AJP - Regulatory, Integrative and Comparative Physiology, Vol 270, Issue 6 1380-R1385, Copyright © 1996 by American Physiological Society
Involvement of nitric oxide in inhibitory innervation of urinary bladder of Atlantic cod, Gadus morhua
C. Olsson and S. Holmgren
Department of Zoophysiology, Goteborg University, Sweden.
The aim of this study was to investigate the involvement of nitric oxide
(NO) in the nonadrenergic, noncholinergic (NANC) relaxation of the urinary
bladder of the Atlantic cod, Gadus morhua. NADPH diaphorase-reactive nerve
cells, presumed to be able to produce NO, were found in the vesicular
nerve. The cells occurred alone and in ganglia together with stained and
unstained cells. The effect of inhibitors of NO synthesis on the relaxation
was examined in vitro in isolated muscle preparations. NG-nitro-L-arginine
methyl ester (10(-4) M) and NG-nitro-L-arginine (L-NNA; 10(-4) M) decreased
the electrically induced relaxation to 32 +/- 6 (n = 8) and 28 +/- 6% (n =
8) of the control, respectively. L-Arginine (10(-3) M) increased the
relaxation to 152 +/- 24% (n = 8), without affecting the inhibition by
L-NNA. The beta-adrenoceptor antagonist propranolol together with
L-arginine analogues abolished the relaxation in 7 of 11 preparations. The
NO donor sodium nitroprusside (NaNP) caused a concentration-dependent
relaxation of the bladder, with a maximal effect obtained at 10(-4) M.
LY-83583 (10(-5) M), a guanylate cyclase inhibitor, decreased both the
electrically (n = 8) and the NaNP (10(-6) M, n = 9)-induced relaxation to
69 +/- 5 and 20 +/- 4% of the control, respectively. Together these
findings suggest that NO is involved in the NANC regulation of the motility
of the urinary bladder of the Atlantic cod.
