ABSTRACT
Nitric oxide (NO), produced by the conversion of the terminal guanidino nitrogen atom(s) from L-arginine into L-citrulline, or a complex molecule yielding NO, accounts for many of the biological properties of endothelium-derived relaxing factor. Endothelium-dependent relaxations of isolated aortic rings from spontaneously hypertensive rats (SHR) are impaired compared to normotensive Wistar Kyoto (WKY) rats, since a simultaneous release of endothelium-dependent contracting factors decreases the relaxing activity of NO despite a greater sensitivity to nitrovasodiolators and to NO and a larger expression of the soluble guanylate cyclase in the smooth muscle from SHR than in WKY rats. Aortic smooth muscle cells from SHR are more sensitive to mitogens and are less affected by the anti-proliferative heparin than cells from WKY rats. This chapter summarizes earlier studies designed to investigate whether or not cytokines induce the L-arginine NO pathway in aortic smooth muscle cells from the SHR, and whether or not there are differences in induction between normotensive and hypertensive strains.
