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Am J Physiol Regul Integr Comp Physiol 278: R19-R27, 2000;
0363-6119/00 $5.00
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Vol. 278, Issue 1, R19-R27, January 2000

Volume expansion natriuresis during servo control of systemic blood pressure in conscious dogs

Jens Lundbæk Andersen1, Lars Juel Andersen1, Niels C. F. Sandgaard1, and Peter Bie2

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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