[Cytochemical demonstration of an endogenous inhibitor of Na-K ATPase and its relationship to familial arterial hypertension].
Acute volume expansion, an increase in sodium intake and a restraint on sodium excretion endow the plasma with the capacity to cause a natriuresis, to inhibit sodium transport and to stimulate vascular reactivity. One natriuretic substance, the atrial natriuretic peptide, has been identified. Cytochemical techniques can detect the presence of a Na-K ATPase inhibitor in the plasma of normal man and the rat, the concentration of which is controlled by salt intake. The substance responsible appears to originate in the hypothalamus. The plasma concentration of the cytochemically detectable Na-K ATPase inhibitor is substantially raised in the plasma of patients with essential hypertension, of the spontaneously hypertensive rat and of the Milan hypertensive rat. An hypothesis is put forward that links salt intake, a genetic renal lesion, the endogenous Na-K ATPase inhibitor, the atrial natriuretic peptide, and the substance responsible for vascular reactivity, with the rise in arterial pressure in hereditary forms of hypertension.
D000818:Animals; D009320:Atrial Natriuretic Factor / Q000378:metabolism*; D004791:Enzyme Inhibitors / Q000032:analysis; D005954:Glucosephosphate Dehydrogenase / Q000378:metabolism; D006651:Histocytochemistry; D006801:Humans; D006973:Hypertension / Q000235:genetics / Q000378:metabolism*; D007668:Kidney / Q000378:metabolism; D051381:Rats; D011918:Rats, Inbred SHR; D012964:Sodium / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors*
D004791:Enzyme Inhibitors; D009320:Atrial Natriuretic Factor; D012964:Sodium; D005954:Glucosephosphate Dehydrogenase; D000254:Sodium-Potassium-Exchanging ATPase
Mise en évidence cytochimique d'un inhibiteur endogène de la Na-K ATPase et ses rapports avec l'hypertension artérielle familiale.