The relation of a circulating sodium transport inhibitor (the natriuretic hormone?) to hypertension.
It is proposed that in essential hypertension the underlying genetic lesion is a renal difficulty in excreting sodium, which becomes more apparent the higher the sodium intake. It is further proposed that the renal lesion is the cause of the observed rise in the plasma's capacity to inhibit Na+-K+-ATPase and that the inhibitor's action on vascular smooth muscle eventually leads to the rise in blood pressure.
D000818:Animals; D001693:Biological Transport, Active; D004285:Dogs; D004790:Enzyme Induction; D004912:Erythrocytes / Q000378:metabolism; D005954:Glucosephosphate Dehydrogenase / Q000096:biosynthesis; D006168:Guinea Pigs; D006801:Humans; D006973:Hypertension / Q000209:etiology* / Q000235:genetics; D007676:Kidney Failure, Chronic / Q000503:physiopathology; D009129:Muscle Tonus; D009130:Muscle, Smooth / Q000502:physiology; D009318:Natriuresis; D045283:Natriuretic Agents; D010455:Peptides; D011506:Proteins / Q000502:physiology*; D051381:Rats; D012964:Sodium / Q000037:antagonists & inhibitors* / Q000378:metabolism / Q000502:physiology; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors
D045283:Natriuretic Agents; D010455:Peptides; D011506:Proteins; C029311:serum sodium transport inhibitor; D012964:Sodium; D005954:Glucosephosphate Dehydrogenase; D000254:Sodium-Potassium-Exchanging ATPase