Hypertension, Vol 22, 49-55, Copyright © 1993 by American Heart Association
FJ Salazar, A Alberola, JM Pinilla, JC Romero and T Quesada
The objective of this study was to determine in conscious dogs the role of
endothelium-derived nitric oxide in mediating the arterial pressure and
renal response to a prolonged increment of sodium intake. After a control
period of 3 days, an inhibitor of nitric oxide synthesis, NG-
nitro-L-arginine-methyl ester, was infused intravenously during 5
consecutive days (0.1 micrograms/kg per minute). Sodium intake (80 mmol/d)
did not change throughout the experiment in one group (n = 4). In another
group (n = 6), 1 day after infusion of this inhibitor was started, sodium
intake increased from 80 to 300 mmol/d during 4 consecutive days.
Inhibition of nitric oxide synthesis in dogs with normal sodium intake
induced a significant decrease in natriuresis and diuresis (P < .05)
without changes in arterial pressure. However, in dogs treated with the
nitric oxide synthesis inhibitor, mean arterial pressure increased from
95.2 +/- 3.3 to 106.2 +/- 4.0 mm Hg (P < .01) the first day that sodium
intake was elevated and remained increased the following 3 days. In a
different group of dogs (n = 5), the increment of sodium intake during 4
days did not induce changes in arterial pressure when nitric oxide
synthesis was not inhibited. Cumulative sodium balance was higher (P <
.01) in dogs treated simultaneously with the nitric oxide synthesis
inhibitor and high sodium intake (158 +/- 21 mmol sodium) than in those
treated only with the nitric oxide synthesis inhibitor (82 +/- 19 mmol
sodium) or with high sodium intake (36 +/- 13 mmol sodium).(ABSTRACT
TRUNCATED AT 250 WORDS)
ARTICLES
Salt-induced increase in arterial pressure during nitric oxide synthesis inhibition
Department of Physiology and Biophysics, Mayo Clinic, Rochester, Minn.
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