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Restoration of Vascular Relaxation in Cerebral Arteries of Congenic Dahl Rats Receiving the Brown Norway (BN) Renin Gene
Author(s) -
Durand Matthew J.,
MorenoQuinn Carol,
Lombard Julian H.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1142.5
Subject(s) - congenic , endocrinology , medicine , renin–angiotensin system , vasodilation , dilator , acetylcholine , biology , gene , blood pressure , genetics
The Dahl Salt Sensitive (SS) rat exhibits impaired regulation of the renin‐angiotensin system (RAS), chronically low levels of angiotensin II, and impaired vascular relaxation in response to vasodilator stimuli. This impaired vascular relaxation is likely due to chronic exposure of the animals to low levels of ANG II. The present study investigates responses to vasodilator stimuli in two different congenic strains in which a portion of the BN chromosome 13 was inserted onto the SS genetic background. Congenic strain SS.BN‐(D13rat88‐D13rat105) contains a 2.9 Mbp portion of chromosome 13 which excludes the BN renin gene, and would not be expected to restore normal regulation of the RAS. Congenic strain SS.BN‐(D13hmgc41‐D13hmgc23) contains a 2.0 Mbp adjacent region that includes the BN renin gene, which should restore normal ANG II levels in animals fed low salt (LS) diet. Males from each congenic strain were fed a LS diet (0.4% NaCl) after weaning. At the age of 10–14 weeks, middle cerebral arteries (MCA) were isolated and cannulated and dilator responses to acetylcholine (10 −10 M–10 −5 M) and reduced PO 2 were assessed using television microscopy. MCA from the congenic strain containing the BN allele for renin dilated in response to acetylcholine and reduced PO 2 while the MCA from the congenic strain containing the SS renin allele did not. These results suggest that the presence of a normally functioning renin gene from the BN rat in the SS genetic background restores normal vasodilator responses in the MCA. [NIH #HL‐29587; #HL‐65289, and #HL‐72920].