Effect of vasopressin and oxytocin on urinary bladder regulation in conditions of hypovolemia

• Grant number: 22/08236-2
• Support Opportunities: Regular Research Grants
• Start date: February 01, 2024
• End date: January 31, 2026
• Field of knowledge: Health Sciences - Medicine - Medical Clinics
• Principal Investigator: Eduardo Mazuco Cafarchio
• Grantee: Eduardo Mazuco Cafarchio
• Host Institution: Centro Universitário FMABC (FMABC). Santo André , SP, Brazil
• Associated researchers: Monica Akemi Sato

Abstract

The involvement of bladder functions is very likely in the world population, especially in women, and the neurogenic bladder is a dysfunction of greater insufficiency. These dysfunctions would be dependent on changes in the control of the detrusor muscle, sphincter muscle or both. The treatments used for these patients, so far, only alleviate the symptoms. Urination and the urinary tract depend on the coordination between two functional units: the bladder and the striated musculature of the urethral sphincter. Central control of urination and urine storage involve a complex mechanism that is not yet well understood. As for the maintenance of excretion and storage of the reflex mechanism apparatus, the micturition initiation reflex can be influenced by Pontine Voiding (PMC). The storage center is at the Urine Storage Point Center (PUSC), which is located ventrolaterally to the PMC. Stimulation of areas that control cardiovascular function such as the Rostroventrolateral Region (RVL), the Nucleus of the Solitary Tract (NTS) and the Caudoventrolateral Region (CVL) changed activities in the medulla, produced from the pelvic nerves. Pelvic nerve regions conversely contractures, when there is occasional nerve sensitivity or relaxing, when there is occasional nerve sensitivity or relaxing. Several neurotransmitters and neuromodulators are found in NTS and RVL, including acetylcholine, which plays an important role in cardiovascular regulation. In NT acetylcholine produces hypo and clamps, voltage-dependent effects, indicating muscarinic receptors. Our grupoinergica results that neurotransmission in accessory bulbs regulates the urinary bladder. This was demonstrated by the fact that a car accident in the 4th cerebral V caused an increase in intraveical pressure, regardless of changes in renal blood flow and arterial pressure. The increase in intravesical pressure was observed for 30 minutes after drug injection, suggesting that this effect would be dependent on a mood mechanism and not only generate the peak of increased mood and economic activity. The 4th-cholin block was created in the protective effect, with blood pressure, intravesical pressure also independent of changes in renal and renal blood flow. Similarly to carbachol, the peak response on intravesical pressure was observed 30 min after the injection in the 4th V of the brain. Previous studies that carbachol can exercise and postsynaptic in C1 neurons of the medulla. On the other hand, evidence also shows that the A/C1 catecholaminergic groups in the medulla have paraventricular projected suprarergic and paraventricular nuclei, which are capable of producing vasopressin and cytokine. In addition, electrical stimulation of the C1 group is capable of increasing plasma levels of vasopressin. The activated peak response can be done with the cholinergic bulb of 30 min, which suggests that the effect presented is dependent on vasopressin. In vitro studies even an effect of bladder regulation, however, there are no effects of oxytocin on bladder regulation, as well as the existence of receptors in this organ. On the other hand, it is known that the maintenance of homeostasis of the internal environment depends on the adequacy of the hydroelectrolytic balance. Different stimuli that activate thirst and lead to water intake also induce vasopressin release. Thus, it is also interesting to investigate the way the extracellular cell works. (AU)