Abstract
We tested the hypotheses: (i) nicotine modifies the interaction of ovarian hormones with adenosine receptor‐mediated renal vasodilations, and (ii) nitric oxide synthase (NOS) and heme oxygenase (HO) modulate this interaction. Vasodilations caused by NECA, adenosine analogue, in perfused kidneys were reduced in ovariectomized (OVX) rats and restored after estrogen (E2) or medroxyprogesterone acetate (MPA) supplementation. The E2 or MPA effect was abolished after blockade of respective receptors by ICI 182780 and mifepristone, and after NOS (L‐NAME) but not HO (ZnPP) inhibition. NECA vasodilations were increased and decreased by nicotine (1 mg/kg/day, 2 weeks) in OVX/E2 and OVX/MPA kidneys, respectively. By contrast, NECA responses were resistant to nicotine in rats with deficient (OVX) or balanced (sham or E2/MPA‐replaced OVX) hormonal milieu. Nicotine enhancement of NECA responses in OVX/E2 kidneys was abolished by L‐NAME but not ZnPP. Alternatively, nicotine attenuation of NECA responses in OVX/MPA kidneys disappeared in presence of hemin (HO inducer) but not L‐arginine (NOS substrate). The hemin effect was compromised by ZnPP. Thus, NOS facilitation and HO inhibition mediate the opposite effects of nicotine on NECA responses in E2‐ or MPA‐replaced OVX rats, respectively.This project was supported financially by the Science and Technology Development Fund (STDF), Egypt, Grant No. 502.
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