[HTML][HTML] Attenuation of salt-induced cardiac remodeling and diastolic dysfunction by the GPER agonist G-1 in female mRen2. Lewis rats
JA Jessup, SH Lindsey, H Wang, MC Chappell… - PloS one, 2010 - journals.plos.org
PloS one, 2010•journals.plos.org
Introduction The G protein-coupled estrogen receptor (GPER) is expressed in various
tissues including the heart. Since the mRen2. Lewis strain exhibits salt-dependent
hypertension and early diastolic dysfunction, we assessed the effects of the GPER agonist
(G-1, 40 nmol/kg/hr for 14 days) or vehicle (VEH, DMSO/EtOH) on cardiac function and
structure. Methods Intact female mRen2. Lewis rats were fed a normal salt (0.5% sodium;
NS) diet or a high salt (4% sodium; HS) diet for 10 weeks beginning at 5 weeks of age …
tissues including the heart. Since the mRen2. Lewis strain exhibits salt-dependent
hypertension and early diastolic dysfunction, we assessed the effects of the GPER agonist
(G-1, 40 nmol/kg/hr for 14 days) or vehicle (VEH, DMSO/EtOH) on cardiac function and
structure. Methods Intact female mRen2. Lewis rats were fed a normal salt (0.5% sodium;
NS) diet or a high salt (4% sodium; HS) diet for 10 weeks beginning at 5 weeks of age …
Introduction
The G protein-coupled estrogen receptor (GPER) is expressed in various tissues including the heart. Since the mRen2.Lewis strain exhibits salt-dependent hypertension and early diastolic dysfunction, we assessed the effects of the GPER agonist (G-1, 40 nmol/kg/hr for 14 days) or vehicle (VEH, DMSO/EtOH) on cardiac function and structure.
Methods
Intact female mRen2.Lewis rats were fed a normal salt (0.5% sodium; NS) diet or a high salt (4% sodium; HS) diet for 10 weeks beginning at 5 weeks of age.
Results
Prolonged intake of HS in mRen2.Lewis females resulted in significantly increased blood pressure, mildly reduced systolic function, and left ventricular (LV) diastolic compliance (as signified by a reduced E deceleration time and E deceleration slope), increased relative wall thickness, myocyte size, and mid-myocardial interstitial and perivascular fibrosis. G-1 administration attenuated wall thickness and myocyte hypertrophy, with nominal effects on blood pressure, LV systolic function, LV compliance and cardiac fibrosis in the HS group. G-1 treatment significantly increased LV lusitropy [early mitral annular descent (e′)] independent of prevailing salt, and improved the e′/a′ ratio in HS versus NS rats (P<0.05) as determined by tissue Doppler.
Conclusion
Activation of GPER improved myocardial relaxation in the hypertensive female mRen2.Lewis rat and reduced cardiac myocyte hypertrophy and wall thickness in those rats fed a high salt diet. Moreover, these advantageous effects of the GPER agonist on ventricular lusitropy and remodeling do not appear to be associated with overt changes in blood pressure.
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