MORDECAI P. BLAUSTEIN, M.D.; JOHN M. HAMLYN, Ph.D.
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.
BLAUSTEIN MP, HAMLYN JM. Role of a Natriuretic Factor in Essential Hypertension: An Hypothesis. Ann Intern Med. 1983;98:785–792. doi: https://doi.org/10.7326/0003-4819-98-5-785
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Published: Ann Intern Med. 1983;98(5_Part_2):785-792.
Cardiology, Coronary Risk Factors, Hypertension, Nephrology.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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