Agmatine Induces Rat Prostate Relaxation through Activation of Peripheral Imidazoline I2-Receptors
Article first published online: 30 APR 2012
© 2012 Blackwell Publishing Asia Pty Ltd
LUTS: Lower Urinary Tract Symptoms
Volume 5, Issue 1, pages 39–43, January 2013
How to Cite
LEE, L.-M., LIN, C.-H., CHUNG, H.-H., CHENG, J.-T., CHEN, I.-H. and TONG, Y.-C. (2013), Agmatine Induces Rat Prostate Relaxation through Activation of Peripheral Imidazoline I2-Receptors. LUTS: Lower Urinary Tract Symptoms, 5: 39–43. doi: 10.1111/j.1757-5672.2012.00158.x
- Issue published online: 21 JAN 2013
- Article first published online: 30 APR 2012
- Received 24 January 2012; revised 21 March 2012; accepted 1 April 2012.
- adenosine-5’-triphosphate-sensitive K+ channel;
- imidazoline receptor;
Objectives: The effect of agmatine on prostate contractility as well as the roles of imidazoline receptors and potassium channels in this action were studied using isolated Wistar rat prostate tissue.
Methods: Rat prostate strips were pre-contracted with 1 µmol/L phenylephrine or 50 mmol/L KCl. The relaxation response to agmatine (1–100 µmol/L) was measured. The effects of imidazoline receptor blockers: efaroxan, BU224, KU14R; ATP-sensitive K+ channels (KATP) channel inhibitor: glibenclamide; cyclic AMP (cAMP) phosphodiesterase inhibitor: IBMX; or protein kinase A (PKA) inhibitor: H-89 on the agmatine-induced relaxation were studied.
Results: Agmatine produced relaxation in prostate strips pre-contracted with phenylephrine or KCl in a dose-dependent manner. This relaxation was significantly reduced by BU224, a selective I2 imidazoline receptor (IR) blocker, but not by I1 or I3 IR blockers (efaroxan, KU14R respectively). Moreover, the agmatine-induced relaxation was attenuated by glibenclamide and H-89, but enhanced by IBMX.
Conclusion: The results suggest that agmatine causes rat prostate relaxation by activation of the I2 IR, which opens KATP channels through cAMP/PKA pathway.