Sodium in blood vessels. A brief review.
Extracellular Na can be accurately partitioned into free and bound components; the latter component is directly related to the hydration and stiffness of the vascular wall. Cell Na can be similarly partitioned: [Na+]i is about 10mM and the transmembrane gradient about 15:1 in a physiological medium. The transmembrane gradient remains constant over a wide range of change in [Na+]0. Although active Na transport is largely responsible for developing the transmembrane ion distribution pattern, the membrane potential depends mainly on movements of K+ and C1-. No certain direct role can be assigned to Na+ in short-term vasoconstriction, but an indirect role through the regulation of catecholamine release and uptake is now established. There is evidence that the entry of Na+ into cells plays a fundamental role in the protein-synthesizing activity of the vascular smooth muscle cell and is thereby involved in the longer term determination of peripheral vascular resistance.
D000818:Animals; D001808:Blood Vessels / Q000166:cytology / Q000378:metabolism / Q000502:physiology*; D006801:Humans; D006973:Hypertension / Q000503:physiopathology; D008564:Membrane Potentials; D009119:Muscle Contraction; D009129:Muscle Tonus; D009130:Muscle, Smooth / Q000166:cytology / Q000378:metabolism / Q000502:physiology; D014176:Protein Biosynthesis; D012964:Sodium / Q000378:metabolism / Q000502:physiology*; D014655:Vascular Resistance; D014661:Vasoconstriction
D012964:Sodium