Central mechanism of the cardiovascular responses caused by L-proline microinjected into the paraventricular nucleus of the hypothalamus in unanesthetized rats

Autor: Cristiane Busnardo, Fernando M.A. Correa, Silvana Lopes-Azevedo
Rok vydání: 2016
Předmět:
0301 basic medicine
Male
endocrine system
medicine.medical_specialty
Vasopressin
Microinjections
Proline
Drug Evaluation
Preclinical
Blood Pressure
Cardiovascular System
Receptors
N-Methyl-D-Aspartate
03 medical and health sciences
chemistry.chemical_compound
0302 clinical medicine
Heart Rate
Internal medicine
medicine
Bradycardia
Animals
Rats
Wistar
Molecular Biology
Microinjection
Neurotransmitter Agents
Dose-Response Relationship
Drug
Chemistry
General Neuroscience
HIPOTÁLAMO
digestive
oral
and skin physiology
Glutamate receptor
Cardiovascular Agents
030104 developmental biology
Endocrinology
nervous system
Hypothalamus
NMDA receptor
Magnocellular cell
NBQX
Neurology (clinical)
hormones
hormone substitutes
and hormone antagonists
030217 neurology & neurosurgery
Developmental Biology
Ionotropic effect
Central Nervous System Agents
Paraventricular Hypothalamic Nucleus
Zdroj: Repositório Institucional da USP (Biblioteca Digital da Produção Intelectual)
Universidade de São Paulo (USP)
instacron:USP
ISSN: 1872-6240
Popis: Previously, we reported that microinjection of L-proline (L-Pro) into the paraventricular nucleus of the hypothalamus (PVN) caused vasopressin-mediated pressor responses in unanesthetized rats. In the present study, we report on the central mechanisms involved in the mediation of the cardiovascular effects caused by the microinjection of L-Pro into the PVN. Microinjection of increasing doses of L-Pro (3-100nmol/100nL) into the PVN caused dose-related pressor and bradycardic responses. No cardiovascular responses were observed after the microinjection of equimolar doses (33nmol/100nL) of its isomer D-Proline (D-Pro) or Mannitol. The PVN pretreatment with either a selective non-NMDA (NBQX) or selective NMDA (LY235959 or DL-AP7) glutamate receptor antagonists blocked the cardiovascular response to L-Pro (33nmol/100nL). The dose-effect curve for the pretreatment with increasing doses of LY235959 was located at the left in relation to the curves for NBQX and DL-AP7, showing that LY235959 is more potent than NBQX, which is more potent than DL-AP7 in inhibiting the cardiovascular response to L-Pro. The cardiovascular response to the microinjection of L-Pro into the PVN was not affected by local pretreatment with Nω-Propyl-l-arginine (N-Propyl), a selective inhibitor of the neuronal nitric oxide synthase (nNOS), suggesting that NO does not mediate the responses to L-Pro in the PVN. In conclusion, the results suggest that ionotropic receptors in the PVN, blocked by both NMDA and non-NMDA receptor antagonists, mediate the pressor response to L-Pro that results from activation of PVN vasopressinergic magnocellular neurons and vasopressin release into the systemic circulation.
Databáze: OpenAIRE
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