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Influence Of Chronic Nicotine On Acetylcholine‐Evoked Renal Vasodilations In Female Rats: Dose Dependency And Ovarian Hormonal Modulation
Author(s) -
El-Mas Mahmoud M,
El-gowilly Sahar M,
Gohar Eman Y,
El-Gowelli Hanan M
Publication year - 2012
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.26.1_supplement.1051.7
Subject(s) - nicotine , medicine , endocrinology , acetylcholine , vasodilation , phenylephrine , hormone , estrogen , ovariectomized rat , chemistry , blood pressure
In this study we report on the interaction of chronic nicotine with cholinergically‐mediated renal vasodilations in female rats and its modulation by ovarian hormones. Dose‐vasodilatory response curves to cumulative bolus doses of acetylcholine (ACh, 0.01–2.43 nmol) were established in phenylephrine‐preconstricted isolated perfused kidneys obtained from sham‐operated (SO) rats treated with or without nicotine (0.5–4.0 mg/kg/day for 2 weeks). The interaction was also evaluated in OVX rats in the absence or presence of progesterone (P), estrogen (E2), or their combination. The vasodilatory effects of ACh were potentiated in a dose‐dependent fashion by the low‐dose range of nicotine (0.5 and 1 mg/kg/day). By contrast, higher nicotine doses (2 and 4 mg/kg/day) failed to alter Ach responses. The co‐existence of both gonadal hormones, P and E2, seems imperative for the display of the potentiating effect of nicotine on ACh vasodilations because: (i) the increase in ACh responses by nicotine was lost in OVX kidneys, and (ii) combined supplementation with P and E2, but not individual treatments, restored the nicotine‐evoked potentiation of ACh vasodilation. Together, the data suggests that nicotine elicits dose‐ and gonadal hormonal‐dependent facilitation of ACh renal vasodilations in female rats. This project was supported financially by the Science and Technology Development Fund (STDF), Egypt, Grant No. 502.