Za. Keskil et al., The contribution of nitric oxide and endothelins to angiotensin II. Evokedresponses in the rat isolated uterus smooth muscle, GEN PHARM, 33(4), 1999, pp. 307-312
The present study was designed to determine the role of endogenous endothel
in peptides and nitric oxide on angiotensin II (AII) responses in the isola
ted nonpregnant rat uterine smooth muscle. AII (10, 20, or 50 ng/ml) increa
ses rhythmic oscillations dose dependently (32.7 +/- 8.9, 55.96 +/- 10.3, a
nd 62.78 +/- 17.7% increase, respectively). L-arginine methyl ester (L-NAME
; 10(-5) M) did not affect the increase in rhythmic oscillations induced by
AII (10, 20, or 50 ng/ml) (17.5 +/- 12.1, 31.5 +/- 18.3, and 52.5 +/- 11.8
% increase, respectively, n = 6, p > 0.05), It reduced the contractile resp
onses to AII(10 ng/ml: from 4.63 +/- 0.6 to 1.8 +/- 0.7 cm(2), p < 0.05; an
d 20 ng/ml: from 5.59 +/- 0.8 to 2.11 +/- 0.4 cm(2), p < 0.05, n = 6). L-ar
ginine (10 mM) decreased the contractile response obtained by AII (10 or 20
ng/ml) (1.93 +/- 1.05, p < 0.05 and 2.14 +/- 0.7 cm(2), p < 0.05, respecti
vely, n = 6). BQ 485 (50 ng/ml) decreased both the number of rhythmic oscil
lations and the contractility increased by AII. Bosentan (10(-5) M) induced
an increase in the number of rhythmic oscillations but decreased the contr
actile responses to the higher concentrations of AII. These data show that
endogenous NO and endothelin peptides contribute to the motility changes in
duced by AII and may play an important role in the pathophysiological event
s of the uterine function. (C) 1999 Elsevier Science Inc. All rights reserv
ed.