Deficiency in angiotensin AT1a receptors prevents diabetes-induced hypertension

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dc.contributor.authorWichi R.B.
dc.contributor.authorFarah V.
dc.contributor.authorChen Y.
dc.contributor.authorIrigoyen M.C.
dc.contributor.authorMorris M.
dc.date.accessioned2024-03-13T01:40:07Z
dc.date.available2024-03-13T01:40:07Z
dc.date.issued2007
dc.description.abstractThe renin-angiotensin system has been implicated in the etiology of the cardiovascular complications of diabetes. Our studies extend these findings to show a specific role for angiotensin AT1a receptors in mediating diabetes-induced hypertension. Male angiotensin AT1a knockout (AT1aKO) and wild-type (AT1aWT) mice with arterial telemetric catheters were injected with streptozotocin (STZ; 150 mg/kg ip). The STZ dose was selected on the basis of a dose-response experiment in C57/BL mice. Blood glucose, water intake, body weight, blood pressure (BP), and heart rate (HR) were measured over a 2-wk period. Estimates of BP and HR variance (BPV and HRV) and their low- and high-frequency domains were also determined. STZ induced similar levels of hyperglycemia and polydypsia in the groups. Mean arterial pressure (MAP) was increased from 100 ± 6 to 124 ± 6 mmHg in diabetic AT1aWT. MAP was unchanged in AT1aKO (80 ± 4 vs. 85 ± 5 mmHg, basal vs. STZ). Treatment with an ACE inhibitor, captopril, produced a greater reduction in MAP (-18%) in diabetic AT1aWT than in AT1aKO (-3.4%). BPV was lower in AT1aKO (19 ± 0.5 vs. 9 ± 2 mmHg2, AT1aWT vs. AT1aKO). Diabetes reduced BPV but only in AT1aWT (19 ± 0.5 vs. 8 ± 1 mmHg 2, basal vs. STZ). There were no changes in HR in either group. In AT1aKO, STZ increased HRV and its high-frequency domain with no changes seen in AT1aWT. Results document that ANG AT1a receptors are critical in diabetes-induced hypertension and in cardiac autonomic responses. Copyright © 2007 the American Physiological Society.
dc.description.issuenumber3
dc.description.volume292
dc.identifier.doi10.1152/ajpregu.00524.2006
dc.identifier.issn0363-6119
dc.identifier.urihttps://dspace.mackenzie.br/handle/10899/37661
dc.relation.ispartofAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
dc.rightsAcesso Restrito
dc.subject.otherlanguageAutonomic function
dc.subject.otherlanguageBlood pressure
dc.subject.otherlanguageCardiovascular
dc.subject.otherlanguageDiabetes
dc.subject.otherlanguageHeart rate
dc.subject.otherlanguageMice
dc.subject.otherlanguageRenin-angiotensin system
dc.subject.otherlanguageStreptozotocin
dc.titleDeficiency in angiotensin AT1a receptors prevents diabetes-induced hypertension
dc.typeArtigo
local.scopus.citations24
local.scopus.eid2-s2.0-33847710302
local.scopus.updated2024-05-01
local.scopus.urlhttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=33847710302&origin=inward
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