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EXPRESSION OF SARCOPLASMIC RETICULUM Ca 2+ ‐ATPase mRNA IN THE HYPERTROPHIED HEART OF YOUNG SPONTANEOUSLY HYPERTENSIVE RATS
Author(s) -
Ohta Kensuke,
Kim Shokei,
Hamaguchi Akinori,
Miura Katsuyuki,
Yukimura Tokihito,
Iwao Hiroshi
Publication year - 1995
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1995.tb02893.x
Subject(s) - medicine , endocrinology , muscle hypertrophy , renin–angiotensin system , angiotensin ii , angiotensin ii receptor type 1 , atpase , pressure overload , endoplasmic reticulum , chemistry , blood pressure , cardiac hypertrophy , enzyme , biochemistry
Summary 1. Recent evidence indicates that cardiac hypertrophy induced by pressure overload is associated with a decrease in sarcoplasmic reticulum (SR) Ca 2+ ‐ATPase of myocytes, which may contribute to a diastolic dysfunction of the heart by causing intracellular Ca 2+ overload. To elucidate whether or not this is also the case in genetic hypertension, we examined cardiac mRNA levels of SR Ca 2+ ‐ATPase in 11 week old spontaneously hypertensive rats (SHR) by northern blot analysis. 2. Furthermore, to test the effects of short‐term inhibition of the renin‐angiotensin system on its expression, we treated 10 week old SHR with angiotensin‐converting enzyme inhibitors (alacepril and imidapril) or an AT1 receptor antagonist (SC‐52458) for 7 days. 3. Though the left ventricular weight of SHR was significantly higher than that of Wistar‐Kyoto (WKY) rats (277 ± 6 vs 237 ± 4mg/100g bodyweight, respectively, P < 0.05), the level of SR Ca 2+ ‐ATPase mRNA showed no difference between SHR and WKY at this age. 4. Moreover, the aforementioned three drugs did not at all affect the SR Ca 2+ ‐ATPase expression of SHR. 5. Thus, the expression of SR Ca 2+ ‐ATPase was not down‐regulated in the heart of 11 week old SHR, and seemed not to be mediated by angiotensin AT1 receptor at this age. Since some evidence on pressure‐overloaded cardiac hypertrophy indicate that the decrease in SR Ca 2+ ‐ATPase expression occur in prominent hypertrophy and in the failured heart, further studies on cardiac SR Ca 2+ ‐ATPase expression in more aged SHR will be required.