Logo image
Early interference with p44/42 mitogen-activated protein kinase signaling in hypothalamic paraventricular nucleus attenuates angiotensin II-induced hypertension
Journal article   Open access   Peer reviewed

Early interference with p44/42 mitogen-activated protein kinase signaling in hypothalamic paraventricular nucleus attenuates angiotensin II-induced hypertension

Yang Yu, Bao-Jian Xue, Zhi-Hua Zhang, Shun-Guang Wei, Terry G Beltz, Fang Guo, Alan Kim Johnson and Robert B Felder
Hypertension (Dallas, Tex. 1979), Vol.61(4), pp.842-849
04/2013
DOI: 10.1161/HYPERTENSIONAHA.111.00080
PMCID: PMC3655907
PMID: 23438934
url
https://doi.org/10.1161/HYPERTENSIONAHA.111.00080View
Published (Version of record) Open Access

Abstract

Blood-borne angiotensin II (ANG II) can upregulate p44/42 mitogen-activated protein kinase (MAPK) signaling and ANG II type-1 receptors in the hypothalamic paraventricular nucleus (PVN), a critical cardiovascular and autonomic center. We tested the hypothesis that brain p44/42 MAPK signaling contributes to the development of ANG II-induced hypertension. The ANG II infusion (120 ng/kg per min, subcutaneously) induced increases in phosphorylated p44/42 MAPK and ANG II type-1 receptors in the PVN after 1 week, before the onset of hypertension, that were sustained as hypertension developed during a 2- or 3-week infusion protocol. Bilateral PVN microinjections of small interfering RNAs for p44/42 MAPK, at the onset of the ANG II infusion or 1 week later, prevented the early increase in p44/42 MAPK activity. The early treatment normalized ANG II type-1 receptor expression in the PVN and attenuated the hypertensive response to the 2-week infusion of ANG II. The later small interfering RNA microinjections had a transient effect on ANG II type-1 receptor expression in PVN and no effect on the hypertensive response to the 3-week infusion of ANG II. The early treatment also normalized the pressure response to ganglionic blockade. The ANG II infusion induced increases in mRNA for proinflammatory cytokines that were not affected by either small interfering RNA treatment. These results suggest that the full expression of ANG II-induced hypertension depends on p44/42 MAPK-mediated effects. A potential role for p44/42 MAPK in modulating the ANG II-induced central inflammatory response might also be considered. MAPK signaling in PVN may be a novel target for early intervention in the progression of ANG II-dependent hypertension.
Blood Pressure RNA, Small Interfering - genetics Up-Regulation Mitogen-Activated Protein Kinase 3 - genetics RNA, Messenger - genetics Rats Signal Transduction - genetics RNA, Messenger - metabolism Rats, Sprague-Dawley Blotting, Western Hypertension - physiopathology Paraventricular Hypothalamic Nucleus - physiopathology Animals Mitogen-Activated Protein Kinase 3 - metabolism Hypertension - chemically induced Mitogen-Activated Protein Kinase 1 - genetics Paraventricular Hypothalamic Nucleus - metabolism Hypertension - genetics Angiotensin II - toxicity Disease Models, Animal Mitogen-Activated Protein Kinase 1 - metabolism

Details

Metrics

Logo image