Role of a natriuretic factor in essential hypertension: an hypothesis.
Excessive dietary intake of sodium appears to play a significant role in human essential hypertension. The underlying mechanism may involve the excessive secretion of a humoral natriuretic factor in response to the salt load. Deproteinized plasma from patients with essential hypertension contains elevated levels of an ouabain-like inhibitor of dog kidney sodium plus potassium-dependent adenosine triphosphatase. This substance, by inhibiting renal sodium transport, should have a natriuretic effect. Plasma from hypertensive patients also produces an ouabain-like sensitization of vascular smooth muscle (rabbit aorta) to exogenous norepinephrine. These data suggest that a circulating inhibitor of the sodium pump may play a key role in generating increased peripheral vascular resistance. Cellular mechanisms that link sodium pump inhibition to increased vascular resistance involve increased norepinephrine release and reduced re-uptake and directly increased smooth muscle contractility and reactivity, as a result of increased cell sodium.
D000818:Animals; D001011:Aorta / Q000378:metabolism; D001794:Blood Pressure; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D004232:Diuretics / Q000627:therapeutic use; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology*; D009131:Muscle, Smooth, Vascular / Q000378:metabolism; D045283:Natriuretic Agents; D009638:Norepinephrine / Q000378:metabolism; D011506:Proteins / Q000502:physiology*; D051381:Rats; D012964:Sodium / Q000378:metabolism; D013572:Synaptic Vesicles / Q000378:metabolism; D014655:Vascular Resistance
D002121:Calcium Channel Blockers; D004232:Diuretics; D045283:Natriuretic Agents; D011506:Proteins; D012964:Sodium; D002118:Calcium; D009638:Norepinephrine