Effects of L-arginine and L-NAME on the renal function in hypertensive and normotensive subjects.
OBJECTIVE
Renal vasodilation in response to L-arginine has been reported to be diminished in hypertensive (HT) subjects. If this diminished renal vasodilator response indicates disturbance of the renal NO pathway, a diminished renal vasoconstrictor response to NO synthase inhibition may be present in HT subjects as well. The present study was conducted to compare the effects of L-arginine and N(G)-nitro-L-arginine methyl ester (L-NAME) on renal and systemic hemodynamics between HT and normotensive (NT) subjects.


METHODS
The responses of renal and systemic vascular resistances (RVR and SVR) and plasma noradrenaline and renin (NOR and PRA) to systemic NO stimulation and inhibition were studied in patients with grade 1 essential HT and age- and sex-matched NT subjects. On separate occasions, after baseline values were obtained, 40-min randomly administered intravenous infusions of L-arginine (12.5 mg.kg(-1).min(-1)) or L-NAME (0.0125 mg.kg(-1).min(-1)) were given.


RESULTS
Baseline values of RVR (129 +/- 21 and 162 +/- 10 resistance units) and SVR (15.1 +/- 4.3 and 21.6 +/- 5.1 resistance units) were higher (p < 0.01) in HT than in NT subjects, whereas the baseline values of NOR and PRA were similar. Infusion of L-arginine caused similar decrements in SVR (29 +/- 10 and 31 +/- 11%), but the decrease in RVR was smaller (22 +/- 8 and 35 +/- 12%, respectively; p < 0.05) in HT than in NT subjects. In response to L-NAME, the increments in RVR (66 +/- 10 and 61 +/- 25%) and SVR (36 +/- 21 and 34 +/- 18%) were similar in HT and NT subjects. In both groups, infusion of L-arginine was associated with similar increments, whereas infusion of L-NAME was associated with similar decrements in NOR and PRA.


CONCLUSIONS
This study confirms the smaller renal vasodilator response to L-arginine in HT than in NT subjects. Whether this is caused by a disturbance of the renal NO pathway remains doubtful considering the observed similar L-NAME-induced increments in RVR and SVR in the two groups of subjects.
van den Meiracker
Anton H
AH
Department of Internal Medicine I, University Hospital Dijkzigt, Room L274, Dr. Molewaterplein 40, NL-3015 GD Rotterdam, The Netherlands. ton.vanden.meiracker@12move.nl
van der Linde
Nicole A J
NA
Broere
Annemieke
A
Derkx
Frans H M
FH
Boomsma
Frans
F
D000328:Adult; D001120:Arginine / Q000494:pharmacology*; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure / Q000502:physiology; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D007328:Insulin / Q000097:blood; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology*; D009569:Nitric Oxide / Q000378:metabolism; D009638:Norepinephrine / Q000097:blood; D012083:Renin / Q000097:blood; D016037:Single-Blind Method; D013997:Time Factors; D014662:Vasoconstrictor Agents / Q000097:blood
D001786:Blood Glucose; D004791:Enzyme Inhibitors; D007328:Insulin; D014662:Vasoconstrictor Agents; D009569:Nitric Oxide; D001120:Arginine; D012083:Renin; D019331:NG-Nitroarginine Methyl Ester; D009638:Norepinephrine