CHRONIC L-NAME HYPERTENSION IN RATS AND AUTOREGULATION OF JUXTAMEDULLARY PREGLOMERULAR VESSELS

The impact of chronic N-G-nitro-L-arginine methyl ester (L-NAME)-induc ed 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 videomicros copy and blood-perfused juxtamedullary nephron (JMN) preparations. Res pective tail-cuff-pressures of control and L-NAME rats were 127 +/- 2 (n = 8) and 173 +/- 4 mmHg (n = 5). Corresponding vessels of both grou ps had similar calibers at 60 mmHg. Increasing blood perfusion pressur e to 200 mmHg constricted control ArcA and JAA by 26 +/- 4% (n = 20) a nd 43 +/- 5% (n = 15), respectively. Instead, a respective 3 +/- 4% (n = 15) and 21 +/- 9% (n = 6) pressure-induced dilation occurred in L-N AME vessels, and 86 +/- 2% of glomeruli expressed or-smooth muscle act in. Responses to acetylcholine (1 mu M) 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 st selective loss of vascular autoregulation in JMNs, which may contr ibute to glomerular injury.