17β-Estradiol treatment reversed left ventricular dysfunction in castrated male rats: an echocardiographic study

Baka, Tomáš; Hodosy, Július; Krajcirovicova, Kristina; Repova, Kristina; Aziriova, Silvia; Domonkos, Emese; Borbélyová, Veronika; Slavkovský, Peter; Zórad, Štefan; Celec, Peter; Paulis, Ludovít; Šimko, Fedor

doi:10.1139/cjpp-2017-0596

Cited by 4 publications

(4 citation statements)

References 20 publications

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“…To asses left ventricular diastolic function, the diastolic transmitral peak early filling velocity (E velocity) and the diastolic transmitral peak late filling velocity (A velocity) were measured, and their ratio (E/A) was calculated from the two-dimensionally guided Doppler spectra of mitral inflow in apical four-chamber view. All measurements were averaged over three consecutive cardiac cycles [ 48 , 49 ].…”

Section: Methodsmentioning

confidence: 99%

Effect of Ivabradine on a Hypertensive Heart and the Renin-Angiotensin-Aldosterone System in L-NAME-Induced Hypertension

Šimko

Baka

Poglitsch³

et al. 2018

IJMS

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Ivabradine, the selective inhibitor of the If current in the sinoatrial node, exerts cardiovascular protection by its bradycardic effect and potentially pleiotropic actions. However, there is a shortage of data regarding ivabradine’s interaction with the renin-angiotensin-aldosterone system (RAAS). This study investigated whether ivabradine is able to protect a hypertensive heart in the model of L-NAME-induced hypertension and to interfere with the RAAS. Four groups (n = 10/group) of adult male Wistar rats were treated as follows for four weeks: control, ivabradine (10 mg/kg/day), L-NAME (40 mg/kg/day), and L-NAME plus ivabradine. L-NAME administration increased systolic blood pressure (SBP) and left ventricular (LV) weight, enhanced hydroxyproline concentration in the LV, and deteriorated the systolic and diastolic LV function. Ivabradine reduced heart rate (HR) and SBP, and improved the LV function. The serum concentrations of angiotensin Ang 1–8 (Ang II), Ang 1–5, Ang 1–7, Ang 1–10, Ang 2–8, and Ang 3–8 were decreased in the L-NAME group and ivabradine did not modify them. The serum concentration of aldosterone and the aldosterone/Ang II ratio were enhanced by L-NAME and ivabradine reduced these changes. We conclude that ivabradine improved the LV function of the hypertensive heart in L-NAME-induced hypertension. The protective effect of ivabradine might have been associated with the reduction of the aldosterone level.

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Section: Methodsmentioning

confidence: 99%

Effect of Ivabradine on a Hypertensive Heart and the Renin-Angiotensin-Aldosterone System in L-NAME-Induced Hypertension

Šimko

Baka

Poglitsch³

et al. 2018

IJMS

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“…Although this study was done in female rats, estrogens have been shown to protect both female and male hearts from various stresses [40][41][42], even though the defense mechanisms involved might be different [43]. Indeed, it would be interesting to investigate rMCPs expression levels in cardiomyocytes from male rats and their corresponding roles in sexspecific cardiac function and morphology.…”

Section: Limitations and Future Studiesmentioning

confidence: 99%

Estrogen modulates the differential expression of cardiac myocyte chymase isoforms and diastolic function

et al. 2019

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Background and objective Cardiac angiotensin II (Ang II) is involved in the diastolic dysfunction in postmenopausal women. Chymases, a family of serine proteases with chymotryptic activity, play a significant role in cardiac Ang II formation from its substrate Ang‐(1–12) in both human and rodent models. While human tissue expresses only the α‐form of chymase, α‐ and β‐forms exist in rodents. Five of the ten rat mast cell proteases (rMCP‐1–5) display chymase activity, and rats express predominantly the β‐chymase isoforms. This study was designed to assess the differences in enzymatic activity among these rMCP isoforms in Ang II formation, particularly in the cardiomyocyte (CM), and the effects of estrogen status on MCP gene expression and activities in female rat models. Methods and results Using conventional polymerase chain reaction (PCR) (Fig. 1A), real‐time PCR (Fig. 1B) and DNA sequencing (Fig. 1C), we demonstrated that MCP‐1, MCP‐2, MCP‐4, and MCP‐5 mRNAs are expressed in the CM of both spontaneously hypertensive rats (SHR) and normotensive Wistar‐Kyoto rats (WKY). While rMCP‐1 and rMCP‐5 gene transcripts were higher than other isoforms in both rat strains, WKY CM exhibits higher levels of rMCP‐1 and rMCP‐5 mRNAs compared to the SHR CM (Fig. 2). Ovariectomy (OVX) increased the expression of rMCP‐1 and rMCP‐5 mRNAs in WKY. In SHR, OVX was associated with a blunted increase in rMCP‐1 mRNA compared to OVX normotensive WKY. Chymase activity, measured by HPLC as Ang II formation from Ang‐(1–12), significantly correlated with rMCP‐1 and rMCP‐5 mRNA expression in both rat strains. Both rMCP‐1 and rMCP‐5 mRNA expressions were positively correlated with progressive diastolic dysfunction (increasing the ratio of early mitral inflow velocity‐to‐early mitral annular velocity, E/e′) and increases in left ventricular internal diameter end diastole. Conclusion These data show rMCP‐1 and rMCP‐5 as the Ang II forming chymase isoforms participating in diastolic dysfunction due to ovariectomy in rodents. Support or Funding Information This work was funded by grants from the National Heart Lung and Blood Institute (CMF and LG) P01‐HL051952 and the National Institute on Aging (LG) AG033727 of the National Institute of Health. This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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“…Estrogen deprivation mitigated this cardioprotection [54][55][56][57] . On the other hand, estrogen reposition was able to increase cardiomyocytes' survival in a murine model of infarction, prevent hypertrophy in cardiomyocytes' culture, and improve cardiac function in the isolated hearts of gonadectomized rats 58,59 . According to literature, the activation of membrane-bound receptor G proteincoupled estrogen receptor (GPER) and estrogen receptor beta (ERβ) modulates Ca 2þ homeostasis.…”

Section: Discussionmentioning

confidence: 98%

Leptin administration during lactation leads to different nutritional, biometric, hemodynamic, and cardiac outcomes in prepubertal and adult female Wistar rats

Souza

Pedro

Rocha

et al. 2021

J Dev Orig Health Dis

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Literature reports that insults, such as hormonal disturbances, during critical periods of development may modulate organism physiology and metabolism favoring cardiovascular diseases (CVDs) later in life. Studies show that leptin administration during lactation leads to cardiovascular dysfunction in young and adult male Wistar rats. However, there are sex differences regarding CVD. Thus, the present work aimed to investigate neonatal leptin administration’s consequences on different outcomes in female rats at prepubertal and adult age. Newborn Wistar female rats were divided into two groups, Leptin and Control, receiving daily subcutaneous injections of this adipokine (8 μg/100 g) or saline for the first 10 of 21 d of lactation. Nutritional, biometric, hemodynamic, and echocardiographic parameters, as well as maximal effort ergometer performance, were determined at postnatal days (PND) 30 and 150. Leptin group presented lower food intake (p = 0.0003) and higher feed efficiency (p = 0.0058) between PND 21 and 30. Differences concerning echocardiographic parameters revealed higher left ventricle internal diameter (LVID) in systole (p = 0.0051), as well as lower left ventricle ejection fraction (LVEF) (p = 0.0111) and fractional shortening (FS) (p = 0.0405) for this group at PND 30. Older rats treated with leptin during lactation presented only higher LVID in systole (p = 0.0270). Systolic blood pressure and maximum effort ergometer test performance was similar between groups at both ages. These data suggest that nutritional, biometric, and cardiac outcomes due to neonatal leptin administration in female rats are age-dependent.

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17β-Estradiol treatment reversed left ventricular dysfunction in castrated male rats: an echocardiographic study

Cited by 4 publications

References 20 publications

Effect of Ivabradine on a Hypertensive Heart and the Renin-Angiotensin-Aldosterone System in L-NAME-Induced Hypertension

Effect of Ivabradine on a Hypertensive Heart and the Renin-Angiotensin-Aldosterone System in L-NAME-Induced Hypertension

Estrogen modulates the differential expression of cardiac myocyte chymase isoforms and diastolic function

Leptin administration during lactation leads to different nutritional, biometric, hemodynamic, and cardiac outcomes in prepubertal and adult female Wistar rats

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