The goal of this study was to determine if there is a basal release of
nitric oxide that affects long-term arterial pressure regulation in d
ogs. Studies were conducted over a 23-day period in eight conscious do
gs with indwelling catheters. Nitric oxide synthesis was blocked by co
ntinuous intravenous infusion of nitro-L-arginine-methyl ester at 37.1
nmol/kg per minute for 11 days. Arterial pressure increased to 120+/-
4% of control on the first day, decreased for a few days, and then inc
reased to a maximum value of 122+/-6% of control on day 7. Bradycardia
was sustained throughout the entire nitro-arginine period. Blockade o
f nitric oxide synthesis was evidenced by attenuated pressure and flow
responses to systemic acetylcholine infusion. The pressor response to
phenylephrine was increased for only 1 day, and the hypotensive effec
ts of nitroprusside were enhanced. Also, the variability of arterial p
ressure was significantly increased during nitro-arginine. Sodium and
water balances were positive the first day of nitro-arginine infusion
but were unchanged for the entire nitro-arginine period. In conclusion
, the data suggest that blockade of the basal release of nitric oxide
in dogs causes an increase in the long-term level of arterial pressure
without any sustained sodium or water retention.