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Urinary Bladder Relaxation through Activation of Imidazoline Receptors Induced by Agmatine is Increased in Diabetic Rats

胍丁胺 咪唑啉受体 内分泌学 内科学 化学 格列本脲 伊达唑嗪 IBMX 磷酸二酯酶抑制剂 敌手 链脲佐菌素 卡巴胆碱 收缩性 受体 糖尿病 医学 生物化学 哌唑嗪 福斯科林 腐胺
作者
Tsung‐Chin Tsai,Chia-Ho Lin,Hsien-Hui Chung,Juei‐Tang Cheng,I-Hung Chen,Yat‐Ching Tong
出处
期刊:Luts: Lower Urinary Tract Symptoms [Wiley]
卷期号:6 (2): 117-123 被引量:7
标识
DOI:10.1111/luts.12031
摘要

ABSTRACT Objectives The effect of agmatine on bladder contractility and the diabetes‐induced alteration of this action were studied in the rat. Methods Bladder strips were isolated from 9‐week‐old streptozotocin ( STZ )‐diabetic rats and control Wistar rats. Strips were hung in an organ bath for measurement of isometric tension and pre‐contracted with either 1 µmol/L acetylcholine ( ACh ) or 50 mmol/L KCl . Dose‐dependent relaxation of the bladder strips was studied by cumulative administration of agmatine 1–100 µmol/L into the organ bath. Effects of specific imidazoline receptor ( IR ) antagonists on the agmatine‐induced relaxation were studied. Western blotting analysis was used to measure bladder IR , sulphonylurea receptor ( SUR ) and inwardly rectifying K + channel subunit 6.2 (Kir 6.2) protein levels. Results Agmatine reduced ACh and KCl pre‐contracted bladder strip tension in a dose‐dependent fashion. Relaxation was significantly increased in STZ ‐diabetic rats. The relaxation was inhibited by BU224 , a selective I 2 IR antagonist; but not by efaroxan ( I 1 IR antagonist) or KU14R ( I 3 IR antagonist). Moreover, the agmatine‐induced relaxation was attenuated by glibenclamide (inhibitor of K ATP channel) and H‐89 (inhibitor of protein kinase A), but enhanced by 3‐isobutyl‐1‐methylxanthine ( IBMX , inhibitor of cyclic AMP phosphodiesterase). Western blotting showed increased expression of bladder IR but not SUR or Kir 6.2 in the STZ ‐diabetic rat. Conclusion Agmatine causes rat bladder relaxation by activation of the I 2 IR , which opens K ATP channels through the cyclic AMP /protein kinase A pathway. Agmatine‐induced bladder relaxation in STZ ‐diabetic rats is increased due to a higher expression of IR .

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