A circulating sodium transport inhibitor and essential hypertension.
Evidence for the hypothesis that the rise in peripheral resistance that occurs in inherited hypertension is due largely to the observed rise in the circulating level of a sodium transport inhibitor is reviewed. A sequence of events is proposed linking a postulated genetic defect in the kidney's ability to excrete sodium, salt intake, and the rise in the circulating concentration of a sodium transport inhibitor and thereby the rise in peripheral resistance in essential hypertension.
D005954:Glucosephosphate Dehydrogenase / Q000097:blood; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D009399:Nephrons / Q000378:metabolism; D010455:Peptides; D012964:Sodium / Q000037:antagonists & inhibitors* / Q000096:biosynthesis / Q000097:blood / Q000502:physiology; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors
D010455:Peptides; C029311:serum sodium transport inhibitor; D012964:Sodium; D005954:Glucosephosphate Dehydrogenase; D000254:Sodium-Potassium-Exchanging ATPase