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Ionotropic glutamate receptors in paraventricular nucleus mediate adipose afferent reflex and regulate sympathetic outflow in rats
Author(s) -
Cui B.P.,
Li P.,
Sun H.J.,
Ding L.,
Zhou Y.B.,
Wang J.J.,
Kang Y.M.,
Zhu G.Q.
Publication year - 2013
Publication title -
acta physiologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.591
H-Index - 116
eISSN - 1748-1716
pISSN - 1748-1708
DOI - 10.1111/apha.12125
Subject(s) - cnqx , medicine , rostral ventrolateral medulla , baroreceptor , endocrinology , nmda receptor , agonist , reflex , ampa receptor , receptor , blood pressure , heart rate
Aim Chemical stimulation of white adipose tissue ( WAT ) induces adipose afferent reflex ( AAR ) and results in increases in renal sympathetic nerve activity ( RSNA ) and mean arterial pressure ( MAP ). The enhanced AAR contributes to sympathetic activation and hypertension in obesity rats. This study was designed to investigate whether N ‐methyl‐ D ‐aspartate receptors ( NMDAR ) and non‐ NMDAR in paraventricular nucleus ( PVN ) modulate AAR and sympathetic outflow. Methods Renal sympathetic nerve activity and MAP were recorded in anesthetized rats. AAR was evaluated by the RSNA and MAP responses to the injection of capsaicin into the four sites of right inguinal WAT (8.0 nmol for each site). Results Bilateral PVN microinjection of NMDAR antagonist AP 5 or MK ‐801, or non‐ NMDAR antagonist CNQX attenuated AAR , RSNA and MAP . AP 5 + CNQX caused greater effects than AP 5 or CNQX alone and almost abolished AAR . NMDAR agonist NMDA or non‐ NMDAR agonist AMPA enhanced the AAR , and increased RSNA and MAP , which were prevented by AP 5 or CNQX pre‐treatment respectively. Casein kinase 2 inhibitor DRB , NR 2 A antagonist NVP ‐ AAM 077 or NR 2 B antagonist CP ‐101,606 attenuated AAR , RSNA and MAP . NVP ‐ AAM 077 + CP ‐101,606 caused greater effects than NVP ‐ AAM 077 or CP ‐101,606 alone. Bilateral baroreceptor denervation and vagotomy enhanced AAR , which was abolished by PVN pre‐treatment with AP 5 + CNQX . Furthermore, AP 5 + CNQX abolished the AAR induced by leptin in i WAT . Conclusion Both NMDAR and non‐ NMDAR in the PVN mediate AAR and contribute to the tonic control of sympathetic outflow and blood pressure. CK 2, NR 2A and NR 2 B subunits of NMDAR in the PVN are involved in the NMDAR ‐mediated tonic control of AAR , RSNA and MAP .