The contribution of nitric oxide to renal vascular wall thickening in ratswith L-NAME-induced hypertension

We investigated the mechanisms of renal vascular wall thickening in a rat m odel of N-nitro L-arginine methyl ester (L-NAME)-induced hypertension. To s eparate the effects of L-NAME-induced hypertension from other effects of ni tric oxide (NO) inhibition, we created two models of L-NAME-induced hyperte nsion: both had the same blood pressure level but NO inhibition was moderat e in one group (group M) and severe in the other (group S). Urinary excreti on of nitrates and nitrites was lower in group S than in group M. Wall thic kening and lipid deposition in renal vessels were significantly great- Intr oduction er in group S than in groups M. Simple and multiple regression ana lyses indicated that renal vascular wall thickening was more strongly corre lated with lipid deposition than with blood pressure. The number of vessels positive for staining with Sudan black B was negatively correlated with ur inary NO excretion. Expression of fibronectin and transforming growth facto r-beta was greater in the Sudan black B-positive than in the Sudan black B- negative vessels, suggesting that extracellular matrix production was incre ased in vessels with lipid deposition. Lipid deposition and increased produ ction of extracellular matrix may contribute to renal vascular wall thicken ing in L-NAME-induced hypertension. Some mechanisms independent of hyperten sion play important roles in vascular wall thickening induced by NO inhibit ion.