Erythropoietin administration in vivo increases vascular nitric oxide synthase expression.

摘要: This study was designed to determine whether recombinant human erythropoietin (rHuEpo) administration increases vascular nitric oxide (NO) production in healthy rats. We hypothesized that rHuEpo hypertension is associated with increased endothelial expression of synthase and augmented NO-dependent vasodilation. Male rats were instrumented pulsed Doppler flow probes around their ascending aorta arterial femoral catheters. Rats treated for 14 days (2 U/d) or vehicle. elevated hematocrit mean pressure (142 +/- 3 versus 116 4 mm Hg). Thoracic segments from had a modest increase relaxation assessed by acetylcholine (10(-10) 10(-5) mol/L) phenylephrine (PE) (10(-6) contracted arteries. Relaxation NO-donor, s-nitrosyl acetylpenicillamine, PE contraction not different control The NO inhibitor, N-omega-nitro-L-arginine, blood total peripheral resistance more at both 10 30 mg/kg. NOS plasma NOx concentrations compared control. Thus, it appears eNOS causes basal vasodilation hypertensive