The regulation of blood pressure by aldosterone-target neurons in the NTS appears independent of kidney function, suggesting that MR-dependent hypertension may have a substantial neurogenic component.22,43 In other salt-sensitive models, increased central sympathetic drive and increased peripheral resistance sustain hypertension.44–46 The salt-induced increase in DBP and heightened pressor responsiveness to α-adrenoreceptor agonism in Hsd11b2.BKO mice are consistent with this hypothesis. The gene discussed is NR3C2; the disease is hypertensive disorder.