It is tempting to speculate that the lower supine levels of ANP seen in patients with orthostatic tachycardia may be due to the lower blood volume and thus absence of mechanical stretching of the atria whereas higher resting levels of ANP could predict decrease in blood pressure due to stimulation of ANP secretion by neurohormones such as for example ET-1 or even by BP-associated gene variants, or by supine hypertension, often seen in OH[22]. The gene discussed is EDN1; the disease is hypertensive disorder.