Key result
Young spontaneously hypertensive rat vascular smooth muscle cells exhibited significantly lower LPS-induced iNOS activity and NO generation compared to normotensive cells, which was further reduced by Angiotensin II.
Why the study?
Does Angiotensin II affect LPS-induced iNOS activity and nitrite production in aortic VSMC from spontaneously hypertensive rats compared to normotensive rats?
Does Angiotensin II affect LPS-induced iNOS activity and nitrite production in aortic VSMC from spontaneously hypertensive rats compared to normotensive rats?
Impaired NO production in vascular smooth muscle cells precedes the development of hypertension in spontaneously hypertensive rats and is further inhibited by Angiotensin II.
May indicate early NO impairment in SHR models; leaves open translational relevance to human hypertension.
Nitric oxide (NO) generation by inducible nitric oxide synthase (iNOS) in the vascular smooth muscle cells (VSMC), may play a role in blood vessel tone regulation. Lipopolysaccharide (LPS) induced iNOS activity and subsequent nitrite production by cultured aortic VSMC, from SHR with an established chronic blood pressure elevation (adult SHR) or during the period preceding the development of hypertension (young SHR) and from age-matched normotensive Wistar (W) rats were compared. Angiotensin II (Ang II) effect was also evaluated. Both basal LPS-induced iNOS activity and nitrite accumulation were significantly lower in young SHR VSMC compared to young W rat cells. In contrast, adult hypertensive and normotensive rat cells did not differ in NO generation. Besides, young SHR cells exhibited a significant smaller iNOS activity and nitrites than adult SHR cells. After 24 h-incubation with Ang II, both variables were markedly reduced in all groups. The proportional reduction of iNOS activity and nitrites by Ang II was not different between hypertensive and normotensive rat cells, at any age. However, this Ang II inhibitory effect was greater in both adult SHR and W cells than in VSMC from young rats. In conclusion, a reduced LPS-induced iNOS activity and NO generation was observed in VSMC form spontaneously hypertensive rats before the raise of blood pressure, but not in adult hypertensive rat cells. Additionally, an inhibitory effect of angiotensin II on these variables is described. We can speculate that the impairment in vascular smooth muscle NO production precedes the development of hypertension in SHR and may play a pathophysiologic role in the early blood pressure elevation in genetically hypertensive rats.
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Cruzado et al. (2002) studied Hypertension. Angiotensin II vs. Normotensive Wistar rat cells and baseline was evaluated on LPS-induced iNOS activity and nitrite production. Young spontaneously hypertensive rat vascular smooth muscle cells exhibited significantly lower LPS-induced iNOS activity and NO generation compared to normotensive cells, which was further reduced by Angiotensin II.
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