Increased renal production of angiotensin II and thromboxane B2 in conscious diabetic rats

Alaa S. Awad, Randy L. Webb, Robert M. Carey, Helmy M. Siragy

Research output: Contribution to journalArticle

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Abstract

Background: The mechanisms involved in development of cardiovascular complications associated with diabetes mellitus are not well elucidated. Among the vasoactive factors that may play a role in development of these complications are angiotensin II and thromboxane B2 (TXB 2). We hypothesized that diabetes increases renal production of TXB2 through stimulation of angiotensin type-1 receptor. Methods: We used a microdialysis technique to monitor changes in renal interstitial fluid (RIF) TXB2 in conscious streptozotocin-induced diabetes rat model. The RIF levels of angiotensin II and TXB2 were monitored before and during 6 weeks after development of diabetes and during treatment with the angiotensin type-1 receptor blocker valsartan at 10 mg/kg. Measurement of the urinary albumin excretion (UAE) was used to monitor the development and progression of diabetic nephropathy. Results: The UAE was 81.62 ± 1.31 ng/min, 184.75 ± 9.41 ng/min (P <. 01), and 229.84 ± 4.49 ng/min (P <. 0001) at baseline, week 3, and week 6, respectively, after induction of diabetes. Basal levels of RIF angiotensin II were 4.28 ± 0.02 pg/mL and significantly increased to 6.24 ± 0.31 pg/mL (P <. 001) and 7.66 ± 0.05 pg/mL (P <. 001) at 3 and 6 weeks after development of diabetes. Similarly, basal RIF TXB2 was 197 ± 27 pg/mL and increased to 488 ± 80 pg/mL (P <. 01) and 703 ± 130 pg/mL (P <. 01) at 3 and 6 weeks after development of diabetes. Valsartan caused further increase in RIF angiotensin II levels. In contrast, valsartan decreased RIF TXB2 levels at baseline to 85 ± 11 pg/mL (P <. 01), at 3 weeks to 141 ± 17 pg/mL (P <. 01), and at 6 weeks to 255 ± 45 pg/mL (P <. 01) after development of diabetes. Conclusions: These results demonstrate that diabetes mellitus is accompanied by increased renal production of angiotensin II and TXB2. The increase in TXB2 is mediated through stimulation of angiotensin type-1 receptor.

Original languageEnglish (US)
Pages (from-to)544-548
Number of pages5
JournalAmerican journal of hypertension
Volume18
Issue number4
DOIs
StatePublished - Apr 2005

Fingerprint

Thromboxane B2
Angiotensin II
Extracellular Fluid
Valsartan
Kidney
Angiotensin Type 1 Receptor
Albumins
Diabetes Mellitus
Angiotensin II Type 1 Receptor Blockers
Experimental Diabetes Mellitus
Microdialysis
Diabetic Nephropathies

All Science Journal Classification (ASJC) codes

  • Internal Medicine

Cite this

Awad, Alaa S. ; Webb, Randy L. ; Carey, Robert M. ; Siragy, Helmy M. / Increased renal production of angiotensin II and thromboxane B2 in conscious diabetic rats. In: American journal of hypertension. 2005 ; Vol. 18, No. 4. pp. 544-548.
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title = "Increased renal production of angiotensin II and thromboxane B2 in conscious diabetic rats",
abstract = "Background: The mechanisms involved in development of cardiovascular complications associated with diabetes mellitus are not well elucidated. Among the vasoactive factors that may play a role in development of these complications are angiotensin II and thromboxane B2 (TXB 2). We hypothesized that diabetes increases renal production of TXB2 through stimulation of angiotensin type-1 receptor. Methods: We used a microdialysis technique to monitor changes in renal interstitial fluid (RIF) TXB2 in conscious streptozotocin-induced diabetes rat model. The RIF levels of angiotensin II and TXB2 were monitored before and during 6 weeks after development of diabetes and during treatment with the angiotensin type-1 receptor blocker valsartan at 10 mg/kg. Measurement of the urinary albumin excretion (UAE) was used to monitor the development and progression of diabetic nephropathy. Results: The UAE was 81.62 ± 1.31 ng/min, 184.75 ± 9.41 ng/min (P <. 01), and 229.84 ± 4.49 ng/min (P <. 0001) at baseline, week 3, and week 6, respectively, after induction of diabetes. Basal levels of RIF angiotensin II were 4.28 ± 0.02 pg/mL and significantly increased to 6.24 ± 0.31 pg/mL (P <. 001) and 7.66 ± 0.05 pg/mL (P <. 001) at 3 and 6 weeks after development of diabetes. Similarly, basal RIF TXB2 was 197 ± 27 pg/mL and increased to 488 ± 80 pg/mL (P <. 01) and 703 ± 130 pg/mL (P <. 01) at 3 and 6 weeks after development of diabetes. Valsartan caused further increase in RIF angiotensin II levels. In contrast, valsartan decreased RIF TXB2 levels at baseline to 85 ± 11 pg/mL (P <. 01), at 3 weeks to 141 ± 17 pg/mL (P <. 01), and at 6 weeks to 255 ± 45 pg/mL (P <. 01) after development of diabetes. Conclusions: These results demonstrate that diabetes mellitus is accompanied by increased renal production of angiotensin II and TXB2. The increase in TXB2 is mediated through stimulation of angiotensin type-1 receptor.",
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Increased renal production of angiotensin II and thromboxane B2 in conscious diabetic rats. / Awad, Alaa S.; Webb, Randy L.; Carey, Robert M.; Siragy, Helmy M.

In: American journal of hypertension, Vol. 18, No. 4, 04.2005, p. 544-548.

Research output: Contribution to journalArticle

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T1 - Increased renal production of angiotensin II and thromboxane B2 in conscious diabetic rats

AU - Awad, Alaa S.

AU - Webb, Randy L.

AU - Carey, Robert M.

AU - Siragy, Helmy M.

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N2 - Background: The mechanisms involved in development of cardiovascular complications associated with diabetes mellitus are not well elucidated. Among the vasoactive factors that may play a role in development of these complications are angiotensin II and thromboxane B2 (TXB 2). We hypothesized that diabetes increases renal production of TXB2 through stimulation of angiotensin type-1 receptor. Methods: We used a microdialysis technique to monitor changes in renal interstitial fluid (RIF) TXB2 in conscious streptozotocin-induced diabetes rat model. The RIF levels of angiotensin II and TXB2 were monitored before and during 6 weeks after development of diabetes and during treatment with the angiotensin type-1 receptor blocker valsartan at 10 mg/kg. Measurement of the urinary albumin excretion (UAE) was used to monitor the development and progression of diabetic nephropathy. Results: The UAE was 81.62 ± 1.31 ng/min, 184.75 ± 9.41 ng/min (P <. 01), and 229.84 ± 4.49 ng/min (P <. 0001) at baseline, week 3, and week 6, respectively, after induction of diabetes. Basal levels of RIF angiotensin II were 4.28 ± 0.02 pg/mL and significantly increased to 6.24 ± 0.31 pg/mL (P <. 001) and 7.66 ± 0.05 pg/mL (P <. 001) at 3 and 6 weeks after development of diabetes. Similarly, basal RIF TXB2 was 197 ± 27 pg/mL and increased to 488 ± 80 pg/mL (P <. 01) and 703 ± 130 pg/mL (P <. 01) at 3 and 6 weeks after development of diabetes. Valsartan caused further increase in RIF angiotensin II levels. In contrast, valsartan decreased RIF TXB2 levels at baseline to 85 ± 11 pg/mL (P <. 01), at 3 weeks to 141 ± 17 pg/mL (P <. 01), and at 6 weeks to 255 ± 45 pg/mL (P <. 01) after development of diabetes. Conclusions: These results demonstrate that diabetes mellitus is accompanied by increased renal production of angiotensin II and TXB2. The increase in TXB2 is mediated through stimulation of angiotensin type-1 receptor.

AB - Background: The mechanisms involved in development of cardiovascular complications associated with diabetes mellitus are not well elucidated. Among the vasoactive factors that may play a role in development of these complications are angiotensin II and thromboxane B2 (TXB 2). We hypothesized that diabetes increases renal production of TXB2 through stimulation of angiotensin type-1 receptor. Methods: We used a microdialysis technique to monitor changes in renal interstitial fluid (RIF) TXB2 in conscious streptozotocin-induced diabetes rat model. The RIF levels of angiotensin II and TXB2 were monitored before and during 6 weeks after development of diabetes and during treatment with the angiotensin type-1 receptor blocker valsartan at 10 mg/kg. Measurement of the urinary albumin excretion (UAE) was used to monitor the development and progression of diabetic nephropathy. Results: The UAE was 81.62 ± 1.31 ng/min, 184.75 ± 9.41 ng/min (P <. 01), and 229.84 ± 4.49 ng/min (P <. 0001) at baseline, week 3, and week 6, respectively, after induction of diabetes. Basal levels of RIF angiotensin II were 4.28 ± 0.02 pg/mL and significantly increased to 6.24 ± 0.31 pg/mL (P <. 001) and 7.66 ± 0.05 pg/mL (P <. 001) at 3 and 6 weeks after development of diabetes. Similarly, basal RIF TXB2 was 197 ± 27 pg/mL and increased to 488 ± 80 pg/mL (P <. 01) and 703 ± 130 pg/mL (P <. 01) at 3 and 6 weeks after development of diabetes. Valsartan caused further increase in RIF angiotensin II levels. In contrast, valsartan decreased RIF TXB2 levels at baseline to 85 ± 11 pg/mL (P <. 01), at 3 weeks to 141 ± 17 pg/mL (P <. 01), and at 6 weeks to 255 ± 45 pg/mL (P <. 01) after development of diabetes. Conclusions: These results demonstrate that diabetes mellitus is accompanied by increased renal production of angiotensin II and TXB2. The increase in TXB2 is mediated through stimulation of angiotensin type-1 receptor.

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