E. Delacretaz et al., LONG-TERM NITRIC-OXIDE SYNTHASE INHIBITION AND DISTENSIBILITY OF CAROTID-ARTERY IN INTACT RATS, Hypertension, 23(6), 1994, pp. 967-970
The goal of the present study was to evaluate the effect of long-term
nitric oxide synthase inhibition by N-G-nitro-L-arginine-methyl ester
(L-NAME) on the morphology and viscoelastic properties of the carotid
arteries in rats. Twelve-week-old Wistar-Kyoto rats were treated for 6
weeks with either the nitric oxide synthase inhibitor L-NAME (0.4 g/L
in drinking water; L-NAME rats, n=13) or tap water (control rats, n=1
3). Age-matched spontaneously hypertensive rats (SHR, n=14) received t
ap water for the same period. The internal diameter of the common caro
tid artery was measured continuously with an echo-tracking device with
the rats under anesthesia with halothane. Intra-arterial pressure was
monitored an the contralateral side. L-NAME rats exhibited arterial p
ressures similar to those of SHR. The distensibility pressure-curve de
termined in L-NAME rats was a direct continuation of that obtained in
control rats. in contrast the distensibility in SHR was increased (P<.
01, SHR versus L-NAME rats). Carotid artery cross-sectional area and l
eft ventricular weight index were increased similarly in SHR and L-NAM
E rats compared with control rats. Thus the hypertension caused by lon
g-term nitric oxide synthesis inhibition was not associated with the i
ncreased arterial distensibility observed in SHR despite similar blood
pressure elevations, similar arterial hypertrophy, and consequently s
imilar wall stress. This suggests a role for nitric oxide in regulatin
g the mechanical behavior of arteries exposed to high blood pressure.