Figures & data
Figure 1 Typical responses of rat aortic rings with or without the endothelium to norepinephrine (NE) and subsequent Hb treatment. In vessel rings with intact endothelium (+E), 10–50 nM NE produced a notable contraction. Subsequent treatment with 0.2–4 µM Hb elicited an additional contraction. In contrast, in vessel rings denuded of the endothelium (−E), Hb mediated additional contraction did not occur despite precontraction with NE. When vessel rings with intact endothelium were treated with 0.5 mM Nω-nitro-L-arginine methyl ester (NAME; a NOS inhibitor), 4 µM Hb had no effect.
Figure 2 Hb mediated additional contraction in NE precontracted rat aortic rings with or without functional endothelium. In endothelium intact vessel rings pretreated with 50 nM NE, 2 µM Hb elicited a significant additional contraction (P < 0.05, N = 6). In vessel rings without functional endothelium, 50 nM NE produced similar precontractions. However, 2 µM Hb did not elicit a significant additional contraction. (P > 0.05, N = 6). When vessel rings with intact endothelium were pretreated with 2 mM NAME, the NE induced contraction responses were not altered but 2 µM Hb did not elicit significant additional contractions. (P > 0.05, N = 6). The Hb mediated additional tension increases in endothelium intact vessel rings were significantly greater than those of vessels with denuded endothelium or pretreated with NAME (P < 0.01, N = 6 each).
Figure 3 Aortic ring tension responses to 0.3 nM–3 µM norepinephrine (NE) in the absence or presence of 2 µM Hb. At NE doses greater than 5 nM, vessel tension increased linearly with NE doses reaching a plateau at around 0.1 µM. At these NE doses, presence of 2 µM Hb allowed generally significantly greater contractions than NE alone (*P < 0.05).
Figure 4 Imposition of passive tension (PT) to a level produced by 50 nM NE did not allow any notable additional contraction following treatment with 4 µM Hb. The magnitude of Hb mediated additional contraction in NE precontracted vessel rings was significantly greater than that of vessel rings with PT (P < 0.01, N = 6).
Figure 5 RT-PCR assay results for iNOS gene expression in the rat thoracic aortic rings. Lane 1: Molecular weight marker (New England Bio Labs, 100 bp DNA ladder); Lanes 2–3: RT-PCR products from 2 normal rat aorta samples. Absence of a 278 bp band indicates lack of iNOS gene expression; Lanes 4–5: Rat iNOS cDNA band (278 bps; positive controls); Lanes 6–8: Glycerol aldehyde-3-phosphate dehydrogenase (GAPDH) cDNA (983 bps; control gene expression).
