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Introgression of chromosome 13 in Dahl salt-sensitive genetic background restores cerebral vascular relaxation

Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226

Submitted 23 February 2003 ; accepted in final form 11 March 2004

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 (PO₂ 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 AT₁ 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.

hypertension; vascular smooth muscle; renin-angiotensin system; physiological genomics

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