There may be a relation between altered venous function, endothelin (ET)-1,
and an impairment in the activity of endothelial-derived nitric oxide (NO)
and prostanoids: in salt-dependent hypertension. The present study examine
d the effects of salt intake on ET-induced changes in venomotor tone and th
e effects of blockade of NO synthase with N-G-nitro-L-arginine methyl ester
(L-NAME) and of cyclooxygenase with indomethacin on venomotor tone caused
by the ETB selective agonist sarafotoxin 6c (S6c) in awake rats. Rats were
anesthetized for permanent placement of catheters for measurements of arter
ial and venous pressures. A silicone balloon catheter was also fixed in the
right atrium to produce brief circulatory arrest. Venomotor tone was estim
ated from measurements of mean circulatory filling pressure (MCFP) in consc
ious rats. There were no differences in mean arterial pressure, heart rate,
or MCFP responses to short-term administration of ET-1 or S6c at different
levels of salt intake. L-NAME or indomethacin did not change MCFP or the r
esponse of MCFP to short-term injection of S6c. In conclusion, neither basa
l MCFP nor integrated venomotor responses to short-term injection of ET-1 o
r S6c were altered by short-term changes in salt intake, blockade of NO syn
thase or cyclooxygenase. These data do not support the hypothesis that incr
eased salt intake alters reactivity of veins to ET-1, NO, or prostanoids.