Endothelin-1 and urinary bladder hyperplasia following partial bladder outlet obstruction.
Endothelin-1 and urinary bladder hyperplasia following partial bladder outlet obstruction.
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DOI：
10.1097/00005344-200036001-00077
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发表时间：
2000
影响因子：
3
通讯作者：
M. Khan;Nileema Shukla;C. Thompson;F. Mumtaz;D. P. Mikhailidis;R. J. Morgan
中科院分区：
文献类型：
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作者：
M. Khan;Nileema Shukla;C. Thompson;F. Mumtaz;D. P. Mikhailidis;R. J. Morgan
膀胱肥大和增生是膀胱出口梗阻（BOO）的常见特征。已知膀胱合成内皮素-1（ET-1）。ET-1是一种有效的血管收缩肽，具有促有丝分裂的特性。采用部分性膀胱梗阻动物模型，我们研究了内皮素-1及其受体亚型[内皮素-A和-B（ET（A）和ET（B）]在膀胱血管平滑肌细胞（SMC）增殖中的潜在作用。在存在3周龄BOO血清的情况下，ET（A）和ET（B）拮抗剂显著（p = 0.008）抑制逼尿肌和膀胱颈SMC增殖。逼尿肌（ET（A）和ET（B）拮抗剂分别为p = 0.03和p = 0.01）和膀胱颈（ET（A）和ET（B）拮抗剂均为p = 0.01）的细胞计数显著减少。这些结果表明，ET-1拮抗剂可以防止SMC增生与部分BOO。
Urinary bladder hypertrophy and hyperplasia is a common feature of bladder outlet obstruction (BOO). The urinary bladder is known to synthesize endothelin-1 (ET-1). ET-1 is a potent vasoconstrictor peptide with mitogenic properties. Using an animal model of partial BOO we investigated the potential role of ET-1 and its receptor subtypes [endothelin-A and -B (ET(A) and ET(B))] in bladder vascular smooth muscle cells (SMC) proliferation. In the presence of 3-week-old BOO serum, ET(A) and ET(B) antagonists significantly (p = 0.008) inhibited detrusor and bladder neck SMC proliferation. Cell counts were significantly reduced from the detrusor (p = 0.03, p = 0.01 with ET(A) and ET(B) antagonists, respectively) and bladder neck (p = 0.01 for both ET(A) and ET(B) antagonists). These results suggest that ET-1 antagonists may prevent SMC hyperplasia associated with partial BOO.