Plasma ProANP1–30 Reflects Salt Sensitivity in Subjects With Heredity for Hypertension
The aim of the present study was to investigate whether plasma concentration of proANP1–30, the N-terminal fragment of the atrial natriuretic peptide prohormone, or 24-hour urinary excretion of urodilatin reflects the degree of salt sensitivity in hypertension-prone individuals. Plasma concentration...
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| Veröffentlicht in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 2002-05, Vol.39 (5), p.996-999 |
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| container_title | Hypertension (Dallas, Tex. 1979) |
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| creator | Melander, Olle Frandsen, Erik Groop, Leif Hulthén, U Lennart |
| description | The aim of the present study was to investigate whether plasma concentration of proANP1–30, the N-terminal fragment of the atrial natriuretic peptide prohormone, or 24-hour urinary excretion of urodilatin reflects the degree of salt sensitivity in hypertension-prone individuals. Plasma concentration of proANP1–30 and urinary urodilatin excretion were determined at baseline, after 1 week on a low-salt diet (10 mmol/d) and after another week on a high-salt diet (240 mmol/d) in 30 healthy subjects with heredity for hypertension. Salt sensitivity was defined as the difference between mean arterial blood pressure after the high-salt diet and the mean arterial blood pressure after the low-salt diet. High- versus low-salt intake increased proANP1–30 (668±330 versus 358±150 pmol/L;P |
| doi_str_mv | 10.1161/01.HYP.0000017552.91014.2A |
| format | Article |
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Plasma concentration of proANP1–30 and urinary urodilatin excretion were determined at baseline, after 1 week on a low-salt diet (10 mmol/d) and after another week on a high-salt diet (240 mmol/d) in 30 healthy subjects with heredity for hypertension. Salt sensitivity was defined as the difference between mean arterial blood pressure after the high-salt diet and the mean arterial blood pressure after the low-salt diet. High- versus low-salt intake increased proANP1–30 (668±330 versus 358±150 pmol/L;P <0.00001) and urodilatin (18.7±5.2 versus 16.0±8.3 pmol/24 h;P <0.05). ProANP1–30 correlated with salt sensitivity at baseline (r =0.76, P <0.000001), after the low- (r =0.80, P <0.0000001) and high-salt diets (r =0.85, P <0.00000001). The increase in proANP1–30 induced by changing from the low- to the high-salt diet was also directly related to salt sensitivity (r =0.78, P <0.000001). ProANP1–30 was not related to urinary sodium excretion. Neither urodilatin nor the sodium-induced change in urodilatin correlated with salt sensitivity. However, urodilatin was related to the urinary sodium excretion at baseline (r =0.58, P <0.01) and after the high-salt diet (r =0.62, P <0.001). In conclusion, the close correlations between proANP1–30 and salt sensitivity suggest that proANP1–30 may serve as a marker for salt sensitivity and could be useful in identifying subjects who would benefit from dietary salt restriction to prevent development of hypertension.]]></description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/01.HYP.0000017552.91014.2A</identifier><identifier>CODEN: HPRTDN</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Arterial hypertension. Arterial hypotension ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Clinical manifestations. Epidemiology. Investigative techniques. Etiology ; Medical sciences</subject><ispartof>Hypertension (Dallas, Tex. 1979), 2002-05, Vol.39 (5), p.996-999</ispartof><rights>2002 American Heart Association, Inc.</rights><rights>2002 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27922,27923</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13679925$$DView record in Pascal Francis$$Hfree_for_read</backlink></links><search><creatorcontrib>Melander, Olle</creatorcontrib><creatorcontrib>Frandsen, Erik</creatorcontrib><creatorcontrib>Groop, Leif</creatorcontrib><creatorcontrib>Hulthén, U Lennart</creatorcontrib><title>Plasma ProANP1–30 Reflects Salt Sensitivity in Subjects With Heredity for Hypertension</title><title>Hypertension (Dallas, Tex. 1979)</title><description><![CDATA[The aim of the present study was to investigate whether plasma concentration of proANP1–30, the N-terminal fragment of the atrial natriuretic peptide prohormone, or 24-hour urinary excretion of urodilatin reflects the degree of salt sensitivity in hypertension-prone individuals. Plasma concentration of proANP1–30 and urinary urodilatin excretion were determined at baseline, after 1 week on a low-salt diet (10 mmol/d) and after another week on a high-salt diet (240 mmol/d) in 30 healthy subjects with heredity for hypertension. Salt sensitivity was defined as the difference between mean arterial blood pressure after the high-salt diet and the mean arterial blood pressure after the low-salt diet. High- versus low-salt intake increased proANP1–30 (668±330 versus 358±150 pmol/L;P <0.00001) and urodilatin (18.7±5.2 versus 16.0±8.3 pmol/24 h;P <0.05). ProANP1–30 correlated with salt sensitivity at baseline (r =0.76, P <0.000001), after the low- (r =0.80, P <0.0000001) and high-salt diets (r =0.85, P <0.00000001). The increase in proANP1–30 induced by changing from the low- to the high-salt diet was also directly related to salt sensitivity (r =0.78, P <0.000001). ProANP1–30 was not related to urinary sodium excretion. Neither urodilatin nor the sodium-induced change in urodilatin correlated with salt sensitivity. However, urodilatin was related to the urinary sodium excretion at baseline (r =0.58, P <0.01) and after the high-salt diet (r =0.62, P <0.001). In conclusion, the close correlations between proANP1–30 and salt sensitivity suggest that proANP1–30 may serve as a marker for salt sensitivity and could be useful in identifying subjects who would benefit from dietary salt restriction to prevent development of hypertension.]]></description><subject>Arterial hypertension. Arterial hypotension</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</subject><subject>Medical sciences</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><recordid>eNotkNFKwzAUhoMoOKfvEAQvW89Jk6y5HKJWGFqc4rwqaZfQzq4dSefYne_gG_okts5zczj8H__P-Qm5RAgRJV4Dhsl7GsIwOBGChQoBecimR2SEgvGACxkdkxGg4oFCXJySM-9XPc05n4zIIq21X2uaunb6mOLP13cE9NnY2hSdp3Ndd3RuGl911WfV7WnV0Pk2X_2Jb1VX0sQ4sxwU2zqa7DfGdQPeNufkxOram4v_PSavd7cvN0kwe7p_uJnOghJjDkFstZU2lsitBm1Yni8lKCVyaVAWKKS2qACYtUYrzcHaSDJciphLXuQQRWNydfDdaF_o2jrdFJXPNq5aa7fPMJITpZjoOX7gdm3dGec_6u3OuKw0_YtlNvTHmYwD1meB6K9gaBSiX7ALZww</recordid><startdate>200205</startdate><enddate>200205</enddate><creator>Melander, Olle</creator><creator>Frandsen, Erik</creator><creator>Groop, Leif</creator><creator>Hulthén, U Lennart</creator><general>American Heart Association, Inc</general><general>Lippincott</general><scope>IQODW</scope></search><sort><creationdate>200205</creationdate><title>Plasma ProANP1–30 Reflects Salt Sensitivity in Subjects With Heredity for Hypertension</title><author>Melander, Olle ; Frandsen, Erik ; Groop, Leif ; Hulthén, U Lennart</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h1840-8faf6f8614fa0ae2bbd60995b6e16c156af19002ffea9a40ff3621d58464cb033</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Arterial hypertension. Arterial hypotension</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</topic><topic>Medical sciences</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Melander, Olle</creatorcontrib><creatorcontrib>Frandsen, Erik</creatorcontrib><creatorcontrib>Groop, Leif</creatorcontrib><creatorcontrib>Hulthén, U Lennart</creatorcontrib><collection>Pascal-Francis</collection><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Melander, Olle</au><au>Frandsen, Erik</au><au>Groop, Leif</au><au>Hulthén, U Lennart</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Plasma ProANP1–30 Reflects Salt Sensitivity in Subjects With Heredity for Hypertension</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><date>2002-05</date><risdate>2002</risdate><volume>39</volume><issue>5</issue><spage>996</spage><epage>999</epage><pages>996-999</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><coden>HPRTDN</coden><abstract><![CDATA[The aim of the present study was to investigate whether plasma concentration of proANP1–30, the N-terminal fragment of the atrial natriuretic peptide prohormone, or 24-hour urinary excretion of urodilatin reflects the degree of salt sensitivity in hypertension-prone individuals. Plasma concentration of proANP1–30 and urinary urodilatin excretion were determined at baseline, after 1 week on a low-salt diet (10 mmol/d) and after another week on a high-salt diet (240 mmol/d) in 30 healthy subjects with heredity for hypertension. Salt sensitivity was defined as the difference between mean arterial blood pressure after the high-salt diet and the mean arterial blood pressure after the low-salt diet. High- versus low-salt intake increased proANP1–30 (668±330 versus 358±150 pmol/L;P <0.00001) and urodilatin (18.7±5.2 versus 16.0±8.3 pmol/24 h;P <0.05). ProANP1–30 correlated with salt sensitivity at baseline (r =0.76, P <0.000001), after the low- (r =0.80, P <0.0000001) and high-salt diets (r =0.85, P <0.00000001). The increase in proANP1–30 induced by changing from the low- to the high-salt diet was also directly related to salt sensitivity (r =0.78, P <0.000001). ProANP1–30 was not related to urinary sodium excretion. Neither urodilatin nor the sodium-induced change in urodilatin correlated with salt sensitivity. However, urodilatin was related to the urinary sodium excretion at baseline (r =0.58, P <0.01) and after the high-salt diet (r =0.62, P <0.001). In conclusion, the close correlations between proANP1–30 and salt sensitivity suggest that proANP1–30 may serve as a marker for salt sensitivity and could be useful in identifying subjects who would benefit from dietary salt restriction to prevent development of hypertension.]]></abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><doi>10.1161/01.HYP.0000017552.91014.2A</doi><tpages>4</tpages></addata></record> |
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| identifier | ISSN: 0194-911X |
| ispartof | Hypertension (Dallas, Tex. 1979), 2002-05, Vol.39 (5), p.996-999 |
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| source | EZB Electronic Journals Library; American Heart Association; Journals@Ovid Complete |
| subjects | Arterial hypertension. Arterial hypotension Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Clinical manifestations. Epidemiology. Investigative techniques. Etiology Medical sciences |
| title | Plasma ProANP1–30 Reflects Salt Sensitivity in Subjects With Heredity for Hypertension |
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