Effect of L-arginine infusion in normotensive subjects with and without a family history of hypertension

Effect of L-arginine infusion in normotensive subjects with and without a family history of hypertension. Experimental studies have shown that nitric oxide (NO) generation in the kidney from L-arginine participates in the regulation of renal function. Our purpose was to study the effect of infusion...

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Veröffentlicht in:Kidney international 1999-11, Vol.56 (5), p.1838-1845
Hauptverfasser: Herlitz, Hans, Jungersten, Lennart U., Wikstrand, John, Widgren, Bengt R.
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Wikstrand, John
Widgren, Bengt R.
description Effect of L-arginine infusion in normotensive subjects with and without a family history of hypertension. Experimental studies have shown that nitric oxide (NO) generation in the kidney from L-arginine participates in the regulation of renal function. Our purpose was to study the effect of infusion of L-arginine (1, 5, and 10 mg/kg/min) on blood pressure (BP), renal hemodynamics, and urinary excretion of sodium and albumin in normotensive subjects with a family history of either severe hypertension (FHSH, N = 17) or mild hypertension (FHMH, N = 20) and in control subjects (N = 18) without a hereditary predisposition for hypertension. The glomerular filtration rate (GFR) and renal plasma flow (RPF) were measured by renal clearances of Cr51 ethylenediaminetetraacetic acid and paramino-hippurate. Renal tubular reabsorption of sodium was estimated by lithium clearance. To evaluate the effect of L-arginine infusion on the L-arginine/NO pathway, we measured the NO-metabolite nitrate in plasma, and urinary excretion of cGMP, the second messenger of NO. The derivative at an L-arginine dose of 7.5 mg/kg/min was used as a measure of sensitivity to L-arginine. There was no difference in baseline systolic BP between the groups, but diastolic BP was significantly higher in FHSH compared with control subjects (P < 0.05). L-arginine caused a significant increase in urine flow, urinary excretion of albumin and sodium, and lithium clearance in all groups. FHSH showed a significantly decreased sensitivity to L-arginine with respect to urine flow rate (P = 0029) compared with FHMH and control subjects. L-arginine caused a significant decrease in the GFR in FHSH (P < 0.02) and control subjects (P < 0.001), but in FHMH, the decrease did not reach statistical significance (P = 0.097). There was no difference in sensitivity to L-arginine with respect to BP, RPF, or GFR between the three groups. In all patients, there was a significant positive relationship between βDgr; urine flow rate or βDgr; urinary sodium excretion and βDgr; GFR during infusion of L-arginine (P = 0.003 and P = 0.03, respectively). Plasma nitrate and urinary cGMP decreased in all groups during the L-arginine infusion. L-Arginine infusion in normotensive subjects caused an enhanced urine flow rate and urinary sodium and albumin excretion and a slight reduction in GFR. The effect of L-arginine on the urine flow rate was significantly less pronounced in subjects with a family history of severe hypertension, whic
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Experimental studies have shown that nitric oxide (NO) generation in the kidney from L-arginine participates in the regulation of renal function. Our purpose was to study the effect of infusion of L-arginine (1, 5, and 10 mg/kg/min) on blood pressure (BP), renal hemodynamics, and urinary excretion of sodium and albumin in normotensive subjects with a family history of either severe hypertension (FHSH, N = 17) or mild hypertension (FHMH, N = 20) and in control subjects (N = 18) without a hereditary predisposition for hypertension. The glomerular filtration rate (GFR) and renal plasma flow (RPF) were measured by renal clearances of Cr51 ethylenediaminetetraacetic acid and paramino-hippurate. Renal tubular reabsorption of sodium was estimated by lithium clearance. To evaluate the effect of L-arginine infusion on the L-arginine/NO pathway, we measured the NO-metabolite nitrate in plasma, and urinary excretion of cGMP, the second messenger of NO. The derivative at an L-arginine dose of 7.5 mg/kg/min was used as a measure of sensitivity to L-arginine. There was no difference in baseline systolic BP between the groups, but diastolic BP was significantly higher in FHSH compared with control subjects (P &lt; 0.05). L-arginine caused a significant increase in urine flow, urinary excretion of albumin and sodium, and lithium clearance in all groups. FHSH showed a significantly decreased sensitivity to L-arginine with respect to urine flow rate (P = 0029) compared with FHMH and control subjects. L-arginine caused a significant decrease in the GFR in FHSH (P &lt; 0.02) and control subjects (P &lt; 0.001), but in FHMH, the decrease did not reach statistical significance (P = 0.097). There was no difference in sensitivity to L-arginine with respect to BP, RPF, or GFR between the three groups. In all patients, there was a significant positive relationship between βDgr; urine flow rate or βDgr; urinary sodium excretion and βDgr; GFR during infusion of L-arginine (P = 0.003 and P = 0.03, respectively). Plasma nitrate and urinary cGMP decreased in all groups during the L-arginine infusion. L-Arginine infusion in normotensive subjects caused an enhanced urine flow rate and urinary sodium and albumin excretion and a slight reduction in GFR. 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Experimental studies have shown that nitric oxide (NO) generation in the kidney from L-arginine participates in the regulation of renal function. Our purpose was to study the effect of infusion of L-arginine (1, 5, and 10 mg/kg/min) on blood pressure (BP), renal hemodynamics, and urinary excretion of sodium and albumin in normotensive subjects with a family history of either severe hypertension (FHSH, N = 17) or mild hypertension (FHMH, N = 20) and in control subjects (N = 18) without a hereditary predisposition for hypertension. The glomerular filtration rate (GFR) and renal plasma flow (RPF) were measured by renal clearances of Cr51 ethylenediaminetetraacetic acid and paramino-hippurate. Renal tubular reabsorption of sodium was estimated by lithium clearance. To evaluate the effect of L-arginine infusion on the L-arginine/NO pathway, we measured the NO-metabolite nitrate in plasma, and urinary excretion of cGMP, the second messenger of NO. The derivative at an L-arginine dose of 7.5 mg/kg/min was used as a measure of sensitivity to L-arginine. There was no difference in baseline systolic BP between the groups, but diastolic BP was significantly higher in FHSH compared with control subjects (P &lt; 0.05). L-arginine caused a significant increase in urine flow, urinary excretion of albumin and sodium, and lithium clearance in all groups. FHSH showed a significantly decreased sensitivity to L-arginine with respect to urine flow rate (P = 0029) compared with FHMH and control subjects. L-arginine caused a significant decrease in the GFR in FHSH (P &lt; 0.02) and control subjects (P &lt; 0.001), but in FHMH, the decrease did not reach statistical significance (P = 0.097). There was no difference in sensitivity to L-arginine with respect to BP, RPF, or GFR between the three groups. In all patients, there was a significant positive relationship between βDgr; urine flow rate or βDgr; urinary sodium excretion and βDgr; GFR during infusion of L-arginine (P = 0.003 and P = 0.03, respectively). Plasma nitrate and urinary cGMP decreased in all groups during the L-arginine infusion. L-Arginine infusion in normotensive subjects caused an enhanced urine flow rate and urinary sodium and albumin excretion and a slight reduction in GFR. The effect of L-arginine on the urine flow rate was significantly less pronounced in subjects with a family history of severe hypertension, which may indicate a tubular disturbance in hypertension.</description><subject>Adult</subject><subject>Arginine - pharmacology</subject><subject>Biological and medical sciences</subject><subject>familial hypertension</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Glomerular Filtration Rate - drug effects</subject><subject>high blood pressure</subject><subject>Humans</subject><subject>Hypertension - genetics</subject><subject>Hypertension - physiopathology</subject><subject>Kidney - drug effects</subject><subject>Kidney - physiology</subject><subject>Male</subject><subject>nitric oxide</subject><subject>Nitric Oxide - physiology</subject><subject>Renal Circulation - drug effects</subject><subject>renal hemodynamics</subject><subject>Renin - blood</subject><subject>Sodium - metabolism</subject><subject>sodium excretion</subject><subject>Vertebrates: urinary system</subject><issn>0085-2538</issn><issn>1523-1755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1v1DAQhi1ERZe2fwH5gLgl-COOkyNU5UNaiQs9W449Zr1K7MVOSvff4-yugBsnjzXPOzN6EMKU1JQ07ft9TQXjFZVC1LTv-5oQyUX9_AJt_jReog0hnaiY4N01ep3znpR_z8krdE2JkFT2bIN2D86BmXF0eFvp9MMHHwD74JbsYygFDjFNcYaQ_RPgvAz7gmf8y887rIM9FXGZscZOT3484p3Pc0zHdeLueIB0isZwi66cHjPcXd4b9Pjp4fv9l2r77fPX-w_byjRNP1ey7cUAwEC3zjaSGy6ccawhWgMbRNdpMjSGMGDc2qYlVrZusEZY6DrHhOE36N157iHFnwvkWU0-GxhHHSAuWbXFAJGSF7A7gybFnBM4dUh-0umoKFGrZbVXq0y1ylSrZXWyrJ5L9M1lxzJMYP8JnrUW4O0F0Nno0SUdjM9_Odox1smCfTxjUIQ8eUgqGw_BgPWpWFY2-v8f8xsTFp36</recordid><startdate>19991101</startdate><enddate>19991101</enddate><creator>Herlitz, Hans</creator><creator>Jungersten, Lennart U.</creator><creator>Wikstrand, John</creator><creator>Widgren, Bengt R.</creator><general>Elsevier Inc</general><general>Nature Publishing</general><scope>6I.</scope><scope>AAFTH</scope><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>19991101</creationdate><title>Effect of L-arginine infusion in normotensive subjects with and without a family history of hypertension</title><author>Herlitz, Hans ; Jungersten, Lennart U. ; Wikstrand, John ; Widgren, Bengt R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c449t-7695bee2ea6fd473c35fcf240aae2b588a0b4c02e23dd460d76fbdc5de88f25c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Adult</topic><topic>Arginine - pharmacology</topic><topic>Biological and medical sciences</topic><topic>familial hypertension</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Glomerular Filtration Rate - drug effects</topic><topic>high blood pressure</topic><topic>Humans</topic><topic>Hypertension - genetics</topic><topic>Hypertension - physiopathology</topic><topic>Kidney - drug effects</topic><topic>Kidney - physiology</topic><topic>Male</topic><topic>nitric oxide</topic><topic>Nitric Oxide - physiology</topic><topic>Renal Circulation - drug effects</topic><topic>renal hemodynamics</topic><topic>Renin - blood</topic><topic>Sodium - metabolism</topic><topic>sodium excretion</topic><topic>Vertebrates: urinary system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Herlitz, Hans</creatorcontrib><creatorcontrib>Jungersten, Lennart U.</creatorcontrib><creatorcontrib>Wikstrand, John</creatorcontrib><creatorcontrib>Widgren, Bengt R.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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>Kidney international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Herlitz, Hans</au><au>Jungersten, Lennart U.</au><au>Wikstrand, John</au><au>Widgren, Bengt R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of L-arginine infusion in normotensive subjects with and without a family history of hypertension</atitle><jtitle>Kidney international</jtitle><addtitle>Kidney Int</addtitle><date>1999-11-01</date><risdate>1999</risdate><volume>56</volume><issue>5</issue><spage>1838</spage><epage>1845</epage><pages>1838-1845</pages><issn>0085-2538</issn><eissn>1523-1755</eissn><coden>KDYIA5</coden><abstract>Effect of L-arginine infusion in normotensive subjects with and without a family history of hypertension. Experimental studies have shown that nitric oxide (NO) generation in the kidney from L-arginine participates in the regulation of renal function. Our purpose was to study the effect of infusion of L-arginine (1, 5, and 10 mg/kg/min) on blood pressure (BP), renal hemodynamics, and urinary excretion of sodium and albumin in normotensive subjects with a family history of either severe hypertension (FHSH, N = 17) or mild hypertension (FHMH, N = 20) and in control subjects (N = 18) without a hereditary predisposition for hypertension. The glomerular filtration rate (GFR) and renal plasma flow (RPF) were measured by renal clearances of Cr51 ethylenediaminetetraacetic acid and paramino-hippurate. Renal tubular reabsorption of sodium was estimated by lithium clearance. To evaluate the effect of L-arginine infusion on the L-arginine/NO pathway, we measured the NO-metabolite nitrate in plasma, and urinary excretion of cGMP, the second messenger of NO. The derivative at an L-arginine dose of 7.5 mg/kg/min was used as a measure of sensitivity to L-arginine. There was no difference in baseline systolic BP between the groups, but diastolic BP was significantly higher in FHSH compared with control subjects (P &lt; 0.05). L-arginine caused a significant increase in urine flow, urinary excretion of albumin and sodium, and lithium clearance in all groups. FHSH showed a significantly decreased sensitivity to L-arginine with respect to urine flow rate (P = 0029) compared with FHMH and control subjects. L-arginine caused a significant decrease in the GFR in FHSH (P &lt; 0.02) and control subjects (P &lt; 0.001), but in FHMH, the decrease did not reach statistical significance (P = 0.097). There was no difference in sensitivity to L-arginine with respect to BP, RPF, or GFR between the three groups. In all patients, there was a significant positive relationship between βDgr; urine flow rate or βDgr; urinary sodium excretion and βDgr; GFR during infusion of L-arginine (P = 0.003 and P = 0.03, respectively). Plasma nitrate and urinary cGMP decreased in all groups during the L-arginine infusion. L-Arginine infusion in normotensive subjects caused an enhanced urine flow rate and urinary sodium and albumin excretion and a slight reduction in GFR. The effect of L-arginine on the urine flow rate was significantly less pronounced in subjects with a family history of severe hypertension, which may indicate a tubular disturbance in hypertension.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>10571792</pmid><doi>10.1046/j.1523-1755.1999.00735.x</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record>
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subjects Adult
Arginine - pharmacology
Biological and medical sciences
familial hypertension
Fundamental and applied biological sciences. Psychology
Glomerular Filtration Rate - drug effects
high blood pressure
Humans
Hypertension - genetics
Hypertension - physiopathology
Kidney - drug effects
Kidney - physiology
Male
nitric oxide
Nitric Oxide - physiology
Renal Circulation - drug effects
renal hemodynamics
Renin - blood
Sodium - metabolism
sodium excretion
Vertebrates: urinary system
title Effect of L-arginine infusion in normotensive subjects with and without a family history of hypertension
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