Renal Sodium Excretion in Sons of Hypertensive Parents

The objective of this study was to evaluate whether renal excretion of sodium is impaired and whether tubular reabsorption of sodium is increased in normotensive white men with a familial predisposition to develop essential hypertension. We compared 11 normotensive sons of two hypertensive parents (...

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Veröffentlicht in:Hypertension (Dallas, Tex. 1979) Tex. 1979), 1993-09, Vol.22 (3), p.323-330
Hauptverfasser: Turner, Stephen T, Reilly, Sharon L
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Reilly, Sharon L
description The objective of this study was to evaluate whether renal excretion of sodium is impaired and whether tubular reabsorption of sodium is increased in normotensive white men with a familial predisposition to develop essential hypertension. We compared 11 normotensive sons of two hypertensive parents (SOHT) with 11 normotensive sons of two normotensive parents (SONT); renal sodium handling was assessed after 1 week of low-sodium diet (10 mmol/d) and after 1 week of high-sodium diet (200 mmol/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 seventh day of each diet, baseline means for filtered load of sodium, absolute excretion of sodium, fractional excretion of sodium (an index of total tubular sodium reabsorption), and fractional excretion of lithium (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 intravenously over a 2-hour period. The means for absolute excretion of sodium, fractional excretion of sodium, and fractional excretion of lithium increased from baseline, but the increases did not differ in magnitude between the groups. With both diets, mean blood pressure was 7 mm Hg greater in the SOHT than in the SONT (P=.O46) and did not change significantly 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 predisposition to develop essential hypertension. If such alterations are underlying characteristics of the familial predisposition to develop essential hypertension, then higher blood pressure in the offspring of hypertensive parents may have compensatory renal effects that restore renal sodium handling to normal.
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To assess renal sodium handling under non-steady-state conditions, we infused 2 L normal saline intravenously over a 2-hour period. The means for absolute excretion of sodium, fractional excretion of sodium, and fractional excretion of lithium increased from baseline, but the increases did not differ in magnitude between the groups. With both diets, mean blood pressure was 7 mm Hg greater in the SOHT than in the SONT (P=.O46) and did not change significantly 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 predisposition to develop essential hypertension. 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We compared 11 normotensive sons of two hypertensive parents (SOHT) with 11 normotensive sons of two normotensive parents (SONT); renal sodium handling was assessed after 1 week of low-sodium diet (10 mmol/d) and after 1 week of high-sodium diet (200 mmol/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 seventh day of each diet, baseline means for filtered load of sodium, absolute excretion of sodium, fractional excretion of sodium (an index of total tubular sodium reabsorption), and fractional excretion of lithium (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 intravenously over a 2-hour period. The means for absolute excretion of sodium, fractional excretion of sodium, and fractional excretion of lithium increased from baseline, but the increases did not differ in magnitude between the groups. With both diets, mean blood pressure was 7 mm Hg greater in the SOHT than in the SONT (P=.O46) and did not change significantly 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 predisposition to develop essential hypertension. 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Etiology</subject><subject>Disease Susceptibility</subject><subject>Endothelins - blood</subject><subject>European Continental Ancestry Group</subject><subject>Family</subject><subject>Humans</subject><subject>Hypertension</subject><subject>Kidney - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Norepinephrine - urine</subject><subject>Sodium - urine</subject><subject>Sodium Chloride - administration &amp; dosage</subject><subject>Sodium, Dietary - administration &amp; dosage</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kEFP3DAQhS3UCrbQMyekHCpuCR57HNvHCkG3ElIRbSV6shxnIgLZZGsnUP59jXbFXEbz3jfv8Bg7BV4B1HDBoVr_ua2EqGQlhTxgK1ACS1S1_MBWHCyWFuD-iH1K6ZFzQER9yA6NRCuFWrH6jkY_FD-ntl82xdW_EGnup7Hox6yNqZi6Yv26pTjTmPpnKm59pHFOJ-xj54dEn_f7mP2-vvp1uS5vfnz7fvn1pgyIxpS61q0W2raGk1WoADg1tUbRKQG1B_Sh5ggKWgtGa6BgDDWh7ZRH1TStPGbnu9xtnP4ulGa36VOgYfAjTUtyWhnLDbcZvNiBIU4pRercNvYbH18dcPfWlOPgclNOCCddbip_nO2jl2ZD7Tu_ryb7X_a-T8EPXfRj6NM7hkYbaUTGcIe9TMNMMT0NywtF90B-mB8cz4OiNiVYK7nNV_kmGfkfwGV-fw</recordid><startdate>199309</startdate><enddate>199309</enddate><creator>Turner, Stephen T</creator><creator>Reilly, Sharon L</creator><general>American Heart Association, Inc</general><general>Lippincott</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>199309</creationdate><title>Renal Sodium Excretion in Sons of Hypertensive Parents</title><author>Turner, Stephen T ; Reilly, Sharon L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4488-767d7279d80e9545110eb6742f5216a14ac604151d918771ec88ebcdf5a45bbd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Blood Pressure</topic><topic>Cardiology. Vascular system</topic><topic>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</topic><topic>Disease Susceptibility</topic><topic>Endothelins - blood</topic><topic>European Continental Ancestry Group</topic><topic>Family</topic><topic>Humans</topic><topic>Hypertension</topic><topic>Kidney - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Norepinephrine - urine</topic><topic>Sodium - urine</topic><topic>Sodium Chloride - administration &amp; dosage</topic><topic>Sodium, Dietary - administration &amp; dosage</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Turner, Stephen T</creatorcontrib><creatorcontrib>Reilly, Sharon L</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Turner, Stephen T</au><au>Reilly, Sharon L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Renal Sodium Excretion in Sons of Hypertensive Parents</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>1993-09</date><risdate>1993</risdate><volume>22</volume><issue>3</issue><spage>323</spage><epage>330</epage><pages>323-330</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><coden>HPRTDN</coden><abstract>The objective of this study was to evaluate whether renal excretion of sodium is impaired and whether tubular reabsorption of sodium is increased in normotensive white men with a familial predisposition to develop essential hypertension. We compared 11 normotensive sons of two hypertensive parents (SOHT) with 11 normotensive sons of two normotensive parents (SONT); renal sodium handling was assessed after 1 week of low-sodium diet (10 mmol/d) and after 1 week of high-sodium diet (200 mmol/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 seventh day of each diet, baseline means for filtered load of sodium, absolute excretion of sodium, fractional excretion of sodium (an index of total tubular sodium reabsorption), and fractional excretion of lithium (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 intravenously over a 2-hour period. The means for absolute excretion of sodium, fractional excretion of sodium, and fractional excretion of lithium increased from baseline, but the increases did not differ in magnitude between the groups. With both diets, mean blood pressure was 7 mm Hg greater in the SOHT than in the SONT (P=.O46) and did not change significantly 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 predisposition to develop essential hypertension. If such alterations are underlying characteristics of the familial predisposition to develop essential hypertension, then higher blood pressure in the offspring of hypertensive parents may have compensatory renal effects that restore renal sodium handling to normal.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>8349325</pmid><doi>10.1161/01.HYP.22.3.323</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record>
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subjects Adult
Aged
Arterial hypertension. Arterial hypotension
Biological and medical sciences
Blood and lymphatic vessels
Blood Pressure
Cardiology. Vascular system
Clinical manifestations. Epidemiology. Investigative techniques. Etiology
Disease Susceptibility
Endothelins - blood
European Continental Ancestry Group
Family
Humans
Hypertension
Kidney - metabolism
Male
Medical sciences
Middle Aged
Norepinephrine - urine
Sodium - urine
Sodium Chloride - administration & dosage
Sodium, Dietary - administration & dosage
title Renal Sodium Excretion in Sons of Hypertensive Parents
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