RENAL SODIUM-EXCRETION IN SONS OF HYPERTENSIVE PARENTS

Citation
St. Turner et Sl. Reilly, RENAL SODIUM-EXCRETION IN SONS OF HYPERTENSIVE PARENTS, Hypertension, 22(3), 1993, pp. 323-330
Citations number
23
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
0194911X
Volume
22
Issue
3
Year of publication
1993
Pages
323 - 330
Database
ISI
SICI code
0194-911X(1993)22:3<323:RSISOH>2.0.ZU;2-R
Abstract
The objective of this study was to evaluate whether renal excretion of sodium is impaired and whether tubular reabsorption of sodium is incr eased in normotensive white men with a familial predisposition to deve lop essential hypertension. We compared 11 normotensive sons of two hy pertensive parents (SOHT) with 11 normotensive sons of two normotensiv e parents (SONT); renal sodium handling was assessed after 1 week of l ow-sodium diet (10 mmol/d) and after 1 week of high-sodium diet (200 m mol/d). The SOHT were on average 5.5 years older than the SONT (46.9 /- 5.2 [SD] vs 41.4 +/- 4.1, P = .012). On the sixth day of each diet, mean urinary sodium excretion did not differ between the two groups ( 12.9 +/- 6.3 vs 12.7 +/- 6.7 mmol/d on low-sodium diet, P = .930; 197 +/- 25 vs 200 +/- 27 mmol/d on high-sodium diet, P = .817). On the sev enth day of each diet, baseline means for filtered load of sodium, abs olute excretion of sodium, fractional excretion of sodium (an index of total tubular sodium reabsorption), and fractional excretion of lithi um (an inverse index of proximal tubular sodium reabsorption) also did not differ between the groups. To assess renal sodium handling under non-steady-state conditions, we infused 2 L normal saline intravenousl y over a 2-hour period. The means for absolute excretion of sodium, fr actional excretion of sodium, and fractional excretion of lithium incr eased from baseline, but the increases did not differ in magnitude bet ween the groups. With both diets, mean blood pressure was 7 mm Hg grea ter in the SOHT than in the SONT (P = .046) and did not change signifi cantly during saline infusion. These results provide no evidence that renal excretion of sodium is impaired or that tubular reabsorption of sodium is increased in normotensive white men who have a familial pred isposition to develop essential hypertension. If such alterations are underlying characteristics of the familial predisposition to develop e ssential hypertension, then higher blood pressure in the offspring of hypertensive parents may have compensatory renal effects that restore renal sodium handling to normal.