Advanced search
Start date
Betweenand
Related content
(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

N-Methyl-D-aspartate Glutamate Receptor Modulates Cardiovascular and Neuroendocrine Responses Evoked by Hemorrhagic Shock in Rats

Full text
Author(s):
Busnardo, Cristiane [1] ; Fassini, Aline [2] ; Rodrigues, Bruno [3] ; Antunes-Rodrigues, Jose [4] ; Crestani, Carlos C. [1] ; Correa, Fernando M. A. [2]
Total Authors: 6
Affiliation:
[1] Sao Paulo State Univ UNESP, Sch Pharmaceut Sci, Dept Drugs & Med, Araraquara, SP - Brazil
[2] Univ Sao Paulo, Sch Med Ribeirao Preto, Dept Pharmacol, Ribeirao Preto, SP - Brazil
[3] Univ Campinas UNICAMP, Fac Phys Educ, Dept Adapted Phys Act, Campinas, SP - Brazil
[4] Univ Sao Paulo, Sch Med Ribeirao Preto, Dept Physiol, Ribeirao Preto, SP - Brazil
Total Affiliations: 4
Document type: Journal article
Source: BIOMED RESEARCH INTERNATIONAL; v. 2021, AUG 13 2021.
Web of Science Citations: 0
Abstract

Here, we report the participation of N-methyl-D-aspartate (NMDA) glutamate receptor in the mediation of cardiovascular and circulating vasopressin responses evoked by a hemorrhagic stimulus. In addition, once NMDA receptor activation is a prominent mechanism involved in nitric oxide (NO) synthesis in the brain, we investigated whether control of hemorrhagic shock by NMDA glutamate receptor was followed by changes in NO synthesis in brain supramedullary structures involved in cardiovascular and neuroendocrine control. Thus, we observed that intraperitoneal administration of the selective NMDA glutamate receptor antagonist dizocilpine maleate (MK801, 0.3 mg/kg) delayed and reduced the magnitude of hemorrhage-induced hypotension. Besides, hemorrhage induced a tachycardia response in the posthemorrhage period (i.e., recovery period) in control animals, and systemic treatment with MK801 caused a bradycardia response during hemorrhagic shock. Hemorrhagic stimulus increased plasma vasopressin levels during the recovery period and NMDA receptor antagonism increased concentration of this hormone during both the hemorrhage and postbleeding periods in relation to control animals. Moreover, hemorrhagic shock caused a decrease in NOx levels in the paraventricular nucleus of the hypothalamus (PVN), amygdala, bed nucleus of the stria terminalis (BNST), and ventral periaqueductal gray matter (vPAG). Nevertheless, treatment with MK801 did not affect these effects. Taken together, these results indicate that the NMDA glutamate receptor is involved in the hemorrhagic shock by inhibiting circulating vasopressin release. Our data also suggest a role of the NMDA receptor in tachycardia, but not in the decreased NO synthesis in the brain evoked by hemorrhage. (AU)

FAPESP's process: 13/00249-9 - Involvement of opioid neurotransmission of the medial amygadala in the mediation of autonomic and hormonal responses evoked by restraint stress in rats
Grantee:Aline Fassini
Support Opportunities: Scholarships in Brazil - Doctorate
FAPESP's process: 21/00148-4 - Genetic study of hypocampus glutamate neurotransmission in central mechanisms of the adaptation of neuroendocrine, cardiovascular and behavioral responses to repeated chronic stress and stress-induced neuroinflamation
Grantee:Cristiane Busnardo Santiago
Support Opportunities: Scholarships in Brazil - Young Researchers
FAPESP's process: 18/04899-1 - Genetic study of hypocampus glutamate neurotransmission in central mechanisms of the adaptation of neuroendocrine, cardiovascular and behavioral responses to repeated chronic stress and stress-induced neuroinflamation
Grantee:Cristiane Busnardo Santiago
Support Opportunities: Research Grants - Young Investigators Grants