Overall, these results do not support the hypothesis that activation of NO-insensitive sGC provides a greater beneficial effect on cardiovascular hemodynamics, including blood pressure, heart rate, vascular resistance, and end-organ damage, than does NO-sensitive sGC stimulation, but suggest that sGC activation might be advantageous over sGC stimulation for mitigating cardiac hypertrophy associated with cardiovascular disease. This evidence concerns the gene SGCB and cardiac hypertrophy.