Investigaton of peripheral and central actions of angiotensin-(1-7) on urinary bla...
| Grant number: | 13/04550-5 |
| Support type: | Regular Research Grants |
| Duration: | October 01, 2013 - September 30, 2015 |
| Field of knowledge: | Biological Sciences - Physiology |
| Principal Investigator: | Monica Akemi Sato |
| Grantee: | Monica Akemi Sato |
| Home Institution: | Faculdade de Medicina do ABC (FMABC). Organização Social de Saúde. Fundação do ABC. Santo André , SP, Brazil |
Abstract
The micturation and urinary storage are dependent on the coordination of two functional units, the urinary bladder and the striate muscle of the external sphincter of the urethra. The central control of micturation and urinary storage is a complex mechanism and still not well known. The urinary storage and voiding depend on reflex mechanisms and the reflex is influenced by the Pontine Micturation Center (PMC). The Pontine Urinary Storage Center (PUSC) is located ventrolaterally from PMC. Evidence has shown the existence of two ascending pathways from urinary bladder to PMC, and two descending pathways from PMC to urinary bladder, nevertheless, one would be a direct pathway and the other one indirect through medullary neurons. The stimulation of medullary areas involved in cardiovascular control, as the Rostral Ventrolateral Medulla (RVLM), Nucleus of the Solitary Tract (NTS), and Caudal Ventrolateral Medulla (CVLM) evokes changes in the pelvic nerve activity. Portions of the urinary bladder innervated by the pelvic nerve contract when the nerve is stimulated, and conversely the nerve inhibition produces vesical relaxation. Several neurotransmitters and neuromodulators are found in the medullary areas. The acetylcholine is one of neurotransmitters and plays an important role on cardiovascular regulation. In the NTS, the acetylcholine elicits hypotension and bradycardia dependent on activation of muscarinic receptors. Conversely, microinjections of cholinergic agonists into the RVLM evokes pressor response and the M2 receptor is the subtype involved in this response as it is found in large density into the RVLM. Considering that acetylcholine is an important neurotransmitter in the medullary areas as the NTS and RVLM, and evidence also indicate that medullary areas involved in cardiovascular regulation can influence the vesical control, our group started to evaluate the role of cholinergic medullary neurotransmission on urinary bladder control. Our previous results have suggested that carbachol injections into the 4th brain ventricle (4th V) elicit differentiated effects on intravesical pressure before and after urether ligature and these effects are independent on alterations in renal blood flow and arterial pressure. The cholinergic blockade into the 4th V induced differentiated effects on intravesical pressure before and after urether ligature, which are also independent on changes in renal blood flow and glomerular filtration. As the carbachol into the 4th V evoked differenciated effects before and after urether ligature, we hypothesized that the activation of cholinergic medullary neurons can release any humoral factor, and through circulation, would act directly on the detrusor muscle. At this point, there is no evidence that vasopressin or oxytocin can be released by SON or PVN neurons evoked by cholinergic medullary neurons. Therefore, it could be interesting to investigate if the cholinergic medullary neurons can exert their effects on urinary bladder by vasopressin or oxytocin release. (AU)