High-salt diet impairs vascular relaxation mechanisms in rat middle cerebral arteries. Am J Physiol Heart Circ Physiol 2003 Apr;284(4):H1124-33
Date
11/29/2002Pubmed ID
12456391DOI
10.1152/ajpheart.00835.2002Scopus ID
2-s2.0-0037378395 (requires institutional sign-in at Scopus site) 63 CitationsAbstract
Male Sprague-Dawley rats were maintained on a low-salt (LS) diet (0.4% NaCl) or a high-salt (HS) diet (4% NaCl) for 3 days or 4 wk. PO(2) reduction to 40-45 mmHg, the stable prostacyclin analog iloprost (10 pg/ml), and stimulatory G protein activation with cholera toxin (1 ng/ml) caused vascular smooth muscle (VSM) hyperpolarization, increased cAMP production, and dilation in cerebral arteries from rats on a LS diet. Arteries from rats on a HS diet exhibited VSM depolarization and constriction in response to hypoxia and iloprost, failed to dilate or hyperpolarize in response to cholera toxin, and cAMP production did not increase in response to hypoxia, iloprost, or cholera toxin. Low-dose angiotensin II infusion (5 ng x kg(-1) x min(-1) i.v.) restored normal responses to reduced PO(2) and iloprost in arteries from animals on a HS diet. These observations suggest that angiotensin II suppression with a HS diet leads to impaired relaxation of cerebral arteries in response to vasodilator stimuli acting at the cell membrane.
Author List
Lombard JH, Sylvester FA, Phillips SA, Frisbee JCMESH terms used to index this publication - Major topics in bold
Angiotensin IIAnimals
Cell Membrane
Cholera Toxin
Colforsin
Cyclic AMP
GTP-Binding Protein alpha Subunits, Gs
Iloprost
Male
Middle Cerebral Artery
Muscle, Smooth, Vascular
Oxygen
Picolines
Prostaglandins F
Pyrans
Rats
Rats, Sprague-Dawley
Sodium Chloride, Dietary
Thromboxane B2
Vasodilation
Vasodilator Agents
