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1 Department of Medical Physiology, University of Copenhagen, DK-2200 Copenhagen; and 2 Department of Physiology and Pharmacology, University of Southern Denmark, Odense, DK-5000 Odense, Denmark
.
The
importance of arterial blood pressure (BP) and ANG II for the renal
natriuretic response (NaEx) to volume expansion (3.5% body wt) was
investigated during converting enzyme blockade (enalaprilate, 2 mg/kg).
In separate experiments, BP was clamped either 30 mmHg above or a few
millimeters mercury below baseline by servo-controlled infusion of ANG
II or sodium nitroprusside, respectively, so that volume expansion did
not change BP. Enalapril decreased BP by 8 mmHg. Without
clamping, volume expansion returned BP to that of preenalapril control
and increased NaEx 10-fold (40 ± 10 to 377 ± 69 µmol/min). During
high pressure clamping (133 ± 2 mmHg), peak NaEx after volume
expansion was 6% of control experiments. During low pressure clamping,
NaEx was 68% of control experiments (45 ± 15 to 256 ± 64 µmol/min). The results show that 1) in absence of ANG II,
volume expansion elicited pronounced natriuresis without increases in
BP beyond baseline, 2) in the presence of hypertensive amounts
of ANG II, the volume expansion-induced natriuresis was almost
eliminated, and 3) nitroprusside prevented the increase in BP
but not sodium excretion during volume expansion. ANG II appears to
dominate the control of NaEx; however, when absent, volume expansion
may still induce marked natriuresis even at constant BP, possibly via
nitric oxide-mediated mechanisms.
sodium excretion; pressure natriuresis; angiotensin II; converting enzyme inhibition; nitric oxide
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