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Fig. 6. Effects of specific receptor antagonists on maximum contractile force
developed by steroid-treated ventricle strips from both male (A) and female
(B) rainbow trout at 0.5 Hz. Strips were pretreated for 10 min with flutamide
(Flut; 0.1 mmol l–1), mifepristone (Mif; 0.1 mmol
l–1) or tamoxifen (Tam; 0.25 mmol l–1) to
inhibit androgen, cortisol and estradiol receptors, respectively. Flut, Mif
and Tam had no independent effects on contractile force in males or females.
Steroid concentrations used were: 0.3 µmol l–1
11-ketotestosterone (11KT), 0.3 µmol l–1 testosterone (T),
0.1 µmol l–1 cortisol (C) in males, 0.01 µmol
l–1 C in females, and 1 nmol l–1 estradiol
(E2) in females. In males, Flut blocked the inotropic effects of androgens
(11KT and T) but not C. Mif blocked the effects of C in males and females but
not 11KT and T in males and E2 in females. In females, Tam prevented the
positive effects of E2 and C. All values are means +
S.E.M. (N=7–10).
*P<0.05 versus EtOH control strips.
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P<0.05, steroid-treated strips
at 0.5 Hz versus steroid-treated strips at 0.2, 0.8 and 1.0 Hz.
–nitro-l-arginine methyl ester) on
contractile force by steroid-treated ventricle strips. Ventricle strips from
both male (A) and female (B) rainbow trout were treated with L-NAME (1.0 mmol
l–1) for 10 min prior to exposure to 11-ketotestosterone
(11KT; 0.3 µmol l–1), testosterone (T; 0.3 µmol
l–1), cortisol (C; 0.1 µmol l–1 in males
and 0.01 µmol l–1 in females) or estradiol (E2; 1.0 nmol
l–1). L-NAME had no independent effect on contractile force;
however, L-NAME limited inotropic effects of androgens, C and E2. All values
are means + S.E.M. (N=6–8).
*P<0.05 versus EtOH control strips.