Kamata K, Inoue K, Kasuya Y
Department of Pharmacology, School of Pharmacy, Hoshi University, Tokyo, Japan.
Res Commun Chem Pathol Pharmacol. 1992 Feb;75(2):143-58.
Functional changes in the urinary bladder obtained from diabetic rats were investigated by determining the responsiveness to acetylcholine (ACh). Maximal contraction of the detrusor strips in response to ACh was significantly enhanced in the diabetic rats. Ca(2+)-induced contracture of the detrusor strips, which had been incubated with 10(-3) M ACh in the presence of nicardipine in Ca(2+)-free medium, was significantly augmented in diabetic rats. Ca(2+)-contracture in Ca(2+)-free, isotonic high-K+ (60 mM) medium was not changed in diabetic state. The density of muscarinic receptors to 3H-QNB was significantly higher in the bladder from diabetic rats compared to age-matched control rats. These results suggest that tone of the autonomic nervous system in the bladder may be decreased in diabetes and, thus, compensatory increase in density of muscarinic receptors may occur. Furthermore, an increased contractile response of the detrusor strips of the urinary bladder to ACh in diabetic rats also may be due to an increased influx of extracellular Ca2+ through the receptor-operated Ca2+ channels but not the voltage-dependent Ca2+ channels.
通过测定对乙酰胆碱（ACh）的反应性，研究了糖尿病大鼠膀胱的功能变化。糖尿病大鼠逼尿肌条对ACh的最大收缩反应显著增强。在无钙培养基中，于尼卡地平存在的情况下，用10⁻³M ACh孵育的逼尿肌条的钙（Ca²⁺）诱导挛缩在糖尿病大鼠中显著增强。在无钙、等渗高钾（60 mM）培养基中的钙（Ca²⁺）挛缩在糖尿病状态下未发生变化。与年龄匹配的对照大鼠相比，糖尿病大鼠膀胱中对³H-QNB的毒蕈碱受体密度显著更高。这些结果表明，糖尿病时膀胱自主神经系统的张力可能降低，因此可能会发生毒蕈碱受体密度的代偿性增加。此外，糖尿病大鼠膀胱逼尿肌条对ACh的收缩反应增加也可能是由于细胞外Ca²⁺通过受体操纵性Ca²⁺通道而非电压依赖性Ca²⁺通道的内流增加所致。
