Faculty Collaboration Database

High-salt diet impairs hypoxia-induced cAMP production and hyperpolarization in rat skeletal muscle arteries. Am J Physiol Heart Circ Physiol 2001 Oct;281(4):H1808-15

Date

09/15/2001

Pubmed ID

11557575

DOI

10.1152/ajpheart.2001.281.4.H1808

Scopus ID

2-s2.0-0034786042 (requires institutional sign-in at Scopus site)   35 Citations

Abstract

This study determined the effects of hypoxia on diameter, vascular smooth muscle (VSM) transmembrane potential (E(m)), and vascular cAMP levels for in vitro cannulated skeletal muscle resistance arteries (gracilis arteries) from Sprague-Dawley rats fed a low-salt (LS) or a high-salt (HS) diet. Arterial diameter and VSM E(m) were measured in response to hypoxia, iloprost, cholera toxin, forskolin, and aprikalim. In HS rats, arterial dilation and VSM hyperpolarization after hypoxia, iloprost, and cholera toxin were impaired versus responses in LS rats, whereas responses to forskolin and aprikalim were unaltered. Blockade of prostaglandin H(2) and thromboxane A(2) receptors had no effect on responses to hypoxia or iloprost in vessels from both rat groups, suggesting that inappropriate activation of these receptors does not contribute to the impaired hypoxic dilation with HS. Hypoxia, cholera toxin, and iloprost increased vascular cAMP levels in vessels of LS rats only, whereas forskolin increased cAMP levels in all vessels. These data suggest that reduced hypoxic dilation of skeletal muscle microvessels in rats on a HS diet may reflect an impaired ability of VSM to produce cAMP after exposure to prostacyclin.

Author List

Frisbee JC, Sylvester FA, Lombard JH

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

Animals
Arteries
Cyclic AMP
Diet, Sodium-Restricted
Electrophysiology
Hypoxia
Male
Muscle, Skeletal
Rats
Rats, Sprague-Dawley
Vascular Resistance
Vasodilation
Vasodilator Agents