A circulating sodium transport inhibitor and essential hypertension.

Abstract	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.
Authors	G A MacGregor, H E de Wardener
Journal	Journal of cardiovascular pharmacology (J Cardiovasc Pharmacol) Vol. 6 Suppl 1 Pg. S55-60 ( 1984) ISSN: 0160-2446 [Print] United States
PMID	6204160 (Publication Type: Journal Article, Review)
Chemical References	Peptides serum sodium transport inhibitor Sodium Glucosephosphate Dehydrogenase Sodium-Potassium-Exchanging ATPase
Topics	Glucosephosphate Dehydrogenase (blood) Humans Hypertension (physiopathology) Nephrons (metabolism) Peptides Sodium (antagonists & inhibitors, biosynthesis, blood, physiology) Sodium-Potassium-Exchanging ATPase (antagonists & inhibitors)

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