What is the clinical evidence from this study?

Population: Cardiac hypertrophy. Intervention: 16alpha-LE2 or 17beta-estradiol vs. Tamoxifen or untreated control. Primary outcome: Cardiac hypertrophy, cardiac output, left ventricular stroke volume, and contractility.

June 14, 2005Cardiovascular ResearchOpen Access

The estrogen receptor-α agonist 16α-LE2 inhibits cardiac hypertrophy and improves hemodynamic function in estrogen-deficient spontaneously hypertensive rats

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Key result

ERalpha agonist 16alpha-LE2 and 17beta-estradiol attenuate cardiac hypertrophy and boost cardiac output in hypertensive rats.

Why the study?

Does activation of ERalpha with 16alpha-LE2 attenuate cardiac hypertrophy and improve hemodynamic function in ovariectomized spontaneously hypertensive rats?

Population

Ovariectomized, spontaneously hypertensive rats (SHR)

Comparison

Subtype-selective ERalpha agonist 16alpha-LE2 or… vs Tamoxifen or ER antagonist ZM-182780

Design

Preclinical

Authors

TPTheo PelzerUniversitätsklinikum Würzburg VJVirginia JazbutyteUniversity of Würzburg KHKai HuUniversity of Science and Technology of China

Discussion

Member takes

Implication

Hypothesis-generating for ERα agonism in estrogen-deficient hypertension; leaves open human translation pending clinical studies.

Structured PICO

Does activation of ERalpha with 16alpha-LE2 attenuate cardiac hypertrophy and improve hemodynamic function in ovariectomized spontaneously hypertensive rats?

Population

Ovariectomized, spontaneously hypertensive rats (SHR) used as an animal model for estrogen-deficient cardiac hypertrophy.

Intervention

Subtype-selective ERalpha agonist 16alpha-LE2 or 17beta-estradiol

Comparator

Tamoxifen or ER antagonist ZM-182780

Outcome

Myocardial hypertrophy, cardiac function (cardiac output, left ventricular stroke volume, papillary muscle strip contractility), and gene expression (cardiac alpha-myosin heavy chain expression)surrogate

Activation of estrogen receptor-alpha with 16alpha-LE2 attenuates cardiac hypertrophy and improves myocardial contractility in a rat model of estrogen deficiency and hypertension.

Limitations

Further studies are required to determine whether activation ERbeta mediates redundant or divergent effects.

Cite This Study

Pelzer et al. (2005) studied Cardiac hypertrophy. 16alpha-LE2 or 17beta-estradiol vs. Tamoxifen or untreated control was evaluated on Cardiac hypertrophy, cardiac output, left ventricular stroke volume, and contractility. The ERalpha agonist 16alpha-LE2 and 17beta-estradiol attenuated cardiac hypertrophy and increased cardiac output in ovariectomized spontaneously hypertensive rats.

synapsesocial.com/papers/6aa353c7aaaedccdac748c72 https://doi.org/10.1016/j.cardiores.2005.04.035

Topics

Hypertension management

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The estrogen receptor-α agonist 16α-LE2 inhibits cardiac hypertrophy and improves hemodynamic function in estrogen-deficient spontaneously hypertensive rats

Discussion

Member takes

Implication

Structured PICO

Limitations

Cite This Study

Topics

The estrogen receptor-α agonist 16α-LE2 inhibits cardiac hypertrophy and improves hemodynamic function in estrogen-deficient spontaneously hypertensive rats

Discussion

Member takes

Implication

Structured PICO

Limitations

Cite This Study

Also Consider

Topics

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