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Department of Internal Medicine I, University Hospital Dijkzigt, 3015 GD Rotterdam, The Netherlands
Experimental
evidence indicates that the renal circulation is more
sensitive to the effects of nitric oxide (NO) synthesis inhibition than
other vascular beds. To explore whether in men the NO-mediated
vasodilator tone is greater in the renal than in the systemic
circulation, the effects of three different intravenous infusions of
NG-nitro-L-arginine
methyl ester (L-NAME; 1, 5, and
25 µg · kg
1 · min1
for 30 min) or placebo on mean arterial pressure (MAP), systemic vascular resistance (SVR), renal blood flow (RBF), renal vascular resistance (RVR), glomerular filtration rate (GFR), and fractional sodium and lithium excretion (FENa
and FELi) were studied in 12 healthy subjects, each receiving randomly two of the four treatments on
two different occasions. MAP was measured continuously by means of the
Finapres device, and stroke volume was calculated by a model flow
method. GFR and RBF were estimated from the clearances of radiolabeled
thalamate and hippuran. Systemic and renal hemodynamics were followed
for 2 h after start of infusions. During placebo, renal and systemic
hemodynamics and FENa and
FELi remained stable. With the low
and intermediate L-NAME doses,
maximal increments in SVR and RVR were similar: 20.4 ± 19.6 and
23.5 ± 16.0%, respectively, with the low dose and 31.4 ± 26.7 and 31.2 ± 14.4%, respectively, with the intermediate dose (means ± SD). With the high L-NAME dose, the increment in RVR was greater than the increment in SVR. Despite a decrease in RBF, FENa
and FELi did not change with the low L-NAME dose, but they
decreased by 31.2 ± 11.0 and 20.2 ± 6.3%,
respectively, with the intermediate dose and by 70.8 ± 8.1 and 31.5 ± 15.9% with the high
L-NAME dose, respectively. It is concluded that in men the renal circulation is not more sensitive to
the effects of NO synthesis inhibition than the systemic circulation and that the threshold for NO synthesis inhibition to produce antinatriuresis is higher than the threshold level to cause renal vasoconstriction.
nitric oxide synthesis inhibition; renal vascular resistance; systemic vascular resistance; fractional sodium excretion; fractional lithium excretion
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