Journal article
Enhanced cardiac inflammation and fibrosis in ovariectomized hypertensive rats: a possible mechanism of diastolic dysfunction in postmenopausal women
Hypertension research, Vol.34(4), pp.496-502
04/01/2011
DOI: 10.1038/hr.2010.261
PMID: 21248760
Abstract
Diastolic dysfunction is more prevalent in individuals with hypertension, particularly postmenopausal women; however, the pathogenesis of diastolic dysfunction remains unknown. Pressure overload activates cardiac inflammation, which induces myocardial fibrosis and diastolic dysfunction in rats with a suprarenal aortic constriction (AC). Therefore, we examined the effects of bilateral ovariectomy (OVX) on left ventricle (LV) remodeling, diastolic dysfunction and cardiac inflammation in hypertensive female rats. Rats were randomized to OVX+AC, OVX and AC groups as well as a Control group receiving sham operations for both the procedures. Rats underwent OVX at 6 weeks and AC at 10 weeks (Day 0). At Day 28, OVX did not appear to affect arterial pressure, cardiac hypertrophy or LV fractional shortening in AC rats. However, OVX increased myocardial fibrosis, elevated LV end-diastolic pressure and reduced the transmitral Doppler spectra early to late filling velocity ratio in AC rats. AC-induced transient myocardial monocyte chemoattractant protein-1 expression and macrophage infiltration, both of which peaked at Day 3 and were augmented and prolonged by OVX. At Day 28, dihydroethidium staining revealed superoxide generation in the intramyocardial arterioles in the OVX+AC group but not in the AC group. NOX1, a functional subunit of nicotinamide adenine dinucleotide phosphate oxidase, was upregulated only in the OVX+AC group at Day 28. Chronic 17 beta-estradiol replacement prevented the increases in macrophage infiltration, NOX1 upregulation, myocardial fibrosis and diastolic dysfunction in OVX+AC rats. In conclusion, we suggest that estrogen deficiency augments cardiac inflammation and oxidative stress and thereby aggravates myocardial fibrosis and diastolic dysfunction in hypertensive female rats. The findings provide insight into the mechanism underlying diastolic dysfunction in hypertensive postmenopausal women. Hypertension Research (2011) 34, 496-502; doi:10.1038/hr.2010.261; published online 20 January 2011
Details
- Title: Subtitle
- Enhanced cardiac inflammation and fibrosis in ovariectomized hypertensive rats: a possible mechanism of diastolic dysfunction in postmenopausal women
- Creators
- Takahiro Mori - Kurume UniversityHisashi Kai - Kurume UniversityHidemi Kajimoto - Kurume UniversityMitsuhisa Koga - Kurume UniversityHiroshi Kudo - Kurume UniversityNarimasa Takayama - Kurume UniversitySuguru Yasuoka - Kurume UniversityTakahiro Anegawa - Kurume UniversityMamiko Kai - Fukuoka UniversityTsutomu Imaizumi - Kurume University
- Resource Type
- Journal article
- Publication Details
- Hypertension research, Vol.34(4), pp.496-502
- DOI
- 10.1038/hr.2010.261
- PMID
- 21248760
- NLM abbreviation
- Hypertens Res
- ISSN
- 0916-9636
- eISSN
- 1348-4214
- Publisher
- Springer Nature
- Number of pages
- 7
- Grant note
- Sharyo-Kyogi Foundation Kimura Memorial Heart Foundation Ministry of Education, Science, Sports and Culture, Japan; Ministry of Education, Culture, Sports, Science and Technology, Japan (MEXT) Kakihara Science Foundation Strategic Support Program for Research Infrastructure Development of Private Universities Science Frontier Research Promotion Centers Program Takeda Science Foundation; Takeda Science Foundation (TSF) Ishibashi Memorial Foundation
- Language
- English
- Date published
- 04/01/2011
- Academic Unit
- Cardiology; Stead Family Department of Pediatrics
- Record Identifier
- 9984961027502771
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