title: Expression of sarcoplasmic reticulum Ca2+ -ATPase mRNA in the hypertrophied heart of young spontaneously hypertensive rats.
abstract: 1. Recent evidence indicates that cardiac hypertrophy induced by pressure overload is associated with a decrease in sarcoplasmic reticulum (SR) Ca2+ -ATPase of myocytes, which may contribute to a diastolic dysfunction of the heart by causing intracellular Ca2+ overload. To elucidate whether or not this is also the case in genetic hypertension, we examined cardiac mRNA levels of SR Ca2+ 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 +/- 4 mg/100 g bodyweight, respectively, P < 0.05), the level of SR Ca2+ -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 Ca2+ -ATPase expression of SHR. 5. Thus, the expression of SR Ca2+ -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 Ca2+ -ATPase expression occur in prominent hypertrophy and in the failured heart, further studies on cardiac SR Ca2+ -ATPase expression in more aged SHR will be required.
authors.affiliation: Department of Pharmacology, Osaka City University Medical School, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Ohta
authors.forename: S
authors.initials: S
authors.lastname: Kim
authors.forename: A
authors.initials: A
authors.lastname: Hamaguchi
authors.forename: K
authors.initials: K
authors.lastname: Miura
authors.forename: T
authors.initials: T
authors.lastname: Yukimura
authors.forename: H
authors.initials: H
authors.lastname: Iwao
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D015152:Blotting, Northern; D000252:Calcium-Transporting ATPases / Q000096:biosynthesis* / Q000235:genetics; D006332:Cardiomegaly / Q000201:enzymology*; D015971:Gene Expression Regulation, Enzymologic / Q000502:physiology*; D008297:Male; D009206:Myocardium / Q000201:enzymology*; D012333:RNA, Messenger / Q000096:biosynthesis* / Q000235:genetics; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D012519:Sarcoplasmic Reticulum / Q000378:metabolism*
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D012333:RNA, Messenger; D000252:Calcium-Transporting ATPases