2026-09-24T08:03:18Z https://www.ideals.illinois.edu/oai-pmh

oai:www.ideals.illinois.edu:2142/21218 2023-07-10 col_2142_5131 col_2142_13007 com_2142_5130 com_2142_13006

Made available in DSpace on 2011-05-07T13:01:59Z (GMT). No. of bitstreams: 2 license.txt: 4922 bytes, checksum: 910b249b4beec47e7ab768910c8f966f (MD5) 9416390.pdf: 5287338 bytes, checksum: 7ad9cc893a5c5e88bc49745c02568e9f (MD5) Previous issue date: 1994 Item marked as restricted to the 'UIUC Users [automated]' Group (id=2) by Howard Ding (hding2@illinois.edu) on 2011-05-07T14:49:17Z Item is restricted indefinitely. Weyhenmeyer, James A. Lark, Lisa Anne 2011-05-07T13:01:59Z 2011-05-07T13:01:59Z 10000-01-01 1994 The brain renin-angiotensin system (RAS) is a known regulator of cardiovascular function. The present studies investigated the cardiovascular effects of the pharmacological interruption of this system in hypertensive inbred Dahl salt-sensitive (DS/JR) rats. Intracerebroventricular (i.c.v.) administration of the angiotensin converting enzyme inhibitor captopril (10 $\mu$g) to conscious, freely moving DS/JR rats produced a sustained depressor response but was without effect in normotensive control inbred Dahl salt-resistant rats. Remaining studies focused on the effects of centrally administered peptide and nonpeptide angiotensin II (ANG II) antagonists in DS/JR rats. Both the peptide antagonist sarthran (20 $\mu$g) and the nonpeptide antagonist losartan (10 $\mu$g), which is specific to the AT$\sb1$ receptor subtype, blocked pressor and dipsogenic responses to i.c.v. ANG II. The AT$\sb2$ receptor antagonist PD 123319 (10 $\mu$g) did not block the responses. Sarthran alone produced a significant and short-lived bradycardia with an accompanying slight depressor response. Losartan and PD 123319 were without effect on blood pressure and heart rate. The sarthran-induced bradycardia was further evaluated by examining its magnitude after preblockade of one or both of the ANG II receptor subtypes. Both losartan and PD 123319 (10 $\mu$g) inhibited the bradycardic response to 20 $\mu$g of sarthran by about 45%. Preblockade of both sites resulted in a slightly greater inhibition suggesting that sarthran's effects are mediated interdependently by the AT$\sb1$ and AT$\sb2$ sites. In summary, the present studies demonstrated that the brain RAS is involved in cardiovascular regulation in the DS/JR rat and, as such, may be a potential target for the treatment of salt-induced hypertension. Furthermore, evidence was presented which suggests that both ANG II receptor subtypes are involved in this function. Restriction data tranferred 2014-07-01T11:22:24-05:00 Original Data Group with Access UIUC Users [automated] Release Date: none Reason: ETDs are only available to UIUC Users without author permission ETDs are only available to UIUC Users without author permission U of I Only AAI9416390 (UMI)AAI9416390 http://hdl.handle.net/2142/21218 eng Copyright 1994 Lark, Lisa Anne Biology, Neuroscience The cardiovascular effects of the pharmacological interruption of the brain renin-angiotensin system in Dahl salt-induced hypertension text Neuroscience Neuroscience University of Illinois at Urbana-Champaign Dissertation Ph.D.