title: Augmentation of pulse wave velocity precedes vascular structural changes of the aorta in rats treated with N(omega)-nitro-L-arginine methyl ester.
abstract: We examined the relationship between structural changes of the aorta and pulse wave velocity (PWV), and the effects of antihypertensive treatments on PWV in N(omega)-nitro-L-arginine methyl ester (L-NAME)-treated rats. Twelve-week-old Wistar-Kyoto (WKY) rats were divided into the following groups, all of which received drug treatment in their drinking water: an untreated control group (n = 36), an L-NAME-treated group (0.7 mg/ml) (n = 32), an L-NAME and angiotensin converting enzyme (ACE) inhibitor (ACEI)-treated group (imidapril: 0.4 mg/ml) (n = 8), and an L-NAME and hydralazine-treated group (0.2 mg/ml) (n = 10). PWV was measured at the same blood pressure (BP) level as in the control group and the wall-to-lumen ratio of the thoracic aorta was evaluated in all groups. In the L-NAME group, PWV increased compared with the value in the control group, at the same time that BP was increasing. After the third day of treatment, PWV was higher in the L-NAME group than in the control group after adjusting BP to the control level, while the wall-to-lumen ratios were equal between the two groups. After the first week of treatment, not only the adjusted PWV, but also the wall-to-lumen ratios were greater in the L-NAME group than in the control group. With administration of antihypertensive agents, both PWV and the thickening of the aortic wall were reduced, but there was no significant difference between the ACEI and hydralazine-treated groups. In conclusion, in a rat model of nitric oxide (NO) synthesis inhibition, the increase in PWV preceded the vascular structural changes, while antihypertensive treatment reduced both changes. There was no significant difference between treatments with ACEI and hydralazine in this model.
authors.affiliation: Division of Hypertension and Nephrology, Department of Internal Medicine, Kyoto Prefectural University of Medicine, Kyoto, Japan. hisako-k@koto.kpu-m.ac.jp
authors.forename: Hisako
authors.initials: H
authors.lastname: Kameyama
authors.forename: Kazuo
authors.initials: K
authors.lastname: Takeda
authors.forename: Tetsurou
authors.initials: T
authors.lastname: Kusaba
authors.forename: Hiromichi
authors.initials: H
authors.lastname: Narumiya
authors.forename: Syuji
authors.initials: S
authors.lastname: Tanda
authors.forename: Noriko
authors.initials: N
authors.lastname: Kuwahara
authors.forename: Keiko
authors.initials: K
authors.lastname: Yamada
authors.forename: Keiichi
authors.initials: K
authors.lastname: Tamagaki
authors.forename: Mitsuhiko
authors.initials: M
authors.lastname: Okigaki
authors.forename: Tsuguru
authors.initials: T
authors.lastname: Hatta
authors.forename: Susumu
authors.initials: S
authors.lastname: Sasaki
mesh_terms: D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects / Q000473:pathology / Q000502:physiology*; D001161:Arteriosclerosis / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology*; D001783:Blood Flow Velocity / Q000502:physiology*; D004195:Disease Models, Animal; D042241:Early Diagnosis; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D011673:Pulsatile Flow / Q000502:physiology*; D051381:Rats; D011921:Rats, Inbred WKY
chemical_list: D004791:Enzyme Inhibitors; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester