Key result
Isolated myocytes from spontaneously hypertensive rats showed a significantly higher extent of shortening compared to Wistar-Kyoto rats (11.3% vs 9.8%, P<0.01).
Absolute Event Rate: 11.3% vs 9.8%
p-value: p=<0.01
Left ventricular diastolic dysfunction in spontaneously hypertensive rats is not caused by intrinsic myocyte contractile depression, but angiotensin II suppresses the function of these hypertrophied myocytes.
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Does not support changes in hypertension care; leaves open translation of enhanced myocyte shortening to human hypertensive cardiomyopathy.
Kobayashi et al. (1995) studied Hypertension. Spontaneous hypertension (SHR) vs. Wistar-Kyoto rats (WKY) was evaluated on Extent of shortening in isolated myocytes (p=<0.01). Isolated myocytes from spontaneously hypertensive rats showed a significantly higher extent of shortening compared to Wistar-Kyoto rats (11.3% vs 9.8%, P<0.01).
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