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Am J Physiol Heart Circ Physiol 279: H2939-H2946, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 6, H2939-H2946, December 2000

Diastolic wall stress and ANG II in cardiac hypertrophy and gene expression induced by volume overload

Hiroshi Yamakawa, Takuroh Imamura, Takeshi Matsuo, Hisamitsu Onitsuka, Yoko Tsumori, Johji Kato, Kazuo Kitamura, Yasushi Koiwaya, and Tanenao Eto

First Department of Internal Medicine, Miyazaki Medical College, Miyazaki 889-1692, Japan

We investigated the effects of diastolic wall stress (WS) and angiotensin II (ANG II) on the left ventricular (LV) hypertrophy (LVH) induced by volume overload and on the gene expression of LV adrenomedullin (AM) and atrial natriuretic peptide (ANP) in volume overload. Diastolic WS was pharmacologically manipulated with (candesartan) or without (calcium channel blocker manidipine) inhibition of ANG II type 1 receptors in aortocaval-shunted rats over 6 wk. Diastolic WS reached a plateau at 2 wk and subsequently declined regardless of further LVH. Although diastolic WS was decreased to a similar extent by both compounds, candesartan blunted LVH over 6 wk, whereas manidipine blunted LVH at 2 wk but not after 4 wk. Levels of AM and ANP gene expression increased as LVH developed but were completely suppressed by candesartan over 6 wk. ANP expression level was also attenuated by manidipine over 6 wk, whereas AM expression level was suppressed at 2 wk but not after 4 wk by manidipine. We concluded that diastolic WS and ANG II might be potent stimuli for the LVH and LV AM and ANP gene expression in volume overload and that diastolic WS could be relatively involved in the early LVH and in the gene expression of ANP rather than of AM.

aortocaval shunt; adrenomedullin; atrial natriuretic peptide; angiotensin II type 1 receptor antagonist; calcium channel blocker; left ventricular hypertropy


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