Administration of BAY 41-2272 prevents bladder dysfunction in nitric-oxide deficient rats

ABSTRACT Objective: to evaluate the protective effects of BAY 41-2272, a soluble guanylate cyclase activator, on changes in cystometric parameters in rats deficient in nitric oxide (NO). Methods: Rats were divided into the following groups: (a) control; (b) DMSO; (c) L-NAME; (d) BAY 41-2272 alone; (e) L-NAME + BAY 41-2272. The NO synthase blocker L-NAME (20 mg/rat/day) was given in drinking water concomitantly or not with BAY 41-2272 (10 mg/kg/day, given by gavage). Results: Chronic L-NAME treatment markedly increased the mean arterial blood pressure, and co-treatment with BAY 41-2272 nearly reversed L-NAME-induced rise on mean arterial blood pressure. Non-void contractions were significantly increased in L-NAME group (0.90 ± 0.1 number/minute) compared with either DMSO or control group (0.49 ± 0.1 number/minute), which were prevented by co-treatment with BAY 41-2272 (0.56 ± 025 number/minute; p摘要 研究目的：评估可溶性鸟苷酸环化酶（soluble guanylate cyclase）激活剂BAY 41-2272对一氧化氮（nitric oxide, NO）缺乏大鼠膀胱测压参数变化的保护作用。 方法：将大鼠分为以下组别：(a) 对照组；(b) 二甲基亚砜（DMSO）组；(c) N-硝基-L-精氨酸甲酯（L-NAME）组；(d) 单独BAY 41-2272给药组；(e) L-NAME联合BAY 41-2272给药组。一氧化氮合酶抑制剂L-NAME（20 mg/大鼠/日）通过饮水给药，可联合或不联合BAY 41-2272（10 mg/kg/日，灌胃给药）。 结果：慢性L-NAME给药可显著升高平均动脉压，而联合BAY 41-2272给药几乎可逆转L-NAME诱导的平均动脉压升高。与DMSO组或对照组（0.49 ± 0.1 次/分钟）相比，L-NAME组的非排尿性收缩显著升高（0.90 ± 0.1 次/分钟），该现象可被BAY 41-2272联合给药抑制（0.56 ± 025 次/分钟；p