The impact of chronic NG-nitro-L-arginine methyl ester (L-NAME)-induced hypertension (20 mg.kg-1.day-1 po, for 25 days) on pressure responsiveness was assessed in vessels ranging from arcuate arteries (ArcA) to juxtaglomerular afferent arterioles (JAA), using videomicroscopy and blood-perfused juxtamedullary nephron (JMN) preparations. Respective tail-cuff pressures of control and L-NAME rats were 127 +/- 2 (n = 8) and 173 +/- 4 mmHg (n = 5). Corresponding vessels of both groups had similar calibers at 60 mmHg. Increasing blood perfusion pressure to 200 mmHg constricted control ArcA and JAA by 26 +/- 4% (n = 20) and 43 +/- 5% (n = 15), respectively. Instead, a respective 3 +/- 4% (n = 15) and 21 +/- 9% (n = 6) pressure-induced dilation occurred in L-NAME vessels, and 86 +/- 2% of glomeruli expressed alpha-smooth muscle actin. Responses to acetylcholine (1 microM) but not to nitroprusside (1 mM) were impaired by L-NAME. Maximal relaxation induced by Mn2+ (10 mM) revealed equal basal tone and similar passive viscoelastic properties in control and L-NAME vessels. No vascular hypertrophy was found in L-NAME vessels. Chronic L-NAME hypertension is therefore associated with a selective loss of vascular autoregulation in JMNs, which may contribute to glomerular injury.
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