April 1, 2002Journal of Hypertension

Inhibition of left ventricular fibrosis by tranilast in rats with renovascular hypertension

Q: What is the clinical evidence from this study?

Study design: Other. Population: Renovascular hypertension. Intervention: Tranilast vs. Untreated 2K1C rats and quinapril. Primary outcome: Cardiac hydroxyproline content (cardiac fibrosis) (p=<0.05).

Q: What question did this study set out to answer?

To examine whether tranilast reduces cardiac fibrosis in rats with renovascular hypertension and its in-vitro effects on cardiac cells.

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Key result

Tranilast significantly reduced cardiac fibrosis (hydroxyproline content 3.97 vs 4.92 mg/mg; P<0.05) in a blood-pressure-independent manner in rats with renovascular hypertension.

Why the study?

Does tranilast reduce cardiac fibrosis in rats with renovascular hypertension?

Population

Rats with two-kidney, one-clip renovascular hypertension, and in-vitro cardiac myocytes and non-myocyte cells

Comparison

Tranilast (400 mg/kg per day) for 12 weeks vs Untreated 2K1C rats, sham-operated controls, and…

Design

Preclinical

Follow-up

12 weeks

Authors

BHBerthold Hocher MGMichael Godes JOJan Olivier

Discussion

Member takes

Overview

May attenuate experimental cardiac fibrosis; leaves open clinical translation from in vitro data.

Key Points

To examine whether tranilast reduces cardiac fibrosis in rats with renovascular hypertension and its in-vitro effects on cardiac cells.
Analyzed hearts from sham-operated controls and three groups of rats with 2K1C renovascular hypertension, treated with either quinapril or tranilast for 12 weeks.
Measured systolic blood pressure, left ventricular weight, and cardiac hydroxyproline content.
Conducted cell culture experiments to assess the effects of tranilast on cardiac myocytes and non-myocyte cells.
Tranilast significantly reduced cardiac fibrosis compared to untreated 2K1C rats (P < 0.01), with a notable reduction in hydroxyproline content (P < 0.05).
Systolic blood pressure was lowered by quinapril, but tranilast did not significantly alter blood pressure levels.
The antiproliferative effect of tranilast on cardiac non-myocyte cells likely contributed to the reduction of cardiac fibrosis.

Structured PICO

Does tranilast reduce cardiac fibrosis in rats with renovascular hypertension?

Population

Rats with two-kidney, one-clip (2K1C) renovascular hypertension treated for 12 weeks.

Intervention

Tranilast (400 mg/kg per day) for 12 weeks

Comparator

Untreated 2K1C rats, sham-operated controls, and 2K1C rats treated with quinapril (6 mg/kg per day) for 12 weeks

Outcome

Cardiac fibrosis (measured by computer-aided image analysis and cardiac hydroxyproline content)surrogate

Main Result

Absolute Event Rate: 3.97% vs 4.92%

p-value: p=<0.05

Long-term treatment with tranilast markedly attenuated left ventricular fibrosis in a rat model of renovascular hypertension, likely via an antiproliferative effect on cardiac non-myocyte cells.

Cite This Study

Hocher et al. (2002) studied Renovascular hypertension. Tranilast vs. Untreated 2K1C rats and quinapril was evaluated on Cardiac hydroxyproline content (cardiac fibrosis) (p=<0.05). Tranilast significantly reduced cardiac fibrosis (hydroxyproline content 3.97 vs 4.92 mg/mg; P<0.05) in a blood-pressure-independent manner in rats with renovascular hypertension.

synapsesocial.com/papers/6a6b3f6945e10bb5bcf2e348 https://doi.org/10.1097/00004872-200204000-00034

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April 1, 2002Journal of Hypertension

Inhibition of left ventricular fibrosis by tranilast in rats with renovascular hypertension

View Full Paper

Ask AI

Bookmark

Key result

Tranilast significantly reduced cardiac fibrosis (hydroxyproline content 3.97 vs 4.92 mg/mg; P<0.05) in a blood-pressure-independent manner in rats with renovascular hypertension.

Why the study?

Does tranilast reduce cardiac fibrosis in rats with renovascular hypertension?

Population

Rats with two-kidney, one-clip renovascular hypertension, and in-vitro cardiac myocytes and non-myocyte cells

Comparison

Tranilast (400 mg/kg per day) for 12 weeks vs Untreated 2K1C rats, sham-operated controls, and…

Design

Preclinical

Follow-up

12 weeks

Authors

BHBerthold Hocher MGMichael Godes JOJan Olivier

Discussion

Member takes

Overview

May attenuate experimental cardiac fibrosis; leaves open clinical translation from in vitro data.

Key Points

To examine whether tranilast reduces cardiac fibrosis in rats with renovascular hypertension and its in-vitro effects on cardiac cells.
Analyzed hearts from sham-operated controls and three groups of rats with 2K1C renovascular hypertension, treated with either quinapril or tranilast for 12 weeks.
Measured systolic blood pressure, left ventricular weight, and cardiac hydroxyproline content.
Conducted cell culture experiments to assess the effects of tranilast on cardiac myocytes and non-myocyte cells.
Tranilast significantly reduced cardiac fibrosis compared to untreated 2K1C rats (P < 0.01), with a notable reduction in hydroxyproline content (P < 0.05).
Systolic blood pressure was lowered by quinapril, but tranilast did not significantly alter blood pressure levels.
The antiproliferative effect of tranilast on cardiac non-myocyte cells likely contributed to the reduction of cardiac fibrosis.

Structured PICO

Does tranilast reduce cardiac fibrosis in rats with renovascular hypertension?

Population

Rats with two-kidney, one-clip (2K1C) renovascular hypertension treated for 12 weeks.

Intervention

Tranilast (400 mg/kg per day) for 12 weeks

Comparator

Untreated 2K1C rats, sham-operated controls, and 2K1C rats treated with quinapril (6 mg/kg per day) for 12 weeks

Outcome

Cardiac fibrosis (measured by computer-aided image analysis and cardiac hydroxyproline content)surrogate

Main Result

Absolute Event Rate: 3.97% vs 4.92%

p-value: p=<0.05

Long-term treatment with tranilast markedly attenuated left ventricular fibrosis in a rat model of renovascular hypertension, likely via an antiproliferative effect on cardiac non-myocyte cells.

Cite This Study

synapsesocial.com/papers/6a6b3f6945e10bb5bcf2e348 https://doi.org/10.1097/00004872-200204000-00034

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