What question did this study set out to answer?

To assess the individual contributions of salt, DOCA, and blood pressure elevation to vascular endothelin-1 expression and determine how this expression correlates with arterial hypertrophy.

September 24, 2008Journal of Vascular Research

Enhanced Expression of the Endothelin-1 Gene in Blood Vessels of DOCA-Salt Hypertensive Rats: Correlation with Vascular Structure

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Why the study?

Does the combined ETA/ETB receptor antagonist bosentan reduce vascular hypertrophy in DOCA-salt-hypertensive rats?

Population

Rats with variable degrees of blood pressure elevation induced by salt and/or deoxycorticosterone acetate…

Comparison

Combined ETA/ETB receptor antagonist bosentan vs Untreated DOCA-salt-hypertensive rats

Design

Preclinical

Follow-up

5 weeks

Authors

ESErnesto L. SchiffrinMontreal Clinical Research Institute RRRichard Larivi egrave reUniversité Laval JLJinsheng LiChinese PLA General Hospital

Discussion

Member takes

Implication

Supports ET-1 role in excess vascular hypertrophy in this rat model; leaves open whether endothelin antagonism prevents remodeling in human hypertension.

Key Points

To assess the individual contributions of salt, DOCA, and blood pressure elevation to vascular endothelin-1 expression and determine how this expression correlates with arterial hypertrophy.
Generated variable hypertension models by administering salt, DOCA, or both to intact or unilaterally nephrectomized rats.
Quantified ET-1 mRNA, immunoreactive ET-1, and morphometric indices (media thickness, cross-sectional area, media-to-lumen ratio) in the aorta and mesenteric arterial bed.
Administered the dual ETA/ETB receptor antagonist bosentan to a subgroup of DOCA-salt hypertensive rats to assess structural responses.
Increased ET-1 mRNA and immunoreactive peptide levels occurred exclusively in unilaterally nephrectomized DOCA-salt-treated rats, whereas other groups reaching systolic blood pressure of 180 mm Hg showed no ET-1 upregulation.
At 5 weeks, DOCA-salt hypertensive rats exhibited vascular hypertrophy disproportionately greater than expected for their blood pressure level.
Treatment with bosentan normalized vascular morphometry relative to blood pressure levels despite producing only a modest reduction in blood pressure.

Structured PICO

Does the combined ETA/ETB receptor antagonist bosentan reduce vascular hypertrophy in DOCA-salt-hypertensive rats?

Population

Rats with variable degrees of blood pressure elevation induced by salt and/or deoxycorticosterone acetate (DOCA), with or without unilateral nephrectomy.

Intervention

Combined ETA/ETB receptor antagonist bosentan

Comparator

Untreated DOCA-salt-hypertensive rats

Outcome

ET-1 gene expression (mRNA abundance and immunoreactive ET-1 content) and vascular morphometric parameters (wet weight of aorta and mesenteric arterial bed, media thickness, media cross-sectional area, and media-to-lumen ratio)surrogate

ET-1 gene overexpression in blood vessels accentuates vascular hypertrophy in DOCA-salt-induced hypertension, an effect that can be mitigated by endothelin receptor antagonism.

Cite This Study

Schiffrin et al. (2008) studied this question.

synapsesocial.com/papers/6a7f930a138fa0ec199fe7d5 https://doi.org/10.1159/000159151

Topics

Hypertension management

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Implication

Supports ET-1 role in excess vascular hypertrophy in this rat model; leaves open whether endothelin antagonism prevents remodeling in human hypertension.