SALT METABOLISM IN HYPERTENSION*†
- JOHN M. WELLER, M.D., F.A.C.P.; and
- SIBLEY W. HOOBLER, M.D., F.A.C.P.
- Requests for reprints should be addressed to John M. Weller, M.D., Department of Internal Medicine, University Hospital, Ann Arbor, Michigan.
Excerpt
It is an established fact that sodium chloride metabolism is abnormal in essential hypertension. However, the exact role which the disordered salt metabolism plays in either the pathogenesis or the perpetuation of this disease is not clear. Both the distribution of sodium within the body and its elimination by the kidney are altered. It has been demonstrated that patients with essential hypertension have slightly elevated serum sodium concentrations.1, 2 In some subjects there is an expansion of the total body sodium, and it has been postulated that this excess sodium is located intracellularly.3 The arterial wall of both hypertensive patients
This 100-word excerpt has been provided in the absence of an abstract.
Summario in Interlingua
Le metabolismo de chloruro de natrium in hypertension essential es anormal. Patientes con hypertension essential pote haber levemente elevate nivellos de natrium seral, un augmentate contento de natrium in le corpore total, e augmentate concentrationes de natrium e de aqua in le parietes arterial.
Hypertension pote esser alleviate per un depletion de natrium. Chlorothiazido, que es un potente agente natriuretic, es capace a producer un effecto antihypertensive tanto in animales hypertensive como etiam in patientes con hypertension. Iste droga produce un potentiation del effectos de varie regimes antihypertensive. Le administration concomitante de chlorothiazido reduce le requirimento de drogas de blocage ganglionic in le tractamento de hypertension. Patientes qui ha essite sympathectomisate responde usualmente al action reductori que chlorothiazido exerce super le tension del sanguine.
Es opinate que le augmentate rejection de natrium, chloruro, e aqua, per que le tubulos renal reage a cargas de sal in hypertension essential, es un effecto e non un causa del elevate tension de sanguine. Il existe nulle prova que le excretion de aqua, occurrente a grados in excesso del excretion de natrium, causa un "retention relative" de natrium in le majoritate del patientes con hypertension.
Es discutite le hypothese que in hypertension essential le contento de natrium in certe compartimentos o in certe histos—possibilemente le lisie musculo vascular—es augmentate e resulta in un elevation del tension del sanguine. Il es possibile que le effecto de chlorothiazido in le tractamento de certe casos de hypertension depende de su capacitate de privar tal histos de natrium. In altere casos le effecto de chlorothiazido pare producer se per le depletion del volumine de plasma.
Article and Author Information
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From the Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan.
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↵† This work has been supported in part by grants from the Michigan Heart Association, American Heart Association, and the National Heart Institute, U. S. Department of Health, Education, and Welfare.
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