1995 Fiscal Year Final Research Report Summary
An evaluation of sympathetic nerve function in fuiling hearts
| Project/Area Number |
06670701
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | TOYAMA MEDICAL AND PHARMACEUTICAL UNIVERSITY |
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Principal Investigator |
INOUE Hiroshi TOYAMA Med. & Pharm. Univ., professor, 医学部, 教授 (60151619)
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| Co-Investigator(Kenkyū-buntansha) |
TAKASHIMA Syuutaro Toyama Med. & Pharm. Univ., assistant professor, 医学部, 助手 (50146586)
NOZAWA Takashi Toyama Med. & Pharm. Univ., assistant professor, 付属病院, 助手 (00180737)
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| Project Period (FY) |
1994 – 1995
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| Keywords | Herat Failure / Dahl Rat / Hypertensive Heart disease / beta-receptor / Cardiac Sympathetic Nerve Function |
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| Research Abstract |
We investigated the cardiac sympathetic nerve function and beta-adrenoreceptors in the process of developing heart failure.
The sympathetic nerve function was assessed by ^<131>I-metaiodobenzylguanidine (MIBG) and beta-receptors by ^<125>I-cyanopindolol (ICYP). Dahl salt sensitive (DS) and salt resistant (DR) rats were fed an 8% NaCl diet from 6 wk of age.
At 12 wk, a cardiac hypertrophy was induced in DS rat but not in DR rat. At 18 wk, a heart falure was developed in DS rats. At the compensated hypertrophic stage (12 wk), DS rats had higher cardiac MIBG uptake but no changes in ICYP uptake. At the heart failure stage in DS rats, MIBG uptake was decreased, especially in the endcardial regions of left ventricle, in an association with a decrease in ICYP uptake. A cardiac norepinephrine (NE) content at 12 wk was significantly lower in DS rats than in DR rats but serum NE level was unchaged. At 18 wk of DS rat, serum NE level increased and cardiac NE content decreased more.
In summary a high salt feeding caused a cardiac sympathetic activation in DS rat. A log term activation of cardiac sympathetic nerve would produce an alteration of the nerve ending and down-regulation of beta-receptors.
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