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Am J Physiol Regul Integr Comp Physiol 282: R1140-R1148, 2002; doi:10.1152/ajpregu.00665.2000
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Vol. 282, Issue 4, R1140-R1148, April 2002

Volume expansion during acute angiotensin II receptor (AT1) blockade and NOS inhibition in conscious dogs

Jens Lundbæk Andersen1, Niels C. F. Sandgaard2, and Peter Bie2

1 Department of Medical Physiology, University of Copenhagen, DK-2200; and 2 Department of Physiology and Pharmacology, University of Southern Denmark, DK-5000 Odense, Denmark

The responses to AT1-receptor blockade (candesartan 1 mg/kg) and to concomitant volume expansion (saline 35 ml/kg for 90 min) with and without nitric oxide synthase (NOS) inhibition (NG-nitro-L-arginine methyl ester 30 µg · kg-1 · min-1) were investigated in separate experiments in normal dogs.

AT1 blockade decreased arterial pressure (106 ± 4 to 96 ± 5 mmHg) and increased glomerular filtration rate (GFR) by 17% and sodium excretion threefold. NOS inhibition increased arterial pressure (103 ± 3 to 116 ± 3 mmHg) and decreased GFR by 21% and reduced sodium excretion by some 80%. Volume expansion increased arterial pressure significantly in all series involving this procedure, most pronounced during combined AT1 blockade and NOS inhibition (21 ± 4 mmHg). Volume expansion during AT1 blockade elicited marked natriuresis (26 ± 11 to 274 ± 55 µmol/min) that was severely reduced by concomitant NOS inhibition (10 ± 3 to 45 ± 11 µmol/min), but still much larger than that seen with volume expansion during NOS inhibition alone (2 ± 1 to 23 ± 7 µmol/min). Volume expansion during AT1 blockade increased GFR (+30%), less so during combined AT1 blockade and NOS inhibition (+13%), but it did not increase GFR significantly (P = 0.07) during NOS inhibition alone. Plasma ANG II increased greater than sevenfold with AT1 blockade and doubled with NOS inhibition (paired t-test, P < 0.05), whereas it decreased by 50-80% during volume expansion irrespective of pretreatment, i.e., during NOS inhibition, volume expansion did not generate subnormal plasma ANG II concentrations.

In conclusion, 1) acute AT1 blockade leads to hyperfiltration, natriuresis, and hyperresponsiveness to volume expansion, 2) these responses are >85% inhibitable by unspecific NOS inhibition, and 3) NOS inhibition alone is followed by increases in plasma ANG II, hypofiltration, and severe antinatriuresis that may be counterbalanced but not overwhelmed by volume expansion. Thus NOS inhibition virtually abolishes the volume expansion natriuresis, at least in part, due to the lack of appropriate inhibition of the renin-angiotensin-aldosterone system.

sodium excretion; blood pressure; glomerular filtration rate; NG-nitro-L-arginine methyl ester; candesartan


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