1991 Fiscal Year Final Research Report Summary
Role of brain natriuretic peptide in arterial pressure regulation
| Project/Area Number |
01570501
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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 | Yokohama City University |
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Principal Investigator |
GOTOH Eiji Yokohama City University, The Second Department of Internal Medicine, Assistant Professor, 医学部, 講師 (30153753)
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| Co-Investigator(Kenkyū-buntansha) |
ISHII Masao Yokohama City University, The Second Department of Internal Medicine, Professor, 医学部, 教授 (90010363)
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| Project Period (FY) |
1989 – 1991
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| Keywords | barin natriuretic peptide / c-type natriuretic peptide / central nervous system / arterial blood pressure / sympathetic nervous system / angiotensin II |
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| Research Abstract |
The brain and sympathetic nervous (SN) system play important roles in cardiovascular regulation. Central administration of atrial natriuretic peptide (ANP) has been reported to oppose pressor response to centrally administered angiotensin (A) II. Recently, two new types of natriuretic peptides were found in the porcine brain, termed brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP). To examine the central action of BNP or CNP on blood pressure, we infused rat-BNP or CNP into the third ventricle and measured arterial blood pressure (AP) and plasma vasopressin (VP) concentration in inactin-anesthetized rats. 1. Although high doses of BNP or CNP produced reductions in AP, these doses, when given intravenously, similarly decreased AP. Plasma VP was decreased. 2. Hypertonic saline or AII given to the ventricle produced significant increases in AP and plasma VP. But BNP or CNP inhibited AP and VP responses to hypertonic saline or AII. These central actions of BNP or CNP we
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re equivalent to those of ANP. 3. Salt-sensitive hypertensive Dahl S rats were subjected. Central administration of high doses of BNP caused significant decreases in AP, but these doses, when given intravenously, showed similar depressor effects. Furthermore, centrally administered BNP did not affect the baroreceptor-mediated reflex function. These data suggest that, in the brain, BNP or CNP as well as ANP antagonizes AII or NaCl in terms of the effects on blood pressure and VP secretion.
Circulating AII has been reported to stimulate SN activity, and ANP may antagonize the SN response to AII. To investigate the interactions between circulating AII and ANP for blood pressure and SN activity, we did intravenous infusions of AII and ANP and measured AP and muscle SN activity in human. Intravenous infusions of AII enhanced SN activities but simultaneous infusions of ANP attenuated the responses. Although the mechanism by which circulating ANP opposes the actions of circulating AII has not been elucidated, it could be related to the interaction between the two peptides in the brain as shown in our studies. Less
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