Neri Luciana S S, de Carvalho Rodrigo P, Daiuto Sergio A, Vale Bárbara do, Cafarchio Eduardo M, Aronsson Patrik, Sato Monica A
Dept. Morphology and Physiology, Faculdade de Medicina do ABC, Centro Universitario FMABC, Santo Andre, SP, Brazil.
Dept. Pharmacology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Curr Res Physiol. 2022 Sep 24;5:399-403. doi: 10.1016/j.crphys.2022.09.004. eCollection 2022.
The mechanisms involved in urinary bladder control are not fully understood, but it is well accepted that a complex central network is involved in micturition control. The micturition reflex can be modulated by direct cortical influence through facilitatory and inhibitory mechanisms. In addition, humoral mechanisms are involved in the bladder control. Vasopressin increases bladder contraction and intravesical pressure. This study sought to investigate the effect of intravenous injections of vasopressin receptor antagonists on cystometric parameters in anesthetized female rats. Isoflurane anesthetized adult female Wistar rats underwent femoral artery and vein cannulation for arterial pressure (AP) and heart rate (HR) recordings, and infusion of drugs, respectively. The bladder was also cannulated for intravesical pressure (IP) recordings and infusion of saline (10 mL/h) for cystometric evaluation. After baseline AP, HR and IP recordings, saline (vehicle, 1 mL/kg), V1a (5 μg/kg) or V2 receptor antagonist (5 μg/kg) was injected i.v. and after 25 min the cystometry was carried out. Neither saline nor V1a or V2 receptor blockade evoked any change in AP, HR and IP. Nevertheless, during cystometry, the threshold pressure of the micturition reflex was significantly reduced in rats with V1a (to 19.30 ± 2.39 mmHg) and V2 receptor blockade (to 19.88 ± 2.49 mmHg) compared to the saline group (28.85 ± 2.06 mmHg, p = 0.014). No difference was observed in the other cystometric parameters. Therefore, the data suggest that blockade of V1a and V2 receptors reduces the threshold pressure of the micturition reflex and does not influence other cystometric parameters in anesthetized female Wistar rats.
膀胱控制所涉及的机制尚未完全明了，但人们普遍认为，一个复杂的中枢网络参与了排尿控制。排尿反射可通过促进和抑制机制受到直接皮质影响的调节。此外，体液机制也参与膀胱控制。血管加压素可增强膀胱收缩及膀胱内压。本研究旨在探讨静脉注射血管加压素受体拮抗剂对麻醉雌性大鼠膀胱测压参数的影响。异氟烷麻醉的成年雌性Wistar大鼠分别进行股动脉和静脉插管，用于记录动脉压（AP）和心率（HR）以及输注药物。膀胱也进行插管，用于记录膀胱内压（IP）以及输注生理盐水（10 mL/h）以进行膀胱测压评估。在记录基线AP、HR和IP后，静脉注射生理盐水（溶媒，1 mL/kg）、V1a（5 μg/kg）或V2受体拮抗剂（5 μg/kg），25分钟后进行膀胱测压。生理盐水、V1a或V2受体阻断均未引起AP、HR和IP的任何变化。然而，在膀胱测压期间，与生理盐水组（28.85±2.06 mmHg，p = 0.014）相比，V1a受体阻断（降至19.30±2.39 mmHg）和V2受体阻断（降至19.88±2.49 mmHg）的大鼠排尿反射阈值压力显著降低。其他膀胱测压参数未见差异。因此，数据表明，阻断V1a和V2受体可降低麻醉雌性Wistar大鼠的排尿反射阈值压力，且不影响其他膀胱测压参数。
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