Introgression of chromosome 13 in Dahl salt-sensitive genetic background restores cerebral vascular relaxation. Am J Physiol Heart Circ Physiol 2004 Aug;287(2):H957-62
Date
03/20/2004Pubmed ID
15031125DOI
10.1152/ajpheart.01087.2003Scopus ID
2-s2.0-3242726790 (requires institutional sign-in at Scopus site) 32 CitationsAbstract
To evaluate the potential role of impaired renin-angiotensin system (RAS) function in contributing to reduced vascular relaxation in Dahl salt-sensitive (S) rats, responses to ACh (10(-6) mol/l) and hypoxia (Po(2) reduction to 40-45 mmHg) were determined in isolated middle cerebral arteries of Dahl S rats, Brown Norway (BN) rats, and consomic rats having chromosome 13 (containing the renin gene) or chromosome 16 of the BN rat substituted into the Dahl S genetic background (SS-13(BN) and SS-16(BN), respectively). Arteries of BN rats on a low-salt (LS) diet (0.4% NaCl) dilated in response to ACh and hypoxia, whereas dilation in response to these stimuli was absent in Dahl S rats on LS diet. Vasodilation to ACh and hypoxia was restored in SS-13(BN) rats on an LS diet but not in SS-16(BN) rats. High-salt diet (4% NaCl), to suppress ANG II, eliminated vasodilation to hypoxia and ACh in BN and in SS-13(BN) rats. Treatment of SS-13(BN) rats with the AT(1) receptor antagonist losartan also eliminated the restored vasodilation in response to ACh and hypoxia. These studies suggest that restoration of normal RAS regulation in SS-13(BN) consomic rats restores vascular relaxation mechanisms that are impaired in Dahl S rats.
Author List
Drenjancevic-Peric I, Lombard JHMESH terms used to index this publication - Major topics in bold
AcetylcholineAngiotensin II Type 1 Receptor Blockers
Animals
Cerebral Arteries
Chromosomes
Diet, Sodium-Restricted
Hybridization, Genetic
Hypoxia
In Vitro Techniques
Losartan
Rats
Rats, Inbred BN
Rats, Inbred Dahl
Renin
Vasodilation
Vasodilator Agents