Dmitrieva Natalia
Program in Neuroscience, Florida State University, Tallahassee, Florida 32306-1270, USA.
J Urol. 2007 Dec;178(6):2677-82. doi: 10.1016/j.juro.2007.07.119. Epub 2007 Oct 22.
It is possible that postmenopausal loss of ovarian hormones leads to sensitization and/or over expression of alpha1-adrenergic receptors. The objective of this study was to determine whether ovariectomy enhances efferent transmission and, hence, increases contractility in the rat bladder by increasing alpha1-adrenergic receptors.
This hypothesis was tested in 4 urethane anesthetized groups of female rats, including regularly cycling rats in metestrus and proestrus, and rats 4 months after ovariectomy with and without estradiol replacement, respectively. The bladder was catheterized through the urethra to measure intravesical pressure. The left femoral artery was also catheterized for local delivery of the nonspecific alpha1-adrenergic agonist phenylephrine, the alpha1-adrenergic antagonist prazosin, the specific alpha1A antagonist 5-methylurapidil or dimethyl sulfoxide (Sigma) in saline vehicle. In some rats bladder contractility was assessed by cystometry, followed by treatment with phenylephrine injected via the femoral artery. In other rats the bladder was denervated and a platinum electrode was wrapped around branches of the left pelvic nerve for electrical stimulation. The amplitude of micturition contractions and contractions evoked by phenylephrine or pelvic nerve stimulation was measured.
Micturition and phenylephrine evoked bladder contractions were significantly increased in ovariectomized rats without estradiol replacement. Prazosin significantly decreased contractions evoked by pelvic stimulation in a dose dependent manner. This decrease was significantly larger in ovariectomized rats without estradiol replacement compared to that in the other groups. The inhibition of stimulation evoked contractions by 5-methylurapidil was also greater in ovariectomized rats without estradiol replacement than in rats with estradiol replacement.
Results suggest that the depletion of ovarian hormones after ovariectomy enhances alpha1-adrenergic activity.
绝经后卵巢激素的丧失可能导致α1 - 肾上腺素能受体致敏和/或过度表达。本研究的目的是确定卵巢切除术是否通过增加α1 - 肾上腺素能受体来增强传出神经传递，从而增加大鼠膀胱的收缩力。
在4组经乌拉坦麻醉的雌性大鼠中验证该假设，包括处于动情后期和动情前期的正常发情周期大鼠，以及分别在卵巢切除术后4个月且有或无雌二醇替代治疗的大鼠。通过尿道将膀胱插管以测量膀胱内压。还将左股动脉插管用于在生理盐水中局部递送非特异性α1 - 肾上腺素能激动剂去氧肾上腺素、α1 - 肾上腺素能拮抗剂哌唑嗪、特异性α1A拮抗剂5 - 甲基尿嘧啶或二甲基亚砜（西格玛）。在一些大鼠中，通过膀胱测压评估膀胱收缩力，然后经股动脉注射去氧肾上腺素进行治疗。在其他大鼠中，使膀胱去神经支配，并将铂电极缠绕在左盆神经分支周围进行电刺激。测量排尿收缩以及由去氧肾上腺素或盆神经刺激引起的收缩幅度。
在未进行雌二醇替代治疗的卵巢切除大鼠中，排尿和去氧肾上腺素引起的膀胱收缩显著增加。哌唑嗪以剂量依赖性方式显著降低盆神经刺激引起的收缩。与其他组相比，在未进行雌二醇替代治疗的卵巢切除大鼠中，这种降低幅度明显更大。5 - 甲基尿嘧啶对刺激引起的收缩的抑制作用在未进行雌二醇替代治疗的卵巢切除大鼠中也比在进行雌二醇替代治疗的大鼠中更大。
结果表明卵巢切除术后卵巢激素的缺乏增强了α1 - 肾上腺素能活性。
Zotero 插件