title: [Sodium ion inhibits angiogenesis of cultured rat aortic and coronary rings].
abstract: High sodium intake is associated with the development of cardiac hypertrophy in man and rats independently of the rise of blood pressure. In addition, the reduced capillary density observed in striated muscle of rats fed a high salt diet suggests that angiogenesis is altered. The aim of the present experiments was to investigate the angiogenic capacities of vascular rings isolated from the aorta and the coronary artery of rats. Vascular rings (external diameter of 1 669 +/- 9 and 323 +/- 26 microm for aorta and coronary artery. respectively) are cultured in a three-dimensional collagen type I lattice and a standard medium (DMEM+HAMF12) containing 152 mM of sodium. Sodium ion associated with chloride or citrate is added to the standard medium to achieve a final concentration of sodium of 160 and 176 mM. The role of sodium-proton exchanger is evaluated through the addition of amiloride to the culture medium. Sprouts formed from vascular explants are counted every second day until days 8 to 10. Kinetics of new vessels formation and the number of sprouts were similar in aortic and coronary rings (83 +/- 5 and 95 +/- 5 sprouts, respectively). Elevation of sodium chloride concentration inhibits by 50 to 80% the neo-vessels formation in both the aorta and the coronary artery. Anti-angiogenic effect of the high sodium medium was not affected when citrate was substituted to chloride. Amiloride (3.10(-5) M) reduced the number of sprouts formed in the standard medium; however, it counteracted the anti-angiogenic effect of elevated sodium concentration. These results indicate that high extracellular concentration of sodium and not chloride anion is accompanied by a deleterious effect on angiogenic capacities of cultured aortic and coronary artery rings through modifications of trans-membrane sodium exchanges.
authors.affiliation: Groupe Rein & Hypertension, Université de Montpellier I, Institut Universitarie de Recherche Clinique.
authors.forename: H
authors.initials: H
authors.lastname: Belabbas
authors.forename: G
authors.initials: G
authors.lastname: Cayla
authors.forename: D
authors.initials: D
authors.lastname: Casellas
authors.forename: B
authors.initials: B
authors.lastname: Jover
mesh_terms: D000818:Animals; D001011:Aorta / Q000473:pathology; D003331:Coronary Vessels / Q000473:pathology*; D008297:Male; D018919:Neovascularization, Physiologic / Q000187:drug effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012964:Sodium / Q000009:adverse effects*; D015222:Sodium Channels / Q000502:physiology; D012982:Sodium, Dietary / Q000009:adverse effects
chemical_list: D015222:Sodium Channels; D012982:Sodium, Dietary; D012964:Sodium