Skip Navigation

Cardiovascular Research 1995 30(6):857-865; doi:10.1016/S0008-6363(95)00120-4
© 1995 by European Society of Cardiology
This Article
Right arrow Full Text (PDF)
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Bohmann, C.
Right arrow Articles by Rump, L. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bohmann, C.
Right arrow Articles by Rump, L. C.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 1995, European Society of Cardiology

Low concentrations of angiotensin II unmask vasoconstrictory {alpha}2-adrenoceptors in isolated perfused kidneys of spontaneously hypertensive rats

Christine Bohmann, Werner Rist, Peter Schollmeyer and Lars Christian Rump*

Medizinische Universitätsklinik Freiburg, Innere Medizin IV, Hugstetter Str. 55, D-79106 Freiburg, Germany

* Corresponding author. Tel.: (+49-761)270-7058; fax: (+49-761)270-7059.

Objectives: The aim of the present study was to evaluate the role of vascular {alpha}1- and {alpha}2-adrenoceptors in kidneys of spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY). Methods: SHR and WKY kidneys (12–14 weeks) were isolated and perfused with Krebs-Henseleit solution. Concentration-response curves for the {alpha}1-adrenoceptor agonist methoxamine and the {alpha}2-adrenoceptor agonist UK 14304 were constructed alone and in the presence of the {alpha}1-adrenoceptor antagonist prazosin, the {alpha}2-adrenoceptor antagonist idazoxan and exogenous angiotensin II. Results: Methoxamine induced a maximal pressor response of 247 ± 9 mmHg with an EC50 of 1.3 ± 0.1 µM in SHR and of 193 ± 4 mmHg with an EC50 of 1.1 ± 0.1 µM in WKY. The concentration-response curve for methoxamine was shifted to the right by prazosin with a pA2 value of 9.29 (SHR) and 9.26 (WKY) and by idazoxan with a pA2 value of 6.45 (SHR) and 6.33 (WKY). UK 14304 induced a maximal pressor response of 41 ± 12 mmHg in SHR and of 37 ± 8 mmHg in WKY. Angiotensin II (0.1 nM) did not significantly alter pressor responses to methoxamine but caused a marked shift to the left of the concentration-response curve for UK 14304. UK 14304 then induced a maximal pressor response of 92 ± 13 mmHg with an EC50 of 0.07 ± 0.01 µM in SHR and of 78 ± 14 mmHg with an EC50 of 0.14 ± 0.01 µM in WKY. In the presence of angiotensin II (0.1 nM) the concentration-response curve for UK 14304 was shifted to the right by prazosin with a pKB of 6.36 (SHR) and 6.33 (WKY) and by idazoxan with a pKB of 7.68 (SHR) and 7.65 (WKY). Conclusions: The results demonstrate a predominant role of vasoconstrictory {alpha}1-adrenoceptors over {alpha}2-adrenoceptors in SHR and WKY isolated kidneys. Low physiological concentrations of angiotensin II unmask functional vascular {alpha}2-adrenoceptors which are slightly more sensitive in SHR than in WKY kidneys.

KEYWORDS Adrenergic receptors; Renal vasculature; Rat; spontaneously hypertensive; Rat; kidney


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Cardiovasc ResHome page
J. Stegbauer, V. Oberhauser, O. Vonend, and L. C. Rump
Angiotensin-(1-7) modulates vascular resistance and sympathetic neurotransmission in kidneys of spontaneously hypertensive rats
Cardiovasc Res, February 1, 2004; 61(2): 352 - 359.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.