1988 Fiscal Year Final Research Report Summary
Roles of neuropeptides in the neural control of cardiovascular function.
| Project/Area Number |
62570078
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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 |
環境生理学(含体力医学･栄養生理学)
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| Research Institution | University of Occupational and Environmental Health |
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Principal Investigator |
KANNAN Hiroshi Univ. of Occup. Environ. Health, Sch. Med.. Associate Professor, 医学部, 助教授 (00049058)
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| Project Period (FY) |
1987 – 1988
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| Keywords | Neural control of cardiovascular system / Sympathetic nerve activity / hypothalamic paraventricular nucleus / Electrical・chemical stimulation / Angiotensin II / Atrial natriuretic hormone / 覚醒ラット |
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| Research Abstract |
Roles of neuropeptides in the neural control of cardiovascular function.
1. Effects of stimulation of the hypothalamic paraventricular nucleus (PVN), where is one of sites of action for the effects of neuropeptides on autonomic functions, were examined on arterial pressure, heart rate and renal sympathetic nerve activity (RSNA) in anesthetized and awake rats. In anesthetized rats, stimulation of the PVN with electrical current and L-glutamate decreased RSNA accompanied by decrease in arterial pressure. On the other hand, the stimulation of the PVN increased the RSNA accompanied by increase in arterial pressure in awake rats. Therefore, it is concluded that PVN neurons are involved in both pressore and depressor controlling system through the sympathetic nerve system, and anesthesia strogly affects the balance of the two controlling system.
2. Effects of intracerebroventricular (i.c.v) administration of neuropeptides on arterial pressure, heart rate and RSNA in anesthetized and awake rats
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. (1). Administration of angiotensin II (AII) evoked an increase in arterial pressure and a decrease in RSNA in dose-dependent manner. Heart rate decreeased in awake rats but did not show any change in anesthetized rats. The responses were greatly attenuated by prior i.c.v. administration of AII antagonist, saralasin. The decrease in RSNA induced by i.c.v. AII persisted in rats with sinoaortic denervation, indicating that the decrease in RSNA is not due to baroreceptors activation. Furthermore, renal blood flow measured by Doppler flow probes did not change significantly. thus, the decrease in rsna observed following i.c.v. aii might be involved in the control of renin release and/or absorption of sodium and water from the renal tubulus, rather than renal hemodynamics. (2). Administration of atrial natriuretic hormone (ANP) did not change arterial pressure, heart rate and RSNA. However, ANP attenuated AII-induced pressor and bradycardia responses but did not affect AII-induced depressant effects on RSNA. Therefore, it is suggested that central interacting sites. of AII and ANP for cardiovascular and renal responses may be different. Less
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