Abstract:
:Transgenic mice overexpressing a transthyretin promoter-ANF structural fusion gene have a life-long reduction in arterial blood pressure compared to nontransgenic littermates. The present study was designed to test the hypothesis that the high plasma level of ANF in the transgenic mice inhibits the renin-angiotensin and/or vasopressin systems, thereby causing the hypotension. Mice were anaesthetized with Inactin and arterial pressure and heart rate were monitored before and during Saralasin infusion and vasopressin V1 receptor blockade. Effectiveness of the blockade was determined by injection of angiotensin and vasopressin before and during Saralasin and V1 receptor antagonist administration. Saralasin was associated with hypotension in both transgenic and nontransgenic mice. The decrease in blood pressure was proportionally greater in the transgenic animals. Vasopressin receptor blockade had little effect on blood pressure in either group. Heart rates were not different between the groups during any maneuver. We conclude that the chronic hypotensive effect of ANF overproduction does not involve the inhibition of either renin-angiotensin or vasopressin systems. The data, however, suggest that the renin-angiotensin system may be stimulated in the ANF-transgenic mice.
journal_name
Physiol Resjournal_title
Physiological researchauthors
Lichardus B,Veress AT,Field LJ,Sonnenberg Hsubject
Has Abstractpub_date
1994-01-01 00:00:00pages
145-50issue
3eissn
0862-8408issn
1802-9973journal_volume
43pub_type
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journal_title:Physiological research
pub_type: 杂志文章
doi:
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pub_type: 杂志文章,评审
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doi:
更新日期:1998-01-01 00:00:00
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journal_title:Physiological research
pub_type: 杂志文章
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journal_title:Physiological research
pub_type: 杂志文章
doi:
更新日期:2007-01-01 00:00:00
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journal_title:Physiological research
pub_type: 杂志文章
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