Patients with heart failure have a decreased vasomotor response to intracoronary L-NMMA, suggesting that basal release of NO in the coronary circulation is reduced in these patients,28 and this might involve a decrease in nNOS-derived NO based on our previous work in the human coronary circulation.9 Furthermore, patients with chronic heart failure also had enhanced inotropic responses to β-adrenergic agonists after intracoronary L-NMMA.29 The gene discussed is NOS1; the disease is heart failure.