David J. Paterson’s team found that an increased cAMP-PKA/cGMP-PKG ratio exacerbated cardiac sympathetic activity in hypertension, in which nitric oxide coupled to the nNOS adaptor protein could increase cGMP-PKG pathway flux; then, researchers overexpressed nos1 in stellate neurons, which inhibited Ca2+ influx to the cytoplasm and restored Ca2+-dependent exocytosis in a model of spontaneously hypertensive [60]. The gene discussed is NOS1; the disease is hypertensive disorder.