Upregulation of autocrine-paracrine renin-angiotensin systems in chronic renovascular hypertension

Javid Sadjadi, Krishna Puttaparthi, M. Burress Welborn, Thomas E. Rogers, Orson Moe, G. Patrick Clagett, Richard H. Turnage, Moshe Levi, J. Gregory Modrall

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

Introduction: The mechanism by which hypertension is maintained in renovascular hypertension remains poorly defined. Because plasma angiotensin II does not correlate with blood pressure in RVH, we postulated that activation of tissue-specific autocrine-paracrine renin-angiotensin systems may upregulate local production of angiotensin II and maintain hypertension in chronic RVH. Methods: RVH was induced with a two-kidney one-clip (2K1C) rat model. Animals were killed at 1 or 12 weeks after surgery (acute or chronic RVH). Angiotensin II was quantitated with radioimmunoassay. Angiotensin II-type 1 (AT 1) receptor density was determined with immunoblotting and immunohistochemistry. Results: Blood pressure was significantly elevated in 2K1C animals compared with sham animals at 1 week (141 ± 5 mm Hg versus 98 ± 3 mm Hg; P < .0005) and at 12 weeks (164 ± 14 mm Hg versus 110 ± 7 mm Hg; P < .0005) after surgery. No significant difference was seen in plasma angiotensin II levels between 2K1C and control animals during acute (38.2 ± 6.5 fmol/mL versus 27.6 ± 6.8 fmol/mL; P = not significant) or chronic (40.1 ± 17.4 fmol/mL versus 27.1 ± 6.5 fmol/mL; P = not significant) RVH. During acute RVH, intrarenal angiotensin II was significantly increased in both the clipped (126.0 ± 16.2 fmol/g versus 62.0 ± 6.2 fmol/g; P < .005) and unclipped (78.9 ± 6.3 fmol/g versus 39.9 ± 2.5 fmol/g; P < .05) kidneys of 2K1C animals compared with control animals. Increased intrarenal angiotensin II levels persisted in chronic RVH in the clipped (147.4 ± 37.7 fmol/g versus 59.2 ± 8.7 fmol/g; P < .05) and unclipped (130.8 ± 31.8 fmol/g versus 63.0 ± 11.0 fmol/g; P < .05) kidneys of 2K1C animals compared with controls. Adrenal angiotensin II content of 2K1C animals was unchanged in acute RVH (493.7 ± 51.4 fmol/g versus 522.6 ± 80.5 fmol/g; P = not significant) but increased nearly three-fold over control animals during chronic RVH (1129.0 ± 149.3 fmol/g versus 400.6 ± 59.1 fmol/g; P < .0005). No significant difference in AT 1 receptor density was noted in renal tubules of clipped and unclipped kidneys or in the adrenal glands of 2K1C animals during acute or chronic RVH compared with control animals. Conclusion: Tissue angiotensin II production is upregulated in the kidneys and adrenal glands in chronic RVH, and AT 1 receptor density is maintained in these tissues, providing a potential mechanism for maintenance of hypertension in RVH.

Original languageEnglish (US)
Pages (from-to)386-392
Number of pages7
JournalJournal of Vascular Surgery
Volume36
Issue number2
StatePublished - Aug 2002

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Renovascular Hypertension
Renin-Angiotensin System
Up-Regulation
Angiotensin II
Kidney
Angiotensin Type 1 Receptor
Adrenal Glands
Hypertension
Blood Pressure
Immunoblotting
Surgical Instruments
Radioimmunoassay
Immunohistochemistry
Maintenance

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Surgery

Cite this

Sadjadi, J., Puttaparthi, K., Welborn, M. B., Rogers, T. E., Moe, O., Clagett, G. P., ... Modrall, J. G. (2002). Upregulation of autocrine-paracrine renin-angiotensin systems in chronic renovascular hypertension. Journal of Vascular Surgery, 36(2), 386-392.

Upregulation of autocrine-paracrine renin-angiotensin systems in chronic renovascular hypertension. / Sadjadi, Javid; Puttaparthi, Krishna; Welborn, M. Burress; Rogers, Thomas E.; Moe, Orson; Clagett, G. Patrick; Turnage, Richard H.; Levi, Moshe; Modrall, J. Gregory.

In: Journal of Vascular Surgery, Vol. 36, No. 2, 08.2002, p. 386-392.

Research output: Contribution to journalArticle

Sadjadi, J, Puttaparthi, K, Welborn, MB, Rogers, TE, Moe, O, Clagett, GP, Turnage, RH, Levi, M & Modrall, JG 2002, 'Upregulation of autocrine-paracrine renin-angiotensin systems in chronic renovascular hypertension', Journal of Vascular Surgery, vol. 36, no. 2, pp. 386-392.
Sadjadi J, Puttaparthi K, Welborn MB, Rogers TE, Moe O, Clagett GP et al. Upregulation of autocrine-paracrine renin-angiotensin systems in chronic renovascular hypertension. Journal of Vascular Surgery. 2002 Aug;36(2):386-392.
Sadjadi, Javid ; Puttaparthi, Krishna ; Welborn, M. Burress ; Rogers, Thomas E. ; Moe, Orson ; Clagett, G. Patrick ; Turnage, Richard H. ; Levi, Moshe ; Modrall, J. Gregory. / Upregulation of autocrine-paracrine renin-angiotensin systems in chronic renovascular hypertension. In: Journal of Vascular Surgery. 2002 ; Vol. 36, No. 2. pp. 386-392.
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abstract = "Introduction: The mechanism by which hypertension is maintained in renovascular hypertension remains poorly defined. Because plasma angiotensin II does not correlate with blood pressure in RVH, we postulated that activation of tissue-specific autocrine-paracrine renin-angiotensin systems may upregulate local production of angiotensin II and maintain hypertension in chronic RVH. Methods: RVH was induced with a two-kidney one-clip (2K1C) rat model. Animals were killed at 1 or 12 weeks after surgery (acute or chronic RVH). Angiotensin II was quantitated with radioimmunoassay. Angiotensin II-type 1 (AT 1) receptor density was determined with immunoblotting and immunohistochemistry. Results: Blood pressure was significantly elevated in 2K1C animals compared with sham animals at 1 week (141 ± 5 mm Hg versus 98 ± 3 mm Hg; P < .0005) and at 12 weeks (164 ± 14 mm Hg versus 110 ± 7 mm Hg; P < .0005) after surgery. No significant difference was seen in plasma angiotensin II levels between 2K1C and control animals during acute (38.2 ± 6.5 fmol/mL versus 27.6 ± 6.8 fmol/mL; P = not significant) or chronic (40.1 ± 17.4 fmol/mL versus 27.1 ± 6.5 fmol/mL; P = not significant) RVH. During acute RVH, intrarenal angiotensin II was significantly increased in both the clipped (126.0 ± 16.2 fmol/g versus 62.0 ± 6.2 fmol/g; P < .005) and unclipped (78.9 ± 6.3 fmol/g versus 39.9 ± 2.5 fmol/g; P < .05) kidneys of 2K1C animals compared with control animals. Increased intrarenal angiotensin II levels persisted in chronic RVH in the clipped (147.4 ± 37.7 fmol/g versus 59.2 ± 8.7 fmol/g; P < .05) and unclipped (130.8 ± 31.8 fmol/g versus 63.0 ± 11.0 fmol/g; P < .05) kidneys of 2K1C animals compared with controls. Adrenal angiotensin II content of 2K1C animals was unchanged in acute RVH (493.7 ± 51.4 fmol/g versus 522.6 ± 80.5 fmol/g; P = not significant) but increased nearly three-fold over control animals during chronic RVH (1129.0 ± 149.3 fmol/g versus 400.6 ± 59.1 fmol/g; P < .0005). No significant difference in AT 1 receptor density was noted in renal tubules of clipped and unclipped kidneys or in the adrenal glands of 2K1C animals during acute or chronic RVH compared with control animals. Conclusion: Tissue angiotensin II production is upregulated in the kidneys and adrenal glands in chronic RVH, and AT 1 receptor density is maintained in these tissues, providing a potential mechanism for maintenance of hypertension in RVH.",
author = "Javid Sadjadi and Krishna Puttaparthi and Welborn, {M. Burress} and Rogers, {Thomas E.} and Orson Moe and Clagett, {G. Patrick} and Turnage, {Richard H.} and Moshe Levi and Modrall, {J. Gregory}",
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T1 - Upregulation of autocrine-paracrine renin-angiotensin systems in chronic renovascular hypertension

AU - Sadjadi, Javid

AU - Puttaparthi, Krishna

AU - Welborn, M. Burress

AU - Rogers, Thomas E.

AU - Moe, Orson

AU - Clagett, G. Patrick

AU - Turnage, Richard H.

AU - Levi, Moshe

AU - Modrall, J. Gregory

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N2 - Introduction: The mechanism by which hypertension is maintained in renovascular hypertension remains poorly defined. Because plasma angiotensin II does not correlate with blood pressure in RVH, we postulated that activation of tissue-specific autocrine-paracrine renin-angiotensin systems may upregulate local production of angiotensin II and maintain hypertension in chronic RVH. Methods: RVH was induced with a two-kidney one-clip (2K1C) rat model. Animals were killed at 1 or 12 weeks after surgery (acute or chronic RVH). Angiotensin II was quantitated with radioimmunoassay. Angiotensin II-type 1 (AT 1) receptor density was determined with immunoblotting and immunohistochemistry. Results: Blood pressure was significantly elevated in 2K1C animals compared with sham animals at 1 week (141 ± 5 mm Hg versus 98 ± 3 mm Hg; P < .0005) and at 12 weeks (164 ± 14 mm Hg versus 110 ± 7 mm Hg; P < .0005) after surgery. No significant difference was seen in plasma angiotensin II levels between 2K1C and control animals during acute (38.2 ± 6.5 fmol/mL versus 27.6 ± 6.8 fmol/mL; P = not significant) or chronic (40.1 ± 17.4 fmol/mL versus 27.1 ± 6.5 fmol/mL; P = not significant) RVH. During acute RVH, intrarenal angiotensin II was significantly increased in both the clipped (126.0 ± 16.2 fmol/g versus 62.0 ± 6.2 fmol/g; P < .005) and unclipped (78.9 ± 6.3 fmol/g versus 39.9 ± 2.5 fmol/g; P < .05) kidneys of 2K1C animals compared with control animals. Increased intrarenal angiotensin II levels persisted in chronic RVH in the clipped (147.4 ± 37.7 fmol/g versus 59.2 ± 8.7 fmol/g; P < .05) and unclipped (130.8 ± 31.8 fmol/g versus 63.0 ± 11.0 fmol/g; P < .05) kidneys of 2K1C animals compared with controls. Adrenal angiotensin II content of 2K1C animals was unchanged in acute RVH (493.7 ± 51.4 fmol/g versus 522.6 ± 80.5 fmol/g; P = not significant) but increased nearly three-fold over control animals during chronic RVH (1129.0 ± 149.3 fmol/g versus 400.6 ± 59.1 fmol/g; P < .0005). No significant difference in AT 1 receptor density was noted in renal tubules of clipped and unclipped kidneys or in the adrenal glands of 2K1C animals during acute or chronic RVH compared with control animals. Conclusion: Tissue angiotensin II production is upregulated in the kidneys and adrenal glands in chronic RVH, and AT 1 receptor density is maintained in these tissues, providing a potential mechanism for maintenance of hypertension in RVH.

AB - Introduction: The mechanism by which hypertension is maintained in renovascular hypertension remains poorly defined. Because plasma angiotensin II does not correlate with blood pressure in RVH, we postulated that activation of tissue-specific autocrine-paracrine renin-angiotensin systems may upregulate local production of angiotensin II and maintain hypertension in chronic RVH. Methods: RVH was induced with a two-kidney one-clip (2K1C) rat model. Animals were killed at 1 or 12 weeks after surgery (acute or chronic RVH). Angiotensin II was quantitated with radioimmunoassay. Angiotensin II-type 1 (AT 1) receptor density was determined with immunoblotting and immunohistochemistry. Results: Blood pressure was significantly elevated in 2K1C animals compared with sham animals at 1 week (141 ± 5 mm Hg versus 98 ± 3 mm Hg; P < .0005) and at 12 weeks (164 ± 14 mm Hg versus 110 ± 7 mm Hg; P < .0005) after surgery. No significant difference was seen in plasma angiotensin II levels between 2K1C and control animals during acute (38.2 ± 6.5 fmol/mL versus 27.6 ± 6.8 fmol/mL; P = not significant) or chronic (40.1 ± 17.4 fmol/mL versus 27.1 ± 6.5 fmol/mL; P = not significant) RVH. During acute RVH, intrarenal angiotensin II was significantly increased in both the clipped (126.0 ± 16.2 fmol/g versus 62.0 ± 6.2 fmol/g; P < .005) and unclipped (78.9 ± 6.3 fmol/g versus 39.9 ± 2.5 fmol/g; P < .05) kidneys of 2K1C animals compared with control animals. Increased intrarenal angiotensin II levels persisted in chronic RVH in the clipped (147.4 ± 37.7 fmol/g versus 59.2 ± 8.7 fmol/g; P < .05) and unclipped (130.8 ± 31.8 fmol/g versus 63.0 ± 11.0 fmol/g; P < .05) kidneys of 2K1C animals compared with controls. Adrenal angiotensin II content of 2K1C animals was unchanged in acute RVH (493.7 ± 51.4 fmol/g versus 522.6 ± 80.5 fmol/g; P = not significant) but increased nearly three-fold over control animals during chronic RVH (1129.0 ± 149.3 fmol/g versus 400.6 ± 59.1 fmol/g; P < .0005). No significant difference in AT 1 receptor density was noted in renal tubules of clipped and unclipped kidneys or in the adrenal glands of 2K1C animals during acute or chronic RVH compared with control animals. Conclusion: Tissue angiotensin II production is upregulated in the kidneys and adrenal glands in chronic RVH, and AT 1 receptor density is maintained in these tissues, providing a potential mechanism for maintenance of hypertension in RVH.

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