Chronic ACE inhibitor treatment increases angiotensin type 1 receptor binding in vivo in the dog kidney

Tamas G. Zober; Maria Elena Fabucci; Wei Zheng; Phillip R. Brown; Esen Seckin; William B. Mathews; Kathryn Sandberg; Zsolt Szabo

doi:10.1007/s00259-007-0667-z

Chronic ACE inhibitor treatment increases angiotensin type 1 receptor binding in vivo in the dog kidney

Tamas G. Zober, Maria Elena Fabucci, Wei Zheng, Phillip R. Brown, Esen Seckin, William B. Mathews, Kathryn Sandberg, Zsolt Szabo

School of Medicine

Research output: Contribution to journal › Article › peer-review

6 Scopus citations

Abstract

Purpose: PET imaging has been recently introduced for investigating the type 1 angiotensin II receptor (AT₁R) in vivo. The goal of the present study was to investigate the effects of acute and chronic exposure to angiotensin converting enzyme inhibitors (ACEI) on the AT₁R in the dog kidney. Methods: Animals were imaged at baseline, after acute intravenous ACEI treatment and after a chronic 2-week exposure to an oral ACEI. Control animals were imaged at identical time points in the absence of ACEI treatment. Results: In vivo AT₁R binding expressed by K _i was increased in the renal cortex by chronic ACEI treatment (p<0.05). In vitro measurements of AT₁R density (B _max) also revealed significant increases in AT₁R in isolated glomeruli (p<0.05). Plasma renin activity was increased, but angiotensin II (Ang II) and the Ang II/Ang I ratio showed a weak correlation with chronic ACEI treatment, consistent with an Ang II escape phenomenon. Conclusion: This study reveals, for the first time, that chronic ACEI treatment increases AT₁R binding in vivo in the dog renal cortex.

Original language	English (US)
Pages (from-to)	1109-1116
Number of pages	8
Journal	European Journal of Nuclear Medicine and Molecular Imaging
Volume	35
Issue number	6
DOIs	https://doi.org/10.1007/s00259-007-0667-z
State	Published - Jun 2008

Keywords

ACE inhibitors
AT receptor
Dogs
In vivo imaging
Positron emission tomography

ASJC Scopus subject areas

Radiology Nuclear Medicine and imaging

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10.1007/s00259-007-0667-z

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@article{3b7f5450d30f4380a12cff95fa64640e,

title = "Chronic ACE inhibitor treatment increases angiotensin type 1 receptor binding in vivo in the dog kidney",

abstract = "Purpose: PET imaging has been recently introduced for investigating the type 1 angiotensin II receptor (AT1R) in vivo. The goal of the present study was to investigate the effects of acute and chronic exposure to angiotensin converting enzyme inhibitors (ACEI) on the AT1R in the dog kidney. Methods: Animals were imaged at baseline, after acute intravenous ACEI treatment and after a chronic 2-week exposure to an oral ACEI. Control animals were imaged at identical time points in the absence of ACEI treatment. Results: In vivo AT1R binding expressed by K i was increased in the renal cortex by chronic ACEI treatment (p<0.05). In vitro measurements of AT1R density (B max) also revealed significant increases in AT1R in isolated glomeruli (p<0.05). Plasma renin activity was increased, but angiotensin II (Ang II) and the Ang II/Ang I ratio showed a weak correlation with chronic ACEI treatment, consistent with an Ang II escape phenomenon. Conclusion: This study reveals, for the first time, that chronic ACEI treatment increases AT1R binding in vivo in the dog renal cortex.",

keywords = "ACE inhibitors, AT receptor, Dogs, In vivo imaging, Positron emission tomography",

author = "Zober, {Tamas G.} and Fabucci, {Maria Elena} and Wei Zheng and Brown, {Phillip R.} and Esen Seckin and Mathews, {William B.} and Kathryn Sandberg and Zsolt Szabo",

note = "Funding Information: Acknowledgment We thank Paige Finley for the help in preparation, monitoring, and postprocedural care of the experimental animals. We also appreciate the contributions of the personnel of the PET center (David Clough, Karen Edmonds, Michael Hans, Hayden Ravert and Robert Smoot) during the organization and performance of the PET studies. This work was supported by the NIH grant #RO1 DK050183.",

year = "2008",

month = jun,

doi = "10.1007/s00259-007-0667-z",

language = "English (US)",

volume = "35",

pages = "1109--1116",

journal = "European Journal of Nuclear Medicine and Molecular Imaging",

issn = "1619-7070",

publisher = "Springer Verlag",

number = "6",

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T1 - Chronic ACE inhibitor treatment increases angiotensin type 1 receptor binding in vivo in the dog kidney

AU - Zober, Tamas G.

AU - Fabucci, Maria Elena

AU - Zheng, Wei

AU - Brown, Phillip R.

AU - Seckin, Esen

AU - Mathews, William B.

AU - Sandberg, Kathryn

AU - Szabo, Zsolt

N1 - Funding Information: Acknowledgment We thank Paige Finley for the help in preparation, monitoring, and postprocedural care of the experimental animals. We also appreciate the contributions of the personnel of the PET center (David Clough, Karen Edmonds, Michael Hans, Hayden Ravert and Robert Smoot) during the organization and performance of the PET studies. This work was supported by the NIH grant #RO1 DK050183.

PY - 2008/6

Y1 - 2008/6

N2 - Purpose: PET imaging has been recently introduced for investigating the type 1 angiotensin II receptor (AT1R) in vivo. The goal of the present study was to investigate the effects of acute and chronic exposure to angiotensin converting enzyme inhibitors (ACEI) on the AT1R in the dog kidney. Methods: Animals were imaged at baseline, after acute intravenous ACEI treatment and after a chronic 2-week exposure to an oral ACEI. Control animals were imaged at identical time points in the absence of ACEI treatment. Results: In vivo AT1R binding expressed by K i was increased in the renal cortex by chronic ACEI treatment (p<0.05). In vitro measurements of AT1R density (B max) also revealed significant increases in AT1R in isolated glomeruli (p<0.05). Plasma renin activity was increased, but angiotensin II (Ang II) and the Ang II/Ang I ratio showed a weak correlation with chronic ACEI treatment, consistent with an Ang II escape phenomenon. Conclusion: This study reveals, for the first time, that chronic ACEI treatment increases AT1R binding in vivo in the dog renal cortex.

AB - Purpose: PET imaging has been recently introduced for investigating the type 1 angiotensin II receptor (AT1R) in vivo. The goal of the present study was to investigate the effects of acute and chronic exposure to angiotensin converting enzyme inhibitors (ACEI) on the AT1R in the dog kidney. Methods: Animals were imaged at baseline, after acute intravenous ACEI treatment and after a chronic 2-week exposure to an oral ACEI. Control animals were imaged at identical time points in the absence of ACEI treatment. Results: In vivo AT1R binding expressed by K i was increased in the renal cortex by chronic ACEI treatment (p<0.05). In vitro measurements of AT1R density (B max) also revealed significant increases in AT1R in isolated glomeruli (p<0.05). Plasma renin activity was increased, but angiotensin II (Ang II) and the Ang II/Ang I ratio showed a weak correlation with chronic ACEI treatment, consistent with an Ang II escape phenomenon. Conclusion: This study reveals, for the first time, that chronic ACEI treatment increases AT1R binding in vivo in the dog renal cortex.

KW - ACE inhibitors

KW - AT receptor

KW - Dogs

KW - In vivo imaging

KW - Positron emission tomography

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ER -

Chronic ACE inhibitor treatment increases angiotensin type 1 receptor binding in vivo in the dog kidney

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