Renal and systemic hemodynamic, natriuretic and neuro-humoral
responses to different doses of l-name in man..
Broere, A., A. H. Van Den Meiracker, F. Boomsma, F. H. M. Derkx, A. J.
Man In _t Veld, and M. A. D. H. Schalekamp.
Department of Internal Medicine I, University Hospital Dijkzigt,
Dr. Molewaterplein 40, 3015 GD Rotterdam, The Netherlands.
APStracts 5:0150F, 1998.
Experimental evidence indicates that the renal circulation is more
sensitive to the effects of NO-synthesis inhibition than other
vascular beds. To explore whether in man the NO-mediated vasodilator
tone is greater in the renal than in the systemic circulation the
effects of three different i.v. infusions of L-NAME (1, 5 and 25
_g/kg/min for 30 minutes) 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 2 of the 4 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 hours after start of infusions. During placebo
renal and systemic hemodynamics and FENa and FEli remained stable.
With the low and intermediate L-NAME dose maximal increments in SVR
and RVR were similar: respectively 20.4+/-19.6 and 23.5+/-16.0% with
the low and 31.4+/-26.7 and 31.2+/-14.4% with the intermediate dose
(mean+/-SD). With the high L-NAME dose the increment in RVR was
greater than the increment in SVR. Despite a decrease in renal blood
flow 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% with the intermediate and by
70.8+/-8.1 and 31.5+/-15.9 % with the high L-NAME dose. It is
concluded that in man 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.
Received 17 February 1998; accepted in final form 18 August 1998.
APS Manuscript Number F37-8.
Article publication pending Am. J. Physiol. (Renal Physiology).
ISSN 1080-4757 Copyright 1998 The American Physiological Society.
Published in APStracts on 21 September 1998