Key result
Spontaneously hypertensive rat hearts show ~26% lower sarcoplasmic reticulum Ca2+ binding capacity than normotensive controls.
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No immediate clinical implications for hypertension; leaves open whether sarcoplasmic reticulum calcium defects contribute to human hypertensive heart disease.
ATPase activity of myofibrils and Ca2+ binding ability of sarcoplasmic reticulum isolated from the hearts of spontaneously hypertensive rats (OkamotoAoki strain, SHR) and normotensive Wistar rats (NR) were measured. Myofibrils isolated from both the hearts of SHR and NR showed essentially the same activity either in the absence or presence of Ca2+. On the other hand, Ca2+ activated ATPase activity of relaxed preparation of myofibrils from SHR was significantly lower than that from NRThe maximum Ca2+ binding capacity of sarcoplasmic reticulum (SR) from SHR (8.80±0.33nmoles/mg) was significantly lower than that from NR (11.95±0.55). Also, SR from SHR had significantly elevated Ca2+ activated ATPase activity (0.171±0.009μmoles/mg/min) compared with that of NR (0.100±0.009). Values were expressed as mean±s.e.m.Reduction of Ca2+ binding capacity of SR may result in increase of intracellular free Ca2+ concentration which probably be one of the important factor for muscle contraction. If the abnormal intracellular distribution of Ca2+ is associated with the smooth muscle of cardiovascular system, it would cause the increase of vascular resistance resulting in hypertension.
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Aoki et al. (1974) studied Hypertension. Spontaneous hypertension (SHR strain) vs. Normotensive Wistar rats was evaluated on Maximum Ca2+ binding capacity of sarcoplasmic reticulum (nmoles/mg) (p=<0.01). Sarcoplasmic reticulum from the hearts of spontaneously hypertensive rats had significantly lower maximum Ca2+ binding capacity (8.80 vs 11.95 nmoles/mg) compared to normotensive rats.
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