What question did this study set out to answer?

To determine whether impaired sarcoplasmic reticulum calcium sequestration causes the loss of load-sensitive relaxation observed in pressure-overload cardiac hypertrophy.

January 1, 1994AJP Heart and Circulatory Physiology

Role of sarcoplasmic reticulum in loss of load-sensitive relaxation in pressure overload cardiac hypertrophy

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Why the study?

Does pressure overload-induced cardiac hypertrophy reduce SR Ca2+ sequestration potential and load-sensitive relaxation in female guinea pig left ventricles?

Population

Female guinea pig left ventricle model of cardiac hypertrophy (Hyp) and sham-operated (Sham) groups

Comparison

21 days of pressure overload induced by… vs Sham-operated

Design

Preclinical

Follow-up

21 days

Authors

CCC. R. CoryOntario Veterinary College RGRobert W. GrangeVirginia Tech MHM. E. HoustonUniversity of Waterloo

Discussion

Member takes

Implication

Supports SR Ca2+-ATPase role in guinea pig hypertrophy relaxation defects; leaves open human translation and clinical relevance.

Key Points

To determine whether impaired sarcoplasmic reticulum calcium sequestration causes the loss of load-sensitive relaxation observed in pressure-overload cardiac hypertrophy.
Induced pressure-overload cardiac hypertrophy in female guinea pigs via 21 days of suprarenal subdiaphragmatic aortic coarctation compared to sham-operated controls.
Assessed in vitro mechanical properties of anterior papillary muscles, including load sensitivity via rapid force step transitions during isotonic contraction.
Quantified left ventricular sarcoplasmic reticulum Ca(2+)-ATPase enzymatic activity, cyclic AMP-dependent protein kinase response, and protein expression using Western blot radioimmunoassays.
Aortic coarctation increased left ventricular mass by 36% and decreased load-sensitive relaxation by 50% in hypertrophic papillary muscles alongside reductions in peak tension and relaxation rates.
Maximal Ca(2+)-ATPase activity at saturating calcium was unaltered, but activity at 0.65 µM free calcium declined by 43% in hypertrophy, correlating strongly with attenuated load sensitivity (r = 0.84, P = 0.009).
Protein kinase stimulation yielded a 1.6-fold activity increase in hypertrophic tissue versus 2.6-fold in controls, despite unchanged protein levels of Ca(2+)-ATPase and phospholamban.

Structured PICO

Does pressure overload-induced cardiac hypertrophy reduce SR Ca2+ sequestration potential and load-sensitive relaxation in female guinea pig left ventricles?

Population

Female guinea pig left ventricle model of cardiac hypertrophy (Hyp) and sham-operated (Sham) groups

Intervention

21 days of pressure overload induced by coarctation of the suprarenal, subdiaphragmatic aorta

Comparator

Sham-operated

Outcome

In vitro mechanical function of anterior papillary muscles and sarcoplasmic reticulum (SR) Ca2+ sequestration potentialsurrogate

Decreased sarcoplasmic reticulum function, specifically a qualitative change in SR Ca2+-ATPase and possibly phospholamban, contributes to the attenuated load sensitivity in pressure overload cardiac hypertrophy.

Cite This Study

Cory et al. (1994) studied this question.

synapsesocial.com/papers/6a723a5e87f921057128808d https://doi.org/10.1152/ajpheart.1994.266.1.h68

Topics

Hypertension management

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Role of sarcoplasmic reticulum in loss of load-sensitive relaxation in pressure overload cardiac hypertrophy

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Topics

Role of sarcoplasmic reticulum in loss of load-sensitive relaxation in pressure overload cardiac hypertrophy

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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Topics

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