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Increased sympathoexcitation to angiotensin II (A II) and AT 1 receptor mRNA in the paraventricular nucleus (PVN) of pregnant rats
Author(s) -
Heesch Cheryl M.,
Kvochina Lyudmyla I.,
Burcks Shan
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.1019.10
Subject(s) - rostral ventrolateral medulla , ionotropic effect , medicine , endocrinology , receptor , medulla oblongata , glutamate receptor , chemistry , glutamatergic , biology , central nervous system
Previously we reported that pressor and sympathetic nerve activity (SNA) responses due to AT 1 receptor activation in the SFO are potentiated in term pregnant (P) compared to nonpregnant (NP) rats. The pathway requires ionotropic glutamate receptors (iGluRs) in the PVN and rostral ventrolateral medulla (RVLM) in both P and NP rats. AT 1 receptors in the PVN and RVLM contribute to potentiated responses to SFO activation in P rats. Since the PVN is obligatory to this pathway, and PVN to RVLM projections are almost exclusively glutamatergic, we considered that the enhanced role of A II in the RVLM might be related to an A II dependent increase in excitatory drive from the PVN, which could then stimulate local production of A II in the RVLM. In sinoaortic denervated inactin anesthetized rats, increases in mean arterial pressure (MAP) and lumbar SNA (LSNA) due to microinjected A II (50 nl, 1.6 mM) in the PVN were greater in P (n = 4) compared to NP (n = 7) rats (ΔMAP: P= 25±5 mmHg; NP= 15±2 mmHg; ΔLSNA: P= 13±3%; NP= 6.5±2%). Real‐time RT‐PCR was used to assess relative expression of AT 1 receptor mRNA (reference gene = GAPDH) in PVN tissue punches from 5 P and 5 NP rats. Expression of AT 1 receptors in the PVN tended (P = 0.1) to be greater in P (2.4±0.82) compared to NP rats (1.0±0.22). These results are consistent with an increased role of PVN AT 1 receptors in sympathoexcitation in pregnancy. (NIH HL 091164)

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