Fibrinolytic function in diuretic-induced volume depletion

Accumulating evidence suggests that the renin-angiotensin system (RAS) may participate in the regulation of fibrinolytic function. In clinical studies, however, angiotensin-converting enzyme (ACE) inhibitors and the angiotensin II receptor antagonist losartan have failed to consistently affect endog...

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Veröffentlicht in:American journal of hypertension 2000-04, Vol.13 (4), p.359-363
Hauptverfasser: Lottermoser, Katja, Hertfelder, H.-J, Vetter, H, Düsing, R
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Hertfelder, H.-J
Vetter, H
Düsing, R
description Accumulating evidence suggests that the renin-angiotensin system (RAS) may participate in the regulation of fibrinolytic function. In clinical studies, however, angiotensin-converting enzyme (ACE) inhibitors and the angiotensin II receptor antagonist losartan have failed to consistently affect endogenous fibrinolysis. Because such an effect may depend on the degree of prestimulation of the RAS, we have studied parameters of fibrinolytic function in 15 healthy volunteer subjects during baseline (day 1) and after 10 days of treatment with 25 mg of hydrochlorothiazide (HCT)/day (day 11). On the last day of the study (day 12), a single oral dose of 50 mg of losartan was given to the volunteers in addition to HCT and fibrinolytic function was assessed at the peak effect of losartan (5 h later). Plasma renin activity (PRA) was significantly stimulated during diuretic treatment (1.35 ± 0.21 v 0.34 ± 0.06 ng mL −1 · h −1 [ P < .001]) and further increased after losartan (6.39 ± 1.16 ng mL −1 · h −1 [ P < .001]). No effects of either the diuretic or losartan could be observed on tissue-type plasminogen activator (t-PA) antigen concentration and activity. However, 10 days of treatment with HCT significantly increased plasminogen activator inhibitor-1 (PAI-1) antigen (26.8 ± 5.8 v 21.1 ± 3.4 ng/mL [p = .037]). In addition, PAI-1 activity was also tentatively raised by HCT treatment (5.48 ± 1.82 v 3.88 ± 0.79 IU/mL [ P = .067]). In spite of the marked further rise in PRA after losartan, the stimulation of PAI-1 antigen and activity was blunted by losartan (24.4 ± 3.6 ng/mL and 4.55 ± 0.99 IU/mL, respectively). Our results demonstrate that volume depletion induced by HCT treatment is associated with a rise in PAI-1. Acute administration of losartan is capable of blunting this effect, suggesting that the angiotensin II type 1 receptor may participate in this effect of angiotensin II.
doi_str_mv 10.1016/S0895-7061(99)00286-1
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In clinical studies, however, angiotensin-converting enzyme (ACE) inhibitors and the angiotensin II receptor antagonist losartan have failed to consistently affect endogenous fibrinolysis. Because such an effect may depend on the degree of prestimulation of the RAS, we have studied parameters of fibrinolytic function in 15 healthy volunteer subjects during baseline (day 1) and after 10 days of treatment with 25 mg of hydrochlorothiazide (HCT)/day (day 11). On the last day of the study (day 12), a single oral dose of 50 mg of losartan was given to the volunteers in addition to HCT and fibrinolytic function was assessed at the peak effect of losartan (5 h later). Plasma renin activity (PRA) was significantly stimulated during diuretic treatment (1.35 ± 0.21 v 0.34 ± 0.06 ng mL −1 · h −1 [ P &lt; .001]) and further increased after losartan (6.39 ± 1.16 ng mL −1 · h −1 [ P &lt; .001]). No effects of either the diuretic or losartan could be observed on tissue-type plasminogen activator (t-PA) antigen concentration and activity. However, 10 days of treatment with HCT significantly increased plasminogen activator inhibitor-1 (PAI-1) antigen (26.8 ± 5.8 v 21.1 ± 3.4 ng/mL [p = .037]). In addition, PAI-1 activity was also tentatively raised by HCT treatment (5.48 ± 1.82 v 3.88 ± 0.79 IU/mL [ P = .067]). In spite of the marked further rise in PRA after losartan, the stimulation of PAI-1 antigen and activity was blunted by losartan (24.4 ± 3.6 ng/mL and 4.55 ± 0.99 IU/mL, respectively). Our results demonstrate that volume depletion induced by HCT treatment is associated with a rise in PAI-1. 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Drug treatments ; plasma renin activity ; plasminogen activator inhibitor 1 ; Plasminogen Activator Inhibitor 1 - blood ; Renin - blood ; Sodium Chloride Symporter Inhibitors - administration &amp; dosage ; tissue plasminogen activator ; Tissue Plasminogen Activator - blood</subject><ispartof>American journal of hypertension, 2000-04, Vol.13 (4), p.359-363</ispartof><rights>2000 American Journal of Hypertension, Ltd.</rights><rights>American Journal of Hypertension, Ltd. © 2000 by the American Journal of Hypertension, Ltd. 2000</rights><rights>2000 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Apr 2000</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c568t-d15ae181763dce65bb98c64d101f103968a9d66bfc3adfef7ee17f419c9c3a23</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=1357713$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10821336$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lottermoser, Katja</creatorcontrib><creatorcontrib>Hertfelder, H.-J</creatorcontrib><creatorcontrib>Vetter, H</creatorcontrib><creatorcontrib>Düsing, R</creatorcontrib><title>Fibrinolytic function in diuretic-induced volume depletion</title><title>American journal of hypertension</title><addtitle>AJH</addtitle><description>Accumulating evidence suggests that the renin-angiotensin system (RAS) may participate in the regulation of fibrinolytic function. In clinical studies, however, angiotensin-converting enzyme (ACE) inhibitors and the angiotensin II receptor antagonist losartan have failed to consistently affect endogenous fibrinolysis. Because such an effect may depend on the degree of prestimulation of the RAS, we have studied parameters of fibrinolytic function in 15 healthy volunteer subjects during baseline (day 1) and after 10 days of treatment with 25 mg of hydrochlorothiazide (HCT)/day (day 11). On the last day of the study (day 12), a single oral dose of 50 mg of losartan was given to the volunteers in addition to HCT and fibrinolytic function was assessed at the peak effect of losartan (5 h later). Plasma renin activity (PRA) was significantly stimulated during diuretic treatment (1.35 ± 0.21 v 0.34 ± 0.06 ng mL −1 · h −1 [ P &lt; .001]) and further increased after losartan (6.39 ± 1.16 ng mL −1 · h −1 [ P &lt; .001]). No effects of either the diuretic or losartan could be observed on tissue-type plasminogen activator (t-PA) antigen concentration and activity. However, 10 days of treatment with HCT significantly increased plasminogen activator inhibitor-1 (PAI-1) antigen (26.8 ± 5.8 v 21.1 ± 3.4 ng/mL [p = .037]). In addition, PAI-1 activity was also tentatively raised by HCT treatment (5.48 ± 1.82 v 3.88 ± 0.79 IU/mL [ P = .067]). In spite of the marked further rise in PRA after losartan, the stimulation of PAI-1 antigen and activity was blunted by losartan (24.4 ± 3.6 ng/mL and 4.55 ± 0.99 IU/mL, respectively). Our results demonstrate that volume depletion induced by HCT treatment is associated with a rise in PAI-1. 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Drug treatments</topic><topic>plasma renin activity</topic><topic>plasminogen activator inhibitor 1</topic><topic>Plasminogen Activator Inhibitor 1 - blood</topic><topic>Renin - blood</topic><topic>Sodium Chloride Symporter Inhibitors - administration &amp; dosage</topic><topic>tissue plasminogen activator</topic><topic>Tissue Plasminogen Activator - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lottermoser, Katja</creatorcontrib><creatorcontrib>Hertfelder, H.-J</creatorcontrib><creatorcontrib>Vetter, H</creatorcontrib><creatorcontrib>Düsing, R</creatorcontrib><collection>Istex</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>ProQuest Central (Corporate)</collection><collection>Health &amp; Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of hypertension</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lottermoser, Katja</au><au>Hertfelder, H.-J</au><au>Vetter, H</au><au>Düsing, R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fibrinolytic function in diuretic-induced volume depletion</atitle><jtitle>American journal of hypertension</jtitle><addtitle>AJH</addtitle><date>2000-04-01</date><risdate>2000</risdate><volume>13</volume><issue>4</issue><spage>359</spage><epage>363</epage><pages>359-363</pages><issn>0895-7061</issn><eissn>1879-1905</eissn><eissn>1941-7225</eissn><coden>AJHYE6</coden><abstract>Accumulating evidence suggests that the renin-angiotensin system (RAS) may participate in the regulation of fibrinolytic function. In clinical studies, however, angiotensin-converting enzyme (ACE) inhibitors and the angiotensin II receptor antagonist losartan have failed to consistently affect endogenous fibrinolysis. Because such an effect may depend on the degree of prestimulation of the RAS, we have studied parameters of fibrinolytic function in 15 healthy volunteer subjects during baseline (day 1) and after 10 days of treatment with 25 mg of hydrochlorothiazide (HCT)/day (day 11). On the last day of the study (day 12), a single oral dose of 50 mg of losartan was given to the volunteers in addition to HCT and fibrinolytic function was assessed at the peak effect of losartan (5 h later). Plasma renin activity (PRA) was significantly stimulated during diuretic treatment (1.35 ± 0.21 v 0.34 ± 0.06 ng mL −1 · h −1 [ P &lt; .001]) and further increased after losartan (6.39 ± 1.16 ng mL −1 · h −1 [ P &lt; .001]). No effects of either the diuretic or losartan could be observed on tissue-type plasminogen activator (t-PA) antigen concentration and activity. However, 10 days of treatment with HCT significantly increased plasminogen activator inhibitor-1 (PAI-1) antigen (26.8 ± 5.8 v 21.1 ± 3.4 ng/mL [p = .037]). In addition, PAI-1 activity was also tentatively raised by HCT treatment (5.48 ± 1.82 v 3.88 ± 0.79 IU/mL [ P = .067]). In spite of the marked further rise in PRA after losartan, the stimulation of PAI-1 antigen and activity was blunted by losartan (24.4 ± 3.6 ng/mL and 4.55 ± 0.99 IU/mL, respectively). Our results demonstrate that volume depletion induced by HCT treatment is associated with a rise in PAI-1. Acute administration of losartan is capable of blunting this effect, suggesting that the angiotensin II type 1 receptor may participate in this effect of angiotensin II.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>10821336</pmid><doi>10.1016/S0895-7061(99)00286-1</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record>
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subjects Adult
Angiotensin II
Angiotensin II - antagonists & inhibitors
Antihypertensive agents
Antihypertensive Agents - administration & dosage
Biological and medical sciences
Blood Volume - drug effects
Cardiovascular system
Diuretics
Drug Therapy, Combination
Fibrinolysis - drug effects
Fibrinolysis - physiology
Humans
hydrochlorothiazide
Hydrochlorothiazide - administration & dosage
Hypertension, Renal - drug therapy
Hypertension, Renal - physiopathology
Losartan - administration & dosage
Male
Medical sciences
Pharmacology. Drug treatments
plasma renin activity
plasminogen activator inhibitor 1
Plasminogen Activator Inhibitor 1 - blood
Renin - blood
Sodium Chloride Symporter Inhibitors - administration & dosage
tissue plasminogen activator
Tissue Plasminogen Activator - blood
title Fibrinolytic function in diuretic-induced volume depletion
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