Scholarship 24/04206-7 - Acetilcolina, Bexiga urinária - BV FAPESP
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Effect of vasopressin and oxytocin on urinary bladder regulation in hypovolemic conditions

Grant number: 24/04206-7
Support Opportunities:Scholarships in Brazil - Scientific Initiation
Start date until: June 01, 2024
End date until: May 31, 2025
Field of knowledge:Health Sciences - Medicine - Medical Clinics
Principal Investigator:Eduardo Mazuco Cafarchio
Grantee:Maria Eduarda de Almeida
Host Institution: Centro Universitário FMABC (FMABC). Santo André , SP, Brazil

Abstract

The impairment of bladder functions has a high incidence in the world population, especially in women, with neurogenic bladder being the dysfunction with the highest incidence. 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 urinary storage depend on the coordination between two functional units: the bladder and the urethral muscles. The central control of urination and urine storage involves a complex mechanism that is not yet well understood. The maintenance of urinary excretion and storage depends on reflex mechanisms, and the reflex to initiate urination can be influenced by the Pontine Voiding Center (PMC). The storage center is in the Pontine Urine Storage Center (PUSC), which is located ventrolateral 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) located in the medulla oblongata, produced changes in the activity of the pelvic nerves. Regions of the bladder innervated by pelvic nerves suffered contractions when stimulated and, conversely, nervous inhibition caused bladder relaxation. Several neurotransmitters and neuromodulators are found in the NTS and RVL, among which is acetylcholine, which plays an important role in cardiovascular regulation. In NTS, acetylcholine produces hypotension and bradycardia, effects that depend on the activation of muscarinic receptors. Results from our group showed that cholinergic neurotransmission in bulbar neurons participates in the regulation of the urinary bladder. This was demonstrated by the fact that the injection of carbachol into the 4th V of the brain caused an increase in intravesical pressure, independently of changes in renal blood flow and arterial pressure. The peak increase in intravesical pressure was observed approximately 30 minutes after drug injection, suggesting that this effect would be dependent on a humoral mechanism and not just generated by changes in the activity of autonomic efferents.Cholinergic blockade of the 4th cerebral V with atropine produced an opposite effect, decreasing intravesical pressure, which was also independent of changes in renal blood flow and blood pressure. Similarly to carbachol, the peak response on intravesical pressure was observed 30 min after the injection into the 4th brain. Previous studies have shown that carbachol can exert pre- and postsynaptic actions on C1 neurons of the medulla oblongata. On the other hand, evidence has also shown that the A1/C1 catecholaminergic groups in the medulla oblongata have projections to the supraoptic and paraventricular nuclei, which are capable of producing vasopressin and oxytocin. Furthermore, electrical stimulation of the C1 group is capable of increasing plasma levels of vasopressin. The injection of carbachol into the 4°V brain led to an increase in the plasma concentration of vasopressin after 30 minutes. Blockade of V1a receptors abolished the increase in intravesical pressure induced by carbachol injection into the 4th brain. In vitro studies have shown that oxytocin produces a relaxing effect on the detrusor muscles and in vivo studies have shown that oxytocin promotes a decrease in intravesical pressure. On the other hand, it is known that the maintenance of homeostasis in the internal environment depends on adequate hydroelectrolyte balance.

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