The purpose of this study was to investigate the effects of endothelial den
udation, inhibitors of nitric oxide (NO) and prostanoid synthesis on vasoco
nstrictor responses in the perfused rabbit ovarian vascular. The experiment
s were conducted using an in vitro perfusion system, where the ovarian vasc
ular bed (en bloc) was perfused with Krebs' solution delivered at a constan
t flow rate using a peristaltic pump. Changes in perfusion pressure, which
reflected peripheral resistance, were measured. Results showed that noradre
naline (NA) (10(-9) to 10(-6) mol) induced reproducible dose-dependent vaso
constrictor responses. Vasoconstrictor effects of low doses of noradrenalin
e were not affected by perfusion of the vascular bed with CHAPS (4.7 mg/ml
for 30 s) to remove the endothelium. The same treatment however, significan
tly reduced responses induced by the higher doses of noradrenaline, thus de
pressing the maximum response. KCl-induced vasoconstriction was not affecte
d by CHAPS. L-N-G-nitroarginine (L-NOARG) (10(-5) mol/l) enhanced NA-induce
d vasoconstriction. D-NOARG, the inactive isomer of L-NOARG and aminoguanid
ine, an inhibitor of inducible nitric oxide synthase reduced rather than en
hanced noradrenaline-induced responses. Methylene blue (3 x 10(-5) mol/l) a
nd LY 83583 (10(-5) mol/l) produced a potentiation of NA-induced vasoconstr
ictor responses. Indomethacin (3 x 10(-6) mol/l) did not significantly enha
nce NA-induced vasoconstriction.