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Superoxide anions in the paraventricular nucleus mediate cardiac sympathetic afferent reflex in insulin resistance rats.
Acta Physiol (Oxf). 2014 Dec; 212(4):267-82.AP

Abstract

AIM

Cardiac sympathetic afferent reflex (CSAR) participates in sympathetic over-excitation. Superoxide anions and angiotensin II (Ang II) mechanisms are associated with sympathetic outflow and CSAR in the paraventricular nucleus (PVN). This study was designed to investigate whether PVN superoxide anions mediate CSAR and Ang II-induced CSAR enhancement response in fructose-induced insulin resistance (IR) rats.

METHODS

CSAR was evaluated with the changes of renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP) responses to the epicardial application of capsaicin (CAP) in anaesthetized rats.

RESULTS

Compared with Control rats, IR rats showed that CSAR, PVN NAD(P)H oxidase activity, superoxide anions, malondialdehyde (MDA), Ang II and AT1 receptor levels were significantly increased, whereas PVN superoxide dismutase (SOD) and catalase (CAT) activities were decreased. In Control and IR rats, PVN microinjection of superoxide anions scavengers tempol, tiron and PEG-SOD (an analogue of endogenous superoxide dismutase) or inhibition of PVN NAD(P)H oxidase with apocynin caused significant reduction of CSAR, respectively, but DETC (a superoxide dismutase inhibitor) strengthened the CSAR. PVN pre-treatment with tempol abolished, whereas DETC potentiated, Ang II-induced CSAR enhancement response. Moreover, PVN pre-treatment with tempol or losartan prevented superoxide anions increase caused by Ang II in IR rats.

CONCLUSION

PVN superoxide anions mediate CSAR and Ang II-induced CSAR response in IR rats. In IR state, increased NAD(P)H oxidase activity and decreased SOD and CAT activities in the PVN promote superoxide anions increase to involve in CSAR enhancement. Ang II may increase NAD(P)H oxidase activity via AT1 receptor to induce superoxide anion production.

Authors+Show Affiliations

Key Laboratory of Cardiovascular Disease and Molecular Intervention, Department of Physiology, Nanjing Medical University, Nanjing, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

25307720

Citation

Sun, H-J, et al. "Superoxide Anions in the Paraventricular Nucleus Mediate Cardiac Sympathetic Afferent Reflex in Insulin Resistance Rats." Acta Physiologica (Oxford, England), vol. 212, no. 4, 2014, pp. 267-82.
Sun HJ, Zhou H, Feng XM, et al. Superoxide anions in the paraventricular nucleus mediate cardiac sympathetic afferent reflex in insulin resistance rats. Acta Physiol (Oxf). 2014;212(4):267-82.
Sun, H. J., Zhou, H., Feng, X. M., Gao, Q., Ding, L., Tang, C. S., Zhu, G. Q., & Zhou, Y. B. (2014). Superoxide anions in the paraventricular nucleus mediate cardiac sympathetic afferent reflex in insulin resistance rats. Acta Physiologica (Oxford, England), 212(4), 267-82. https://doi.org/10.1111/apha.12405
Sun HJ, et al. Superoxide Anions in the Paraventricular Nucleus Mediate Cardiac Sympathetic Afferent Reflex in Insulin Resistance Rats. Acta Physiol (Oxf). 2014;212(4):267-82. PubMed PMID: 25307720.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Superoxide anions in the paraventricular nucleus mediate cardiac sympathetic afferent reflex in insulin resistance rats. AU - Sun,H-J, AU - Zhou,H, AU - Feng,X-M, AU - Gao,Q, AU - Ding,L, AU - Tang,C-S, AU - Zhu,G-Q, AU - Zhou,Y-B, Y1 - 2014/10/30/ PY - 2014/04/22/received PY - 2014/05/26/revised PY - 2014/09/29/revised PY - 2014/10/06/accepted PY - 2014/10/14/entrez PY - 2014/10/14/pubmed PY - 2015/10/9/medline KW - angiotensin II KW - cardiac sympathetic afferent reflex KW - insulin resistance KW - paraventricular nucleus KW - superoxide anions SP - 267 EP - 82 JF - Acta physiologica (Oxford, England) JO - Acta Physiol (Oxf) VL - 212 IS - 4 N2 - AIM: Cardiac sympathetic afferent reflex (CSAR) participates in sympathetic over-excitation. Superoxide anions and angiotensin II (Ang II) mechanisms are associated with sympathetic outflow and CSAR in the paraventricular nucleus (PVN). This study was designed to investigate whether PVN superoxide anions mediate CSAR and Ang II-induced CSAR enhancement response in fructose-induced insulin resistance (IR) rats. METHODS: CSAR was evaluated with the changes of renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP) responses to the epicardial application of capsaicin (CAP) in anaesthetized rats. RESULTS: Compared with Control rats, IR rats showed that CSAR, PVN NAD(P)H oxidase activity, superoxide anions, malondialdehyde (MDA), Ang II and AT1 receptor levels were significantly increased, whereas PVN superoxide dismutase (SOD) and catalase (CAT) activities were decreased. In Control and IR rats, PVN microinjection of superoxide anions scavengers tempol, tiron and PEG-SOD (an analogue of endogenous superoxide dismutase) or inhibition of PVN NAD(P)H oxidase with apocynin caused significant reduction of CSAR, respectively, but DETC (a superoxide dismutase inhibitor) strengthened the CSAR. PVN pre-treatment with tempol abolished, whereas DETC potentiated, Ang II-induced CSAR enhancement response. Moreover, PVN pre-treatment with tempol or losartan prevented superoxide anions increase caused by Ang II in IR rats. CONCLUSION: PVN superoxide anions mediate CSAR and Ang II-induced CSAR response in IR rats. In IR state, increased NAD(P)H oxidase activity and decreased SOD and CAT activities in the PVN promote superoxide anions increase to involve in CSAR enhancement. Ang II may increase NAD(P)H oxidase activity via AT1 receptor to induce superoxide anion production. SN - 1748-1716 UR - https://www.unboundmedicine.com/medline/citation/25307720/Superoxide_anions_in_the_paraventricular_nucleus_mediate_cardiac_sympathetic_afferent_reflex_in_insulin_resistance_rats_ L2 - https://doi.org/10.1111/apha.12405 DB - PRIME DP - Unbound Medicine ER -