P-360: Renin release in response to renin system blockade: further evidence for activation of the intrarenal renin system in type-1 diabetes mellitus
In type-1 diabetics, Captopril (Cap) and Candesartan (Cande) administration results in a supra normal rise in renal plasma flow (RPF), thought to reflect activation of the intrarenal renin angiotensin system (RAS). Because of implications for diabetic nephropathy, we explored, in 43 type-1 diabetics...
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| Veröffentlicht in: | American journal of hypertension 2003-05, Vol.16 (S1), p.168A-168A |
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| creator | Stevanovic, Radomir D. Deborah, Price A. Cecilia, Lansang M. Lori, Laffel M. Norman, Hollenberg K. |
| description | In type-1 diabetics, Captopril (Cap) and Candesartan (Cande) administration results in a supra normal rise in renal plasma flow (RPF), thought to reflect activation of the intrarenal renin angiotensin system (RAS). Because of implications for diabetic nephropathy, we explored, in 43 type-1 diabetics (D) (27.7 ± 1.5) and 34 normal subjects (NL) (37.7 ± 2.7 years) in high salt balance, the control of renin response to blockade of the RAS with 25 mg of Cap and 16 mg of Cande on consecutive days. All were white with normal renal function. Baseline PRA was higher in D 0.6 ± 0.08 vs NL 0.4 ± 0.06 ng/mLAngI/hr, (p< 0.001). After Cap, PRA peaked after 90 mn to 5.9 ± 1 in D and 1.6 ± 1 ng/mLAngI/hr in NL (p< 0.001). Baseline PRA was positively correlated with peak PRA in D (r= 0.682, p= 0.0012), and in NL (r= 0.843, p |
| doi_str_mv | 10.1016/S0895-7061(03)00525-9 |
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Because of implications for diabetic nephropathy, we explored, in 43 type-1 diabetics (D) (27.7 ± 1.5) and 34 normal subjects (NL) (37.7 ± 2.7 years) in high salt balance, the control of renin response to blockade of the RAS with 25 mg of Cap and 16 mg of Cande on consecutive days. All were white with normal renal function. Baseline PRA was higher in D 0.6 ± 0.08 vs NL 0.4 ± 0.06 ng/mLAngI/hr, (p< 0.001). After Cap, PRA peaked after 90 mn to 5.9 ± 1 in D and 1.6 ± 1 ng/mLAngI/hr in NL (p< 0.001). Baseline PRA was positively correlated with peak PRA in D (r= 0.682, p= 0.0012), and in NL (r= 0.843, p<0.0001). Baseline RPF before Cap was 631.6 ± 18.6 in D and 566.5 ± 14 mL/mn/1.73m2 in NL (p= 0.008). After Cap, peak RPF was 685.3 ± 19.4 in D, and 590.2 ± 17.6 mL/mn/1.73m2 in NL (p< 0.0001). Responses to Cande were similar to Cap. Peak PRA was reached after 8hrs: 6.6 ± 2.1 for D, and 2 ± 0.8 ng/mLAngI/hr for NL (p= 0.88). Baseline RPF before Cande was 609.1 ± 22.5 in D, and 546.7 ± 20.8 mL/mn/1.73m2 in NL (p= 0.07) After Cande, it was 692 ± 29 in D, and 592.5 mL/mn/1.73m2 in NL (p= 0.03). Baseline RPF was positively correlated with peak RPF after Cap and after Cande(r = 0.8, p < 0.0001) for both D and NL. Diabetics whose baseline PRA was below the mean [=25: “non-activated” (NA) group], were separated from those in whom it was above [=18: “activated” (A) group]. Mean baseline PRA before Cap, was 0.3 ± 0.03 for the NA, and 1.07 ± 0.1 ng/mLAngI/hr for the A (p < 0.001). These two groups differed in age: 30.4 ± 2 (NA), vs 21.9 years (A) (p< 0.001). After Cap: peak PRA was 3.1 ± 1.3 (NA) vs 7.6 ± 1.3 ng/mLAngI/hr (A) (p= 0.03), and peak RPF was 639.8 ± 24.7 (NA) vs 738.7 ± 23.3 mL/mn/1.73m2 (A) (p = 0.009). The Delta RPF after Cande was 44.6 ± 16.6 (NA) vs 118.1 ± 21.4 mL/mn/1.73m2 (A) (p = 0.01). After the administration of Cap or Cande, PRA levels are much higher in D than in NL subjects, suggesting suppression of renin secretion by intrarenal Angiotensin II. RPF parallels PRA response, suggesting that similar forces drive them, probably contributing to the pathogenesis of nephropathy.]]></description><identifier>ISSN: 0895-7061</identifier><identifier>EISSN: 1941-7225</identifier><identifier>DOI: 10.1016/S0895-7061(03)00525-9</identifier><identifier>CODEN: AJHYE6</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>diabetic nephropathy ; Plasma Renin Activity ; Renal Plasma Flow</subject><ispartof>American journal of hypertension, 2003-05, Vol.16 (S1), p.168A-168A</ispartof><rights>Copyright Nature Publishing Group May 2003</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>314,776,780,27903,27904</link.rule.ids></links><search><creatorcontrib>Stevanovic, Radomir D.</creatorcontrib><creatorcontrib>Deborah, Price A.</creatorcontrib><creatorcontrib>Cecilia, Lansang M.</creatorcontrib><creatorcontrib>Lori, Laffel M.</creatorcontrib><creatorcontrib>Norman, Hollenberg K.</creatorcontrib><title>P-360: Renin release in response to renin system blockade: further evidence for activation of the intrarenal renin system in type-1 diabetes mellitus</title><title>American journal of hypertension</title><addtitle>AJH</addtitle><description><![CDATA[In type-1 diabetics, Captopril (Cap) and Candesartan (Cande) administration results in a supra normal rise in renal plasma flow (RPF), thought to reflect activation of the intrarenal renin angiotensin system (RAS). Because of implications for diabetic nephropathy, we explored, in 43 type-1 diabetics (D) (27.7 ± 1.5) and 34 normal subjects (NL) (37.7 ± 2.7 years) in high salt balance, the control of renin response to blockade of the RAS with 25 mg of Cap and 16 mg of Cande on consecutive days. All were white with normal renal function. Baseline PRA was higher in D 0.6 ± 0.08 vs NL 0.4 ± 0.06 ng/mLAngI/hr, (p< 0.001). After Cap, PRA peaked after 90 mn to 5.9 ± 1 in D and 1.6 ± 1 ng/mLAngI/hr in NL (p< 0.001). Baseline PRA was positively correlated with peak PRA in D (r= 0.682, p= 0.0012), and in NL (r= 0.843, p<0.0001). Baseline RPF before Cap was 631.6 ± 18.6 in D and 566.5 ± 14 mL/mn/1.73m2 in NL (p= 0.008). After Cap, peak RPF was 685.3 ± 19.4 in D, and 590.2 ± 17.6 mL/mn/1.73m2 in NL (p< 0.0001). Responses to Cande were similar to Cap. Peak PRA was reached after 8hrs: 6.6 ± 2.1 for D, and 2 ± 0.8 ng/mLAngI/hr for NL (p= 0.88). Baseline RPF before Cande was 609.1 ± 22.5 in D, and 546.7 ± 20.8 mL/mn/1.73m2 in NL (p= 0.07) After Cande, it was 692 ± 29 in D, and 592.5 mL/mn/1.73m2 in NL (p= 0.03). Baseline RPF was positively correlated with peak RPF after Cap and after Cande(r = 0.8, p < 0.0001) for both D and NL. Diabetics whose baseline PRA was below the mean [=25: “non-activated” (NA) group], were separated from those in whom it was above [=18: “activated” (A) group]. Mean baseline PRA before Cap, was 0.3 ± 0.03 for the NA, and 1.07 ± 0.1 ng/mLAngI/hr for the A (p < 0.001). These two groups differed in age: 30.4 ± 2 (NA), vs 21.9 years (A) (p< 0.001). After Cap: peak PRA was 3.1 ± 1.3 (NA) vs 7.6 ± 1.3 ng/mLAngI/hr (A) (p= 0.03), and peak RPF was 639.8 ± 24.7 (NA) vs 738.7 ± 23.3 mL/mn/1.73m2 (A) (p = 0.009). The Delta RPF after Cande was 44.6 ± 16.6 (NA) vs 118.1 ± 21.4 mL/mn/1.73m2 (A) (p = 0.01). After the administration of Cap or Cande, PRA levels are much higher in D than in NL subjects, suggesting suppression of renin secretion by intrarenal Angiotensin II. RPF parallels PRA response, suggesting that similar forces drive them, probably contributing to the pathogenesis of nephropathy.]]></description><subject>diabetic nephropathy</subject><subject>Plasma Renin Activity</subject><subject>Renal Plasma Flow</subject><issn>0895-7061</issn><issn>1941-7225</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNpVjl9LwzAUR4MoOKcfQQj4og_R_GnSdm8i6oRtDh04fClpe4vZunYm6XAfxO9rdCL4dA_8DoeL0Cmjl4wydfVMk1SSmCp2TsUFpZJLku6hHksjRmLO5T7q_SmH6Mi5BaU0Uor10OeUCEUH-Aka02ALNWgH-Afdum0C-zbw9-i2zsMK53VbLHUJA1x11r-BxbAxJTQF4Kq1WBfebLQ3bYPbCoc9xLzVIaHr_6FAfrsGwnBpdA4eHF5BXRvfuWN0UOnawcnv7aPZ3e3sZkhGj_cPN9cjYpSSpAJIqUoizQFYXFDOWZJERRXleZUKITRVvJRS5Cp4lFU8hzxSQhZlKqJcc9FHZ7vs2rbvHTifLdrOhkddxihXKomFksEiO8uEtz-ytTUrbbeZtstMxSKW2XD-mk0myXg8nU-yF_EF79t52Q</recordid><startdate>200305</startdate><enddate>200305</enddate><creator>Stevanovic, Radomir D.</creator><creator>Deborah, Price A.</creator><creator>Cecilia, Lansang M.</creator><creator>Lori, Laffel M.</creator><creator>Norman, Hollenberg K.</creator><general>Oxford University Press</general><scope>BSCLL</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>200305</creationdate><title>P-360: Renin release in response to renin system blockade: further evidence for activation of the intrarenal renin system in type-1 diabetes mellitus</title><author>Stevanovic, Radomir D. ; Deborah, Price A. ; Cecilia, Lansang M. ; Lori, Laffel M. ; Norman, Hollenberg K.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-i665-fee90684a2ee17c0221884cf4bbf9333a062d553b6e9001f2beb4635cd934ba23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>diabetic nephropathy</topic><topic>Plasma Renin Activity</topic><topic>Renal Plasma Flow</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Stevanovic, Radomir D.</creatorcontrib><creatorcontrib>Deborah, Price A.</creatorcontrib><creatorcontrib>Cecilia, Lansang M.</creatorcontrib><creatorcontrib>Lori, Laffel M.</creatorcontrib><creatorcontrib>Norman, Hollenberg K.</creatorcontrib><collection>Istex</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & 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)</collection><collection>ProQuest Central</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 & Medical Complete (Alumni)</collection><collection>Health & 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>ProQuest Central China</collection><jtitle>American journal of hypertension</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Stevanovic, Radomir D.</au><au>Deborah, Price A.</au><au>Cecilia, Lansang M.</au><au>Lori, Laffel M.</au><au>Norman, Hollenberg K.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>P-360: Renin release in response to renin system blockade: further evidence for activation of the intrarenal renin system in type-1 diabetes mellitus</atitle><jtitle>American journal of hypertension</jtitle><addtitle>AJH</addtitle><date>2003-05</date><risdate>2003</risdate><volume>16</volume><issue>S1</issue><spage>168A</spage><epage>168A</epage><pages>168A-168A</pages><issn>0895-7061</issn><eissn>1941-7225</eissn><coden>AJHYE6</coden><abstract><![CDATA[In type-1 diabetics, Captopril (Cap) and Candesartan (Cande) administration results in a supra normal rise in renal plasma flow (RPF), thought to reflect activation of the intrarenal renin angiotensin system (RAS). Because of implications for diabetic nephropathy, we explored, in 43 type-1 diabetics (D) (27.7 ± 1.5) and 34 normal subjects (NL) (37.7 ± 2.7 years) in high salt balance, the control of renin response to blockade of the RAS with 25 mg of Cap and 16 mg of Cande on consecutive days. All were white with normal renal function. Baseline PRA was higher in D 0.6 ± 0.08 vs NL 0.4 ± 0.06 ng/mLAngI/hr, (p< 0.001). After Cap, PRA peaked after 90 mn to 5.9 ± 1 in D and 1.6 ± 1 ng/mLAngI/hr in NL (p< 0.001). Baseline PRA was positively correlated with peak PRA in D (r= 0.682, p= 0.0012), and in NL (r= 0.843, p<0.0001). Baseline RPF before Cap was 631.6 ± 18.6 in D and 566.5 ± 14 mL/mn/1.73m2 in NL (p= 0.008). After Cap, peak RPF was 685.3 ± 19.4 in D, and 590.2 ± 17.6 mL/mn/1.73m2 in NL (p< 0.0001). Responses to Cande were similar to Cap. Peak PRA was reached after 8hrs: 6.6 ± 2.1 for D, and 2 ± 0.8 ng/mLAngI/hr for NL (p= 0.88). Baseline RPF before Cande was 609.1 ± 22.5 in D, and 546.7 ± 20.8 mL/mn/1.73m2 in NL (p= 0.07) After Cande, it was 692 ± 29 in D, and 592.5 mL/mn/1.73m2 in NL (p= 0.03). Baseline RPF was positively correlated with peak RPF after Cap and after Cande(r = 0.8, p < 0.0001) for both D and NL. Diabetics whose baseline PRA was below the mean [=25: “non-activated” (NA) group], were separated from those in whom it was above [=18: “activated” (A) group]. Mean baseline PRA before Cap, was 0.3 ± 0.03 for the NA, and 1.07 ± 0.1 ng/mLAngI/hr for the A (p < 0.001). These two groups differed in age: 30.4 ± 2 (NA), vs 21.9 years (A) (p< 0.001). After Cap: peak PRA was 3.1 ± 1.3 (NA) vs 7.6 ± 1.3 ng/mLAngI/hr (A) (p= 0.03), and peak RPF was 639.8 ± 24.7 (NA) vs 738.7 ± 23.3 mL/mn/1.73m2 (A) (p = 0.009). The Delta RPF after Cande was 44.6 ± 16.6 (NA) vs 118.1 ± 21.4 mL/mn/1.73m2 (A) (p = 0.01). After the administration of Cap or Cande, PRA levels are much higher in D than in NL subjects, suggesting suppression of renin secretion by intrarenal Angiotensin II. RPF parallels PRA response, suggesting that similar forces drive them, probably contributing to the pathogenesis of nephropathy.]]></abstract><cop>Oxford</cop><pub>Oxford University Press</pub><doi>10.1016/S0895-7061(03)00525-9</doi></addata></record> |
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| subjects | diabetic nephropathy Plasma Renin Activity Renal Plasma Flow |
| title | P-360: Renin release in response to renin system blockade: further evidence for activation of the intrarenal renin system in type-1 diabetes mellitus |
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