Nitric oxide shear stress-induced release

Buga, G. M., Gold, M. E., Fukuto, J. M., and Ignarro, L. J. (1991). Shear-stress-induced release of nitric oxide from endothelial cells grown on beads. Hypertension (Dallas) 17, 187-193. 

FIGURE 2 Inhibition of shear stress-induced release of nitric oxide in isolated endothelial cells by S-nitroso-N-acetylpenicillamine (SNAP). Relaxant responses of the first arterial strip in a three-tissue cascade are illustrated. The flow rate through the column of endothelial cells was varied from 0.3 to 3 ml/min. Three sets of control responses were obtained at 15-min intervals before the addition of SNAP. After the third set of control responses, 1 /rmol/liter SNAP was perfused through the column for 15 min (positioned away from the target arterial strips), following which the column was perfused with plain Krebs bicarbonate solution for a further 15 min. The perfusate was then directed over the target strips, and responses to shear stress were obtained. Data represent the means se from at least four separate experiments. 

Kanai, A.J., H.C. Strauss, G.A. Truskey, A. L. Crews, S. Grunfeld, and T. Malinski (1995). Shear-stress induces ATP-independent transient nitric-oxide release from vascular endothelial-cells, measured directly with a porphyrinic microsensor. Cir. Res. 77(2), 284-293. 

In vitro NO, released fiom fiesh or cultured endothelial cells, inhibits aggregation induced by a variety of agonists as well as by shear stress (Radomski et al, 1987c,d Furlong et al, 1987 Busse et al, 1987 Macdonald et al, 1988 Alheid et al, 1989 Houston et al, 1990 Brockman et al, 1991). Nitric oxide also causes disaggregation of preformed platelet aggregates (Radomski et al, 1987d) and inhibits platelet recruitment (Freedman et al, 1997). 

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