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Arteriolar responses to vasodilator stimuli and elevated P(O2) in renin congenic and Dahl salt-sensitive rats. Microcirculation 2004 Dec;11(8):669-77 PMID: 15726834

Abstract

OBJECTIVES: Angiotensin II suppression leads to impaired vascular relaxation in normotensive animals on a high-salt diet. The goal of this study was to determine whether normal vascular reactivity could be restored by transferring the chromosomal region carrying the Dahl salt-resistant (R) renin gene into the Dahl salt-sensitive (SS) genetic background in a strain of renin congenic rats (RGRR).

METHODS: Male RGRR and SS rats were fed low-salt (0.4%) and high-salt (4%) diets for 4 weeks. The responses of cremaster muscle arterioles to acetylcholine (ACh), sodium nitroprusside (SNP), and elevated PO2 were assessed using video microscopy.

RESULTS: ACh-induced dilation was significantly enhanced in RGRR on a high-salt diet compared to SS rats, while dilation to the NO donor SNP was similar in both strains. A high-salt diet significantly enhanced arteriolar constriction in response to elevated PO2, in both SS and RGRR rats.

CONCLUSIONS: These data suggest that transfer of the chromosomal region containing the renin gene is crucial in the recovery of ACh-induced dilation of arterioles in RGRR rats vs. SS rats, and that factors in the SS genetic background contribute to an enhanced sensitivity to elevated PO2, independent of genes on chromosome 13.

Author List

Drenjancevic-Peric I, Greene AS, Kunert MP, Lombard JH

Authors

Andrew S. Greene PhD Interim Vice Chair, Chief, Professor in the Biomedical Engineering department at Medical College of Wisconsin
Julian H. Lombard PhD Professor in the Physiology department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Animals
Arterioles
Chromosomes, Mammalian
Male
Microscopy, Video
Muscles
Oxygen
Rats
Rats, Inbred Dahl
Renin
Renin-Angiotensin System
Sodium Chloride
Transgenes
Vasoconstriction
Vasodilation
Vasodilator Agents



View this publication's entry at the Pubmed website PMID: 15726834
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