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(Hypertension. 2008;52:203.)
© 2008 American Heart Association, Inc.

Editorial Commentaries

Ethnic Differences in Renal Handling of Water and Solutes in Hypertension

Michel Burnier

From the Service de Néphrologie et Consultation d’Hypertension, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.

Correspondence to Michel Burnier, Service de Néphrologie et Consultation d’Hypertension, Rue du Bugnon 17, CHUV, 1011 Lausanne, Switzerland. E-mail michel.burnier@chuv.ch

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Ethnic differences in hypertension are well recognized and have been attributed to several factors, including genetic susceptibility, environmental factors, and lifestyle. This latter increases the likelihood of developing hypertension in some populations by favoring the development of risk factors such as obesity, a low level of physical activity, a high sodium intake, and a low dietary intake of potassium and calcium. Thus, high blood pressure is clearly more frequent among black subjects, and hypertensive disease in black subjects differs from that seen in the white population in several aspects: black hypertensive patients more frequently exhibit salt sensitivity, a tendency toward expanded plasma volume, lower plasma renin activity, and increased renal vascular resistance.^1,2 Moreover, difference in the urinary excretion of natriuretic and vasodilatory substances, such as dopamine and prostaglandins, and in sodium-potassium and sodium-lithium countertransport have been reported in black and white hypertensive subjects, suggesting once again that subjects of black descent excrete sodium less efficiently than white subjects, an observation that also explains the increased percentage of salt-sensitive hypertension in the black population.³

However, the important unanswered question remains, "Where within the kidney does the greater sodium reabsorption occur?" The characterization of the molecular mechanisms of several monogenic forms of human salt-sensitive hypertension has focused much of the attention on an excessive sodium reabsorption by the distal segments of the nephron.⁴ However, these forms of hypertension are rare, and so far primary disturbances in distal reabsorption of sodium that could explain the increased sodium sensitivity of hypertension in some populations . . . [Full Text of this Article]

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