![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
|
|
|
|
|
||
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Received for publication March 10, 2005.
Revised May 16, 2005.
Accepted for publication May 17, 2005.
2-Adrenoceptor Interaction
2-Adrenoceptors potentiate vascular responses to angiotensin II. The goal of this study was to test the hypothesis that the phospholipase C (PLC)/protein kinase C (PKC)/c-src/phosphatidylinositol 3-kinase (PI3K) pathway contributes to the vascular angiotensin II/2-adrenoceptor interaction. In rats in vivo, intrarenal infusions of angiotensin II (10 ng/kg/min) increased renal vascular resistance by 5.8 ± 0.5 units, and this response was enhanced (p<0.05) to 9.1 ± 1.2 units by UK 14,304 (3 µg/kg/min; 2-adrenoceptor agonist). Intrarenal infusions of U73122 (3 µg/min; PLC inhibitor), GF 109203X (10 µg/min; PKC inhibitor), CGP77675 (5 µg/min; c-src inhibitor) and wortmannin (1 µg/min; PI3K inhibitor) abolished the angiotensin II/2-adrenoceptor interaction. In isolated, perfused rat kidneys, angiotensin II (0.3, 1 and 3 nmoles/L) increased perfusion pressure (by 15 ± 8, 39 ± 4 and 93 ± 9 mm Hg, respectively), and UK 14,304 (1 µmole/L) potentiated these responses (to 36 ± 4, 67 ± 7 and 135 ± 17 mm Hg, respectively). This angiotensin II/2-adrenoceptor interaction was abolished by U73122 (10 µmoles/L), GF 109203X (3 µmoles/L), CGP77675 (5 µmoles/L) and wortmannin (0.2 µmoles/L). Preglomerular microvascular smooth muscle cells expressed PLC-
2, PLC-3, c-src, phospho(tyrosine 416)-c-src and PI3K. In these cells, angiotensin II (0.1 µmole/L) and UK 14304 (1 µmole/L) per se did not increase phospho-c-src; however the combination of angiotensin II plus UK 14,304 doubled phospho-c-src, and this interaction was abolished by U73122 (10 µmoles/L) and GF 109203X (3 µmoles/L). Conclusion: The PLC/PKC/c-src/PI3K pathway may contribute importantly to the interaction between 2-adrenoceptors and angiotensin II on renal vascular resistance.
Key words:
UK 14,304, angiotensin II, c-src, phosphatidylinositol 3-kinse, phospho-c-src, phospholipase C
This article has been cited by other articles:
|
|
 |
|
  H. Kinoshita, N. Matsuda, H. Kaba, N. Hatakeyama, T. Azma, K. Nakahata, Y. Kuroda, K. Tange, H. Iranami, and Y. Hatano Roles of Phosphatidylinositol 3-Kinase-Akt and NADPH Oxidase in Adenosine 5'-Triphosphate-Sensitive K+ Channel Function Impaired by High Glucose in the Human Artery Hypertension, September 1, 2008; 52(3): 507 - 513. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. K. Jackson, D. G. Gillespie, C. Zhu, J. Ren, L. C. Zacharia, and Z. Mi {alpha}2-Adrenoceptors Enhance Angiotensin II-Induced Renal Vasoconstriction: Role for NADPH Oxidase and RhoA Hypertension, March 1, 2008; 51(3): 719 - 726. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. K. Jackson, M. Zhang, W. Liu, and Z. Mi Inhibition of Renal Dipeptidyl Peptidase IV Enhances Peptide YY1 36-Induced Potentiation of Angiotensin II-Mediated Renal Vasoconstriction in Spontaneously Hypertensive Rats J. Pharmacol. Exp. Ther., November 1, 2007; 323(2): 431 - 437. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. H. Dubinion, Z. Mi, and E. K. Jackson Role of Renal Sympathetic Nerves in Regulating Renovascular Responses to Angiotensin II in Spontaneously Hypertensive Rats J. Pharmacol. Exp. Ther., June 1, 2006; 317(3): 1330 - 1336. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. H. Dubinion, Z. Mi, C. Zhu, L. Gao, and E. K. Jackson Pancreatic Polypeptide-Fold Peptide Receptors and Angiotensin II-Induced Renal Vasoconstriction Hypertension, March 1, 2006; 47(3): 545 - 551. [Abstract] [Full Text] [PDF]
|
|
 |
 |
 |
|
 |
 |
 |
