kg) were constructed in proestrus, ovarictomized (OVX), and estrogen (50 μg/kg s.c., 5 days)‐replaced OVX (OVXE 2 ) rats. Slopes of the curves were taken as a measure of baroreflex sensitivity (BRS). Nicotine (100 μg/kg) reduced BRS in OVX rats but not in proestrus or OVXE 2 rats. The attenuation of reflex tachycardia by nicotine was also evident in diestrus rats, which exhibit low plasma estrogen, and in OVX rats treated simultaneously with E 2 and the estrogen receptor antagonist tamoxifen. Experiments were then extended to determine whether central estrogenic pathways modulate the nicotine‐BRS interaction. Intracisteral (i.c.) treatment of OVX rats with E 2 (0.2 μg/rat) abolished the BRS attenuating effect of nicotine. This protective effect of E 2 disappeared when OVX rats were pretreated with i.c. ICI 182,780, a selective estrogen receptor antagonist. Together, central pathways of estrogen receptors seem to play integral role in the protection offered by E 2 against nicotine‐induced barorecetor dysfunction.