Abstract
Mitogen‐Activated Protein Kinase Mediates the Effects of Chemokine Stromal Cell‐Derived Factor‐1 (SDF‐1) on Cardiovascular Function and Sympathetic Drive in Rats
The FASEB journal, Vol.26(S1), pp.891.8-891.8
04/2012
DOI: 10.1096/fasebj.26.1_supplement.891.8
Abstract
The chemokine SDF-1 and its receptors are expressed by neurons and glial cells in cardiovascular autonomic regions of the brain. SDF-1 expression increases in these regions in rats with heart failure (HF). Intracerebroventricular (ICV) administration of SDF-1 elicits increases in mean blood pressure (MBP, mmHg), heart rate (HR, bpm) and renal sympathetic nerve activity (RSNA) that are exaggerated in rats with HF. SDF-1 is known to activate mitogen-activated protein kinase (MAPK) intracellular signaling. We hypothesized that p44/42 MAPK, which has recently been implicated in sympathetic activation in HF, mediates the sympathetic and hemodynamic responses to SDF-1. In urethane anesthetized adult male rats, ICV injection of SDF-1 (100 ng) induced significant (p<0.05) increases in MBP (27.6 ± 3.5), HR (55 ± 6) and RSNA (90.1 ± 6.8 %). Pretreatment with ICV PD98059 (1 μg), a selective p44/42 MAPK inhibitor, prevented these SDF-1 induced responses. ICV minocycline (20 μg), an inhibitor of glial cell activation, significantly (p<0.05) attenuated but did not block the SDF-1 induced increases in MBP (11.2 ± 2.4), HR (27 ± 4) and RSNA (38.8 ± 4.2 %). These data identify p44/42 MAPK signaling as an obligatory intracellular mechanism mediating the cardiovascular and sympathetic responses to SDF-1. MAPK signaling in both neurons and glial cells may contribute to these responses. Supported by NIH RO1 HL073986 & HL096671.
Details
- Title: Subtitle
- Mitogen‐Activated Protein Kinase Mediates the Effects of Chemokine Stromal Cell‐Derived Factor‐1 (SDF‐1) on Cardiovascular Function and Sympathetic Drive in Rats
- Creators
- Shun-Guang WeiZhi-Hua ZhangYang YuRobert B. Felder
- Resource Type
- Abstract
- Publication Details
- The FASEB journal, Vol.26(S1), pp.891.8-891.8
- DOI
- 10.1096/fasebj.26.1_supplement.891.8
- ISSN
- 0892-6638
- eISSN
- 1530-6860
- Grant note
- DOI: 10.13039/100000002, name: National Institutes of Health, award: RO1 HL073986, HL096671
- Language
- English
- Date published
- 04/2012
- Academic Unit
- Cardiovascular Medicine; Internal Medicine; Iowa Neuroscience Institute
- Record Identifier
- 9984256795602771
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