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Development of gender‐specific cardiac hypertrophy: role of the nitric oxide synthase system
Author(s) -
Wong Philip G,
Brander Emily PA,
Tse M Yat,
Armstrong David WJ,
Pang Stephen C.
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.402.4
Subject(s) - atrial natriuretic peptide , medicine , endocrinology , enos , nitric oxide synthase , estrogen , downregulation and upregulation , nitric oxide , endothelial nos , estrous cycle , natriuretic peptide , biology , heart failure , gene , biochemistry
Gender‐specific differences in hormonal regulation may influence susceptibility to cardiac hypertrophy (CH). The nitric oxide synthase (NOS) and natriuretic peptide (NP) systems are homeostatic regulators of blood pressure; ablation of either system increases predisposition to hypertension and CH. Objective To elucidate how the NOS and NP systems work in concert, as well as the impact of estrogen on these systems using the atrial natriuretic peptide gene‐disrupted (ANP −/− ) mouse model. Methods At 13–16 weeks, female ANP +/+ and ANP −/− mice were euthanized during either the estrus (high estrogen) or proestrus (low estrogen) phases of their estrus cycle. Organs were harvested and left ventricle tissue gene expression of NOS system components were assessed using real‐time quantitative RT‐PCR. Results Female ANP +/+ at estrus had a decreased expression of iNOS, eNOS, sGCα1 and sGCβ1 as compared to female ANP +/+ at proestrus. Female ANP −/− at estrus had an increased expression of iNOS, eNOS, sGCα1 and sGCβ1 as compared to female ANP −/− at proestrus. Conclusions High estrogen levels led to a downregulation of the NOS system in ANP +/+ mice, and an upregulation of the NOS system in ANP −/− mice. Whether alteration in NOS system gene expression is a result of hypertension or reduction in circulating ANP levels remains to be determined. (Support from the Heart & Stroke Foundation of Ontario) Grant Funding Source : Heart and Stroke Foundation of Ontario