title: Effects of normal pregnancy on cellular cation metabolism and peripheral vascular resistance.
abstract: Normal pregnancy is associated with a poorly understood loss of vascular responsiveness to the pressor effects of infused angiotensin II. Since cellular cation metabolism appears to be a critical determinant of basal vascular tone and vascular reactivity, we have evaluated platelet ionized calcium, erythrocyte sodium, calcium and magnesium levels, and erythrocyte Ca-ATPase and Na/K ATPase activity in 15 normal black pregnant women (37.5 +/- 0.6 weeks gestation) and 10 normal age-matched nonpregnant black women. Plasma levels of factors potentially affecting vascular reactivity (endoxin, renin activity (PRA), and atrial natriuretic peptide (ANP] were measured by RIA and peripheral vascular resistance by biolectrical impedance. Peripheral vascular resistance was almost twice as high (P less than .003) in the normal group as in the pregnant women. Intracellular calcium concentrations were not significantly different in erythrocytes or platelets of the two groups. Although erythrocyte membrane Ca-ATPase was similar, Na/K ATPase activity was significantly higher in the pregnant subjects than in the nonpregnant controls, and intracellular sodium was lower. All three measured plasma factors, ANP, endoxin and PRA, were significantly elevated in the pregnant women. Our results suggest that the decrease in peripheral vascular resistance seen in normal pregnancy is probably not the result of alterations in cellular cation concentrations and/or cell membrane pump activity. However, the significant correlation between vascular reactivity and circulating ANP indicates this potent vasodilator may play a role in the observed decrease in peripheral vascular resistance associated with pregnancy.
authors.affiliation: Department of Internal Medicine, Wayne State University School of Medicine, Detroit, MI 48201.
authors.forename: J R
authors.initials: JR
authors.lastname: Sowers
authors.forename: M B
authors.initials: MB
authors.lastname: Zemel
authors.forename: M F
authors.initials: MF
authors.lastname: Walsh
authors.forename: P R
authors.initials: PR
authors.lastname: Standley
authors.forename: P C
authors.initials: PC
authors.lastname: Zemel
authors.forename: R A
authors.initials: RA
authors.lastname: Bronsteen
authors.forename: J
authors.initials: J
authors.lastname: Kraniak
authors.forename: R J
authors.initials: RJ
authors.lastname: Sokol
mesh_terms: D000328:Adult; D009320:Atrial Natriuretic Factor / Q000097:blood; D044383:Black People; D001794:Blood Pressure; D001798:Blood Proteins / Q000032:analysis; D017301:Ca(2+) Mg(2+)-ATPase / Q000097:blood; D000252:Calcium-Transporting ATPases / Q000097:blood; D002298:Cardenolides; D016022:Case-Control Studies; D004077:Digoxin; D004573:Electrolytes / Q000097:blood* / Q000378:metabolism; D005260:Female; D006801:Humans; D007474:Ion Exchange; D011247:Pregnancy / Q000502:physiology*; D012083:Renin / Q000097:blood; D012503:Saponins; D000254:Sodium-Potassium-Exchanging ATPase / Q000097:blood; D014655:Vascular Resistance
chemical_list: D001798:Blood Proteins; D002298:Cardenolides; D004573:Electrolytes; D012503:Saponins; C034504:digoxin-like factors; D004077:Digoxin; D009320:Atrial Natriuretic Factor; D012083:Renin; D017301:Ca(2+) Mg(2+)-ATPase; D000252:Calcium-Transporting ATPases; D000254:Sodium-Potassium-Exchanging ATPase