Forman A, Andersson K E, Henriksson L, Rud T, Ulmsten U
Acta Pharmacol Toxicol (Copenh). 1978 Aug;43(2):111-8. doi: 10.1111/j.1600-0773.1978.tb02244.x.
Smooth muscle preparations of the urethra, bladder, and ureter were obtained from patients undergoing operations for various urological disorders. The urethral preparations were contracted by noradrenaline (0.1-3 microgram . ml-1), prostaglandin F2alpha (1-10 microgram . ml-1), and potassium (127 mM), the bladder preparations by carbacholine (0.004-1 microgram . ml-1), prostaglandin F2alpha (1-10 microgram . ml-1), potassium (127 mM), and barium chloride (3 mM), and the ureter preparations by potassium (127 mM), and barium chloride (3 mM). Irrespective of the mode of activation, pretreatment with nifedipine (0.1 microgram . ml-1) for 10 min. reduced the responses. Nifedipine also relaxed preparations contracted by the contractile agents used. In 19 female patients, aged 20 to 73 years, undergoing investigation because of urgency and/or urge incontinence, simultaneous urethrocystometry at rest was performed before and after oral administration of 20 to 40 mg nifedipine. Bladder capacity and residual urine were also determined. Nifedipine did not affect the pressures within the bladder and urethra, nor did it increase the bladder capacity. However, after nifedipine intake there was a statistically significant increase in residual urine. The results suggest that nifedipine can inhibit contractile activity induced by drugs with different modes of action; the drug does not affect the tone in bladder and urethra.
尿道、膀胱和输尿管的平滑肌标本取自因各种泌尿系统疾病接受手术的患者。尿道标本可被去甲肾上腺素（0.1 - 3微克·毫升⁻¹）、前列腺素F2α（1 - 10微克·毫升⁻¹）和钾（127毫摩尔）收缩；膀胱标本可被卡巴胆碱（0.004 - 1微克·毫升⁻¹）、前列腺素F2α（1 - 10微克·毫升⁻¹）、钾（127毫摩尔）和氯化钡（3毫摩尔）收缩；输尿管标本可被钾（127毫摩尔）和氯化钡（3毫摩尔）收缩。无论激活方式如何，用硝苯地平（0.1微克·毫升⁻¹）预处理10分钟可降低反应。硝苯地平还可使被所用收缩剂收缩的标本舒张。在19名年龄20至73岁、因尿急和/或急迫性尿失禁接受检查的女性患者中，在口服20至40毫克硝苯地平前后进行了静息状态下的同步尿道膀胱测压。还测定了膀胱容量和残余尿量。硝苯地平不影响膀胱和尿道内的压力，也不增加膀胱容量。然而，服用硝苯地平后，残余尿量有统计学意义的增加。结果表明，硝苯地平可抑制由不同作用方式的药物诱导的收缩活动；该药物不影响膀胱和尿道的张力。
