| Project/Area Number |
60480233
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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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 | Kyushu University |
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Principal Investigator |
TAKESHITA Akira Kyushu University, Faculty of Medicine, associate professor, 医学部, 助教授 (30038814)
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| Co-Investigator(Kenkyū-buntansha) |
IMAIZUMI Tsutomu Kyushu University, Faculty of Medicine, Assistant, 医学部, 助手 (60148947)
KANAIDE Hideo Kyushu University, Faculty of Medicine, Lecture, 医学部, 講師 (80038851)
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| Project Period (FY) |
1985 – 1986
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| Project Status |
Completed (Fiscal Year 1986)
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| Budget Amount *help |
¥6,600,000 (Direct Cost: ¥6,600,000)
Fiscal Year 1986: ¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1985: ¥4,700,000 (Direct Cost: ¥4,700,000)
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| Keywords | Cardiopulmonary baroreflex / High salt intake / Spontaneously hypertensive rat / Atrial natriuretic peptide / 心房筋伸展 |
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| Research Abstract |
1) We investigated the effects of high salt intake on cardiopulmonary baroreflex control of renal sympathetic nerve activity (RSNA) in SHR and WKY. The stimulus ( <DELTA> LV end-diastolic pressure)-response ( <DELTA> RSNA) relationship in SHR with normal salt intake was shifted toward a higher pressure range compared with that in WKY with normal salt intake. High salt intake decereased the gain of the reflex both in SHR and WKY. However, changes in the gain caused by salt loading were comparable between SHR and WKY.
2) We also examined release of atrial natriuretic peptide (ANP) in response to atrail stretch in vitro. We found, first, that ANP release decreased gradually with time despite that an increase in resting tension was maintained, Which suggests that adaptation occures in ANP release in response to atrial stretch. Second, we found that ANP release did not occure when the atria were stretched in the medium with diltiazem <10^(-5)> M or the calciums-free medium. However, repetitive stretch at a frequency of 300 beats/min increased ANP release despite the presence of diltiazem <10^(-5)> M. These results indicate that active muscle contraction or calcium entry into myocytes is not prerequisite for ANP release.
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