Key Points
- To examine sarcomere shortening and relaxation dynamics in single left ventricular myocytes from renovascular hypertensive rats to pinpoint the cellular basis of impaired relaxation.
- Isolated single left ventricular cardiac myocytes from renovascular hypertensive (Hyp) and normotensive control (Sham) rats.
- Measured sarcomere shortening and relaxation velocities at 18 hours post-isolation using an optical-digital Fourier-transform processor, confirming results with whole-cell video tracking in both fresh and cultured myocytes.
- Resting sarcomere length, maximal shortening percentage, time to peak shortening, and average shortening velocity showed no differences between Sham and Hyp myocytes.
- Average sarcomere relaxation velocity was significantly reduced and half-relaxation time was significantly prolonged in Hyp myocytes compared to Sham controls, an impairment maintained in both freshly isolated and cultured cells.
Structured PICO
PPopulationSingle left ventricular (LV) cardiac myocytes isolated from renovascular hypertensive (Hyp) rats and normotensive (Sham) rats
IInterventionRenovascular hypertension model
CComparatorNormotensive (Sham) model
OOutcomeSarcomere shortening and relaxation velocities, and half-relaxation timesurrogate
Renovascular hypertension induces intrinsic relaxation abnormalities in isolated cardiac myocytes, potentially explaining diastolic dysfunction at the cellular level.