Premium
Afferent arteriolar responses to endothelin‐1 are attenuated by a high salt diet
Author(s) -
Schneider Markus Peter,
Inscho Edward W,
Pollock David M
Publication year - 2006
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.20.4.a758-b
Subject(s) - afferent arterioles , endocrinology , medicine , chemistry , afferent , blood pressure , endothelin receptor , nephron , vascular resistance , endothelin 1 , norepinephrine , kidney , angiotensin ii , receptor , dopamine
Background Endothelin‐1 (ET‐1) is a strong vasoconstrictor of afferent arterioles, and ET‐1 expression increases during a high salt (HS) diet. However, the responsiveness of these vessels to ET‐1 during a HS diet has not been examined. Methods Sprague‐Dawley rats (300–350 gm) were fed either normal salt chow (NS, 0.66% NaCl) or HS (8%) for one week. Systolic blood pressure (SBP) was determined before and during HS by tail cuff plethysmography. Afferent arteriolar responsiveness was determined using the in vitro blood perfused juxtamedullary nephron technique. Kidneys were superfused with increasing concentrations of either ET‐1 (10 −12 to 10 −8 M) or norepinephrine (NE) (10 −8 to 10 −6 M). Each concentration was superfused for 5 minutes and measurements of vascular diameters were averaged from the last two minutes of each period. Results SBP was similar between NS and HS groups and averaged 111±5 mmHg and 110±5 mmHg, respectively. Baseline afferent arteriolar diameter was similar between the NS and HS groups: 18.5±1.5 and 17.6±2.9 μm, respectively. Afferent arteriolar responses to ET‐1 were significantly attenuated in rats fed a HS diet, resulting in a rightward shift of the concentration‐response relationship (figure). In contrast, vasoconstrictor responses to NE were not altered in rats fed a HS diet. Conclusion The response of afferent arterioles to ET‐1 is attenuated by HS. Reduced arteriolar responses to ET‐1 could lead to reduced preglomerular resistance, facilitatingsodium excretion. Supported by the DFG (SCHN 769/1‐1, M.P.S.) and the NIH: HL74167 (E.I.W., D.M.P.), HL64776 (D.M.P.), DK44628 (E.I.W.).