title: Effect of cilazapril and salt on Ca2+ extrusion in arterial smooth muscle of Dahl rats.
abstract: We examined effects of salt and cilazapril on the Ca pump and Na/Ca exchange system in arterial smooth muscle of Dahl salt-sensitive (DS) rats. Twenty-four DS rats were assigned to four groups. H and H+ rats were fed a high salt diet; L- and L+ rats were fed a low salt diet. H+ and L+ were administered cilazapril. Aortic rings were superfused with physiologic saline and isometric tension was measured. Relaxation of low Na+-induced contraction was promoted by the removal of external Ca. Cilazapril significantly decreased blood pressure in both the high and low salt diet groups. The inhibition of renin-angiotensin system by cilazapril showed that Ca extrusion by ATP-driven Ca pump was decreased by salt loading, and that Ca extrusion by Na/Ca exchange was increased by salt loading. There was a negative correlation between Ca extrusion by Ca pump and blood pressure, and a positive correlation between Ca extrusion by Na/Ca exchange and blood pressure. These results suggest that the decrease of Ca2+ extrusion by ATP-driven Ca pump resulting from a high salt diet might lead to an elevation in the concentration of cellular Ca2+ and contribute to the mechanism of hypertension in DS rats, and that Ca2+ extrusion by the Na/Ca exchange might be increased in compensation for an increase in cellular Ca2+ concentration on the high salt diet.
authors.affiliation: Division of Cardiovascular Diseases, The Institute for Adult Diseases, Asahi Life Foundation, Shinjuku, Tokyo, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Ashida
authors.forename: H
authors.initials: H
authors.lastname: Yoshimi
authors.forename: Y
authors.initials: Y
authors.lastname: Kawano
authors.forename: H
authors.initials: H
authors.lastname: Matsuoka
authors.forename: T
authors.initials: T
authors.lastname: Omae
mesh_terms: D000255:Adenosine Triphosphate / Q000502:physiology; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology*; D001158:Arteries / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism*; D000252:Calcium-Transporting ATPases / Q000378:metabolism; D002352:Carrier Proteins / Q000378:metabolism; D017315:Cilazapril / Q000494:pharmacology*; D004351:Drug Resistance / Q000235:genetics; D006973:Hypertension / Q000139:chemically induced* / Q000235:genetics* / Q000378:metabolism; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains / Q000235:genetics; D012965:Sodium Chloride / Q000494:pharmacology*; D019831:Sodium-Calcium Exchanger
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D002352:Carrier Proteins; D019831:Sodium-Calcium Exchanger; D017315:Cilazapril; D012965:Sodium Chloride; D000255:Adenosine Triphosphate; D000252:Calcium-Transporting ATPases; D002118:Calcium