Gotoh M, Hassouna M, Elhilali M M
J Urol. 1986 Feb;135(2):431-7. doi: 10.1016/s0022-5347(17)45659-x.
Interactions of prostaglandin E2 (PGE2), F2 alpha (PGF2 alpha) and prostacyclin (PGI2) with Ca2+ on the isometric contraction of rabbit detrusor muscle strips were studied using two types of Ca2+ antagonists of different mechanisms of action: verapamil and sodium nitroprusside (NP). The effects of PGI2 on vesicourethral smooth muscle and their relationship with cholinergic, adrenergic receptors and nervous activity were also investigated. PGE2 and F2 alpha (3 X 10(-8) to 3 X 10(-5) M) caused dose-dependent contraction of the strips. Pretreatment of the strips with verapamil (10(-7) to 10(-5)M) significantly inhibited PGs-induced contraction in a dose-dependent manner, whereas NP(10(-7) to 10(-5)M) failed to suppress the contraction. Relaxation of the preparations once contracted by PGE2 and F2 alpha (3 X 10(-6)M) was induced completely by addition of verapamil (10(-5)M), and incompletely by NP(10(-5) to 10(-3)M). Washing of the strips with Ca2+-free solution containing 0.01 mM EGTA completely eliminated spontaneous activity and diminished basal tension, but replenishment of Ca2+ (0.5 to 10 mM) to the medium caused dose-related contraction and spontaneous activity of the strips. Addition of PGE2 and F2 alpha to the Ca2+-free medium enhanced Ca2+-induced contraction and spontaneous activity during Ca2+ replenishment, which were significantly inhibited by pretreatment with verapamil (10(-7) to 10(-5)M) in a dose-dependent manner, but not affected by NP (10(-7) to 10(-5)M). In Ca2+-free medium containing 0.1 mM EGTA, PGE2 and F2 alpha caused a slight degree of tension increase of the strips dose-dependently at the higher concentration exceeding 3 X 10(-6)M. PGI2 (10(-9) to 3 X 10(-4)M) caused dose-dependent contraction of the strips from the bladder body, base and the urethra. The contractile action of PGI2 was greatest on the bladder body, less on the base and minimal on the urethra. The effect of PGI2 was less potent than those of PGE2 and F2 alpha. The PGI2-induced contraction was slow in onset, short lasting, and not affected by pretreatment with phentolamine, propranolol, atropine, hexamethonium, hemicholinium-3 and tetrodotoxin. The interactions of PGI2 with Ca2+ were similar to those of PGE2 and F2 alpha.(ABSTRACT TRUNCATED AT 400 WORDS)
维拉帕米和硝普钠（NP），研究了前列腺素E2（PGE2）、F2α（PGF2α）和前列环素（PGI2）与钙离子对兔逼尿肌条等长收缩的相互作用。还研究了PGI2对膀胱尿道平滑肌的作用及其与胆碱能、肾上腺素能受体和神经活动的关系。PGE2和F2α（3×10⁻⁸至3×10⁻⁵M）引起肌条剂量依赖性收缩。用维拉帕米（10⁻⁷至10⁻⁵M）预处理肌条可显著抑制PGs诱导的收缩，且呈剂量依赖性，而NP（10⁻⁷至10⁻⁵M）不能抑制收缩。对于一旦被PGE2和F2α（3×10⁻⁶M）收缩的制剂，加入维拉帕米（10⁻⁵M）可完全诱导其舒张，而加入NP（10⁻⁵至10⁻³M）则不完全舒张。用含0.01 mM EGTA的无钙溶液冲洗肌条可完全消除自发活动并降低基础张力，但向培养基中补充Ca²⁺（0.5至10 mM）会引起肌条剂量相关的收缩和自发活动。在无钙培养基中加入PGE2和F2α可增强Ca²⁺补充期间Ca²⁺诱导的收缩和自发活动，用维拉帕米（10⁻⁷至10⁻⁵M）预处理可显著抑制，且呈剂量依赖性，但不受NP（10⁻⁷至10⁻⁵M）影响。在含0.1 mM EGTA的无钙培养基中，PGE2和F2α在浓度超过3×10⁻⁶M时可引起肌条轻微的剂量依赖性张力增加。PGI2（10⁻⁹至3×10⁻⁴M）可引起膀胱体、底部和尿道肌条的剂量依赖性收缩。PGI2对膀胱体的收缩作用最大，对底部的作用较小，对尿道的作用最小。PGI2的作用比PGE2和F2α弱。PGI2诱导的收缩起效缓慢、持续时间短，且不受酚妥拉明、普萘洛尔、阿托品、六甲铵、半胱氨酸-3和河豚毒素预处理的影响。PGI2与钙离子的相互作用与PGE2和F2α相似。（摘要截短于400字）
