Myocardial Na, K-ATPase in one-kidney, one-clip hypertensive rats
Myocardial ventricular Na, K-ATPase activity of normotensive rats was compared with that of healthy rats with chronic benign one-kidney, one-clip hypertension. The yield of protein (mg/g wet wt left plus right ventricles) in microsomal and sarcolemmal membrane fractions was the same for both normote...
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Published in | Journal of molecular and cellular cardiology Vol. 18; no. 10; pp. 1085 - 1095 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
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England
Elsevier Ltd
01.10.1986
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Abstract | Myocardial ventricular Na, K-ATPase activity of normotensive rats was compared with that of healthy rats with chronic benign one-kidney, one-clip hypertension. The yield of protein (mg/g wet wt left plus right ventricles) in microsomal and sarcolemmal membrane fractions was the same for both normotensive and hypertensive rat ventricles. However, the yield of protein (mg/ventricle) was 26% greater in the hypertensive relative to the normotensive animals, consistent with the presence of hypertrophy, as also indicated by an increase in the ratio of ventricular to body weight and a shift in the isomyosin composition. Na, K-ATPase activity, sodium-dependent phosphorylation and ouabain binding were significantly (
P<0.05) decreased (by 20%, 40%, and 45%, respectively) in the hypertensive rat ventricles when the data were expressed in units/g tissue wet weight. However, when expressed in units per ventricle, values in normotensive and hypertensive animals were similar. The molecular activity or turnover number of ventricular (and also renal) Na, K-ATPase activity was the same in both groups of animals. These results suggest that the decrease in myocardial specific Na, K-ATPase activity in the rat made hypertensive by removing one kidney and constricting the renal artery of the other kidney is related to the presence of cardiac hypertrophy. |
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AbstractList | Myocardial ventricular Na, K-ATPase activity of normotensive rats was compared with that of healthy rats with chronic benign one-kidney, one-clip hypertension. The yield of protein (mg/g wet wt left plus right ventricles) in microsomal and sarcolemmal membrane fractions was the same for both normotensive and hypertensive rat ventricles. However, the yield of protein (mg/ventricle) was 26% greater in the hypertensive relative to the normotensive animals, consistent with the presence of hypertrophy, as also indicated by an increase in the ratio of ventricular to body weight and a shift in the isomyosin composition. Na, K-ATPase activity, sodium-dependent phosphorylation and ouabain binding were significantly (P less than 0.05) decreased (by 20%, 40%, and 45%, respectively) in the hypertensive rat ventricles when the data were expressed in units/g tissue wet weight. However, when expressed in units per ventricle, values in normotensive and hypertensive animals were similar. The molecular activity or turnover number of ventricular (and also renal) Na, K-ATPase activity was the same in both groups of animals. These results suggest that the decrease in myocardial specific Na, K-ATPase activity in the rat made hypertensive by removing one kidney and constricting the renal artery of the other kidney is related to the presence of cardiac hypertrophy. Myocardial ventricular Na, K-ATPase activity of normotensive rats was compared with that of healthy rats with chronic benign one-kidney, one-clip hypertension. The yield of protein in microsomal and sarcolemmal membrane fractions was the same for both normotensive and hypertensive rat ventricles. However, the yield of protein was greater in the hypertensive relative to the normotensive animals. Na, K-ATPase activity, sodium-dependent phosphorylation and ouabain binding were significantly decreased in the hypertensive rat ventricles when the data were expressed in units/g tissue wet weight. The molecular activity or turnover number of ventricular (and also renal) Na, K-ATPase activity was the same in both groups of animals. The results suggest that the decrease in myocardial specific Na, K-ATPase activity in the rat made hypertensive by removing one kidney and constricting the renal artery of the other kidney is related to the presence of cardiac hypertrophy. Myocardial ventricular Na, K-ATPase activity of normotensive rats was compared with that of healthy rats with chronic benign one-kidney, one-clip hypertension. The yield of protein (mg/g wet wt left plus right ventricles) in microsomal and sarcolemmal membrane fractions was the same for both normotensive and hypertensive rat ventricles. However, the yield of protein (mg/ventricle) was 26% greater in the hypertensive relative to the normotensive animals, consistent with the presence of hypertrophy, as also indicated by an increase in the ratio of ventricular to body weight and a shift in the isomyosin composition. Na, K-ATPase activity, sodium-dependent phosphorylation and ouabain binding were significantly ( P<0.05) decreased (by 20%, 40%, and 45%, respectively) in the hypertensive rat ventricles when the data were expressed in units/g tissue wet weight. However, when expressed in units per ventricle, values in normotensive and hypertensive animals were similar. The molecular activity or turnover number of ventricular (and also renal) Na, K-ATPase activity was the same in both groups of animals. These results suggest that the decrease in myocardial specific Na, K-ATPase activity in the rat made hypertensive by removing one kidney and constricting the renal artery of the other kidney is related to the presence of cardiac hypertrophy. |
Author | Schwartz, A. Whitmer, K.R. Martin, A.F. Lane, L.K. Wallick, E.T. Lee, S.W. Overbeck, H.W. Lee, J.H. |
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Keywords | Hypertension K-ATPase Sodium pump Na Hypertrophy |
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References | Lowry, Rosebrough, Farr, Randall (bib11) 1951; 193 Hoh, McGrath, Hale (bib8) 1977; 10 Akera, Yamamoto, Temma, Kim, Brody (bib3) 1981; 640 Haddy, Pamnani (bib7) 1983; 42 Martin, Pagani, Solaro (bib12) 1982; 50 Khatter, Hoeschen (bib9) 1984; 79 Haddy, Overbeck (bib6) 1976; 19 Silver, Houser (bib18) 1985; 37 Lee, Schwartz, Adams, Yamori, Whitmer, Lane, Wallick (bib10) 1983; 5 Schwartz, Allen, Harigaya (bib17) 1969; 168 Yazaki, Fujii (bib21) 1972; 13 Anversa, Loud, Giacomelli, Wiener (bib1) 1978; 38 Clough, Pamnani, Haddy (bib4) 1983; 245 Mercadier, Lompre, Wisnewsky, Samuel, Bercovici, Swynghedauw, Schwartz (bib13) 1981; 49 Rupp (bib16) 1981; 76 Wallick, Anner, Ray, Schwartz (bib20) 1978; 253 Folkow (bib5) 1982; 62 Akera, Cheng (bib2) 1977; 470 Van Alstyne, Burch, Knickelbein, Hungerford, Gower, Webb, Poe, Lindenmayer (bib19) 1980; 602 Overbeck, Pamnani, Akera, Brody, Haddy (bib14) 1976; 38 Overbeck, Gressette (bib15) 1982; 4 |
References_xml | – volume: 602 start-page: 131 year: 1980 end-page: 143 ident: bib19 article-title: Isolation of sealed vesicles highly enriched with sarcolemma markers from canine ventricles publication-title: Biochim Biophys Acta contributor: fullname: Lindenmayer – volume: 76 start-page: 79 year: 1981 end-page: 88 ident: bib16 article-title: The adaptive changes in the isoenzyme pattern of myosin from hypertrophied rat myocardium as a result of pressure overload and physical training publication-title: Basic Res Cardiol contributor: fullname: Rupp – volume: 38 start-page: 597 year: 1978 end-page: 609 ident: bib1 article-title: Absolute morphometric study of myocardial hypertrophy in experimental hypertension II. Ultrastructure of myocytes and interstitium publication-title: Lab Invest contributor: fullname: Wiener – volume: 19 start-page: 935 year: 1976 end-page: 948 ident: bib6 article-title: The role of humoral agents in volume-expanded hypertension publication-title: Life Sci contributor: fullname: Overbeck – volume: 50 start-page: 117 year: 1982 end-page: 124 ident: bib12 article-title: Thyroxine-induced redistribution of isoenzymes of rabbit ventricular myosin publication-title: Circ Res contributor: fullname: Solaro – volume: 62 start-page: 347 year: 1982 end-page: 504 ident: bib5 article-title: Physiological aspects of primary hypertension publication-title: Physiol Rev contributor: fullname: Folkow – volume: 38 start-page: 48 year: 1976 end-page: 52 ident: bib14 article-title: Depressed function of a ouabain-sensitive sodium-potassium pump in blood vessels from renal hypertensive dogs publication-title: Circ Res contributor: fullname: Haddy – volume: 640 start-page: 779 year: 1981 end-page: 790 ident: bib3 article-title: Is ouabain-sensitive rubidium or potassium uptake a measure of sodium pump activity in isolated cardiac muscle publication-title: Biochim Biophys Acta contributor: fullname: Brody – volume: 470 start-page: 412 year: 1977 end-page: 423 ident: bib2 article-title: A simple method for the determination of affinity and binding site concentration in receptor binding studies publication-title: Biochim Biophys Acta contributor: fullname: Cheng – volume: 10 start-page: 1053 year: 1977 end-page: 1076 ident: bib8 article-title: Electrophoretic analysis of multiple forms of rat cardiac myosin: Effects of hypophysectomy and thyroxine replacement publication-title: J Mol Cell Carbiol contributor: fullname: Hale – volume: 168 start-page: 31 year: 1969 end-page: 41 ident: bib17 article-title: Possible involvement of cardiac Na publication-title: J Pharmacol Exp Ther contributor: fullname: Harigaya – volume: 37 start-page: 607 year: 1985 end-page: 615 ident: bib18 article-title: Decreased sodium-potassium pump activity in isolated hypertrophied feline ventricular myocytes publication-title: Life Sci contributor: fullname: Houser – volume: 13 start-page: 73 year: 1972 end-page: 83 ident: bib21 article-title: Depressed Na, K-ATPase activity in the failing rabbit heart publication-title: Jpn Heart J contributor: fullname: Fujii – volume: 79 start-page: 396 year: 1984 end-page: 410 ident: bib9 article-title: Reduced number of digitalis receptor sites in the hypertrophied pig myocardium publication-title: Basic Res Cardiol contributor: fullname: Hoeschen – volume: 193 start-page: 265 year: 1951 end-page: 275 ident: bib11 article-title: Protein measurement with the Folin phenol reagent publication-title: J Biol Chem contributor: fullname: Randall – volume: 42 start-page: 2673 year: 1983 end-page: 2680 ident: bib7 article-title: The role of a humoral sodium-potassium pump inhibitor in low-renin hypertension publication-title: Fed Proc contributor: fullname: Pamnani – volume: 49 start-page: 525 year: 1981 end-page: 532 ident: bib13 article-title: Myosin isoenzymic changes in several models of rat cardiac hypertrophy publication-title: Circ Res contributor: fullname: Schwartz – volume: 4 start-page: 132 year: 1982 end-page: 139 ident: bib15 article-title: Sodium pump activity in arteries of rats with Goldblatt hypertension publication-title: Hypertension contributor: fullname: Gressette – volume: 245 start-page: H244 year: 1983 end-page: H251 ident: bib4 article-title: Decreased myocardial Na publication-title: Am J Physiol contributor: fullname: Haddy – volume: 5 start-page: 682 year: 1983 end-page: 688 ident: bib10 article-title: Decrease in Na publication-title: Hypertension contributor: fullname: Wallick – volume: 253 start-page: 8778 year: 1978 end-page: 8786 ident: bib20 article-title: Effect of temperature on phosphorylation and ouabain binding to N-ethylmaleimide treated Na, K-ATPase publication-title: J Biol Chem contributor: fullname: Schwartz |
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SubjectTerms | adenosinetriphosphatase Animals Cardiomegaly - enzymology Hypertension Hypertension, Renal - enzymology Hypertrophy K-ATPase Kidney - enzymology Kidney - ultrastructure Male Microsomes - enzymology myocardium Myocardium - enzymology Ouabain - metabolism Phosphorylation Rats Rats, Inbred Strains Sarcolemma - enzymology Sodium pump Sodium-Potassium-Exchanging ATPase - metabolism |
Title | Myocardial Na, K-ATPase in one-kidney, one-clip hypertensive rats |
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