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Effect of High Salt Diet on Response of Rat Mesenteric Resistance Arteries to Angiotensin (1‐7)
Author(s) -
Raffai Gabor,
Lombard Julian H.
Publication year - 2009
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.23.1_supplement.952.1
Subject(s) - myograph , endocrinology , medicine , vasodilation , mesenteric arteries , angiotensin ii , chemistry , acetylcholine , nitric oxide synthase , nitric oxide , bradykinin , renin–angiotensin system , endothelium , vasoactive intestinal peptide , receptor , artery , blood pressure , neuropeptide
This study determined the vasoactive effects of acetylcholine (ACh) and angiotensin 1‐7 (ANG 1‐7) on isolated mesenteric resistance arteries (100‐300 μm) from male Sprague‐Dawley rats fed either normal salt (NS, 0.4% NaCl) or high salt (HS, 4% NaCl) diet, with water ad libitum . Diameter changes from pretreatment control (Δ μm) were recorded in NE‐pre‐constricted vessels maintained at 75 mmHg in a tissue culture myograph system. Dilation (Δ μm) to ACh was suppressed in HS (19±14 μm) vs. NS (44±4 μm) vessels, while ANG 1‐7 dilated arteries from rats fed HS diet (32±6 μm) but not NS diet (‐1±7 μm). ANG (1‐7) dilations were abolished by the mas ‐receptor antagonist d‐Ala‐angiotensin (1‐7) (7±7 μm) and endothelium removal (1±10 μm). Inhibition of nitric oxide synthase with L‐NAME (4±5 μm) and cyclooxygenase inhibition with indomethacin (11±7 μm) also inhibited vasodilator responses to ANG (1‐7) in HS vessels. These results indicate that ANG (1‐7) causes endothelium dependent vasodilation via the mas receptor in rats fed HS diet, but not during NS diet. (NIH #HL‐65289 and #HL‐72920).