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Department of Physiology and Biophysics, Mayo Medical School, and Division of Hypertension, Mayo Clinic, Rochester, Minnesota 55905
Nitric oxide
(NO) synthesis inhibition with
NG-nitro-L-arginine methyl ester
(L-NAME) (10 µg · kg
1 · min1
iv), cyclooxygenase inhibition with meclofenamate (Meclo;
5 mg/kg iv bolus), and combination of drugs
(L-NAME+Meclo) were used to investigate the roles of NO and prostaglandins (PG) in the hemodynamic and natriuretic responses to isotonic saline volume expansion (VE; 5%
body wt over 60 min) in anesthetized dogs. Before VE, L-NAME
(n = 6), Meclo
(n = 6), and
L-NAME+Meclo
(n = 6) produced significant
increments in mean arterial pressure (MAP) of 12 ± 2, 15 ± 3, and 17 ± 3 mmHg, respectively. VE did not change MAP in
Meclo-treated dogs, but produced a significant elevation in the control
dogs (14 ± 6 mmHg), in
L-NAME-treated dogs (17 ± 6 mmHg), and in dogs pretreated with
L-NAME+Meclo (12 ± 5 mmHg). VE alone induced marked natriuretic responses in the control (38 ± 9 to 562 ± 86 µmol/min),
L-NAME (31 ± 9 to 664 ± 65 µmol/min), and Meclo groups (41 ± 10 to 699 ± 51 µmol/min). However, this natriuretic response was attenuated in dogs
pretreated with L-NAME+Meclo (12 ± 4 to 185 ± 52 µmol/min). These results indicate that
1) blockade of both NO and PGs has
significant diminishing effects on volume-induced natriuresis,
2) NO blockade alone impairs
volume-induced natriuresis in a manner that requires further increases
in MAP to restore the natriuresis, and
3) PG blockade alone does not curtail volume-induced natriuresis.
NG-nitro-L-arginine methyl ester; pressure-natriuresis sensitivity
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