Nitric oxide (NO)-mediated responses were investigated in corpora cavernosa
isolated from 8-week diabetic rats. Relaxations to field stimulation were
abolished by N-G-nitro-L-arginine (NOARG, 100 mu M). Responses to stimulati
on and sodium nitroprusside were reduced in tissues from diabetic rats comp
ared to control rats, when data were expressed as g tension, but not when e
xpressed as g/g tissue. The endothelium-dependent vasodilator, acetylcholin
e, failed to relax tissues. Stimulation-induced contractions were smaller i
n the diabetic group compared to the control group when data were expressed
as g tension, but not g/g tissue. Contractions were enhanced by NOARG, and
inhibited by acetylcholine (300 mu M), by a similar degree in both groups.
NOARG reduced the inhibitory effect of acetylcholine in tissues from contr
ol, but not diabetic rats. The results suggest diabetes caused a general im
pairment in responsiveness of rat corpus cavernosum, which may be a consequ
ence of tissue weight change. A role for endothelium-dependent NO could not
be identified; however, NO-mediated modulation of noradrenergic transmissi
on by acetylcholine, may be defective in diabetes. (C) 1999 Elsevier Scienc
e B.V. All rights reserved.