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Obesity-hypertension: the effects on cardiovascular and renal systems
Longitudinal and cross-sectional studies suggest that a large number of obese patients have a high prevalence of hypertension. This association causes the following changes: insulin and leptin resistance with a suppressed biologic activity of natriuretic peptide, which contributes to sodium retentio...
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Published in: | American Journal of Hypertension 2000-12, Vol.13 (12), p.1308-1314 |
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container_title | American Journal of Hypertension |
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description | Longitudinal and cross-sectional studies suggest that a large number of obese patients have a high prevalence of hypertension. This association causes the following changes: insulin and leptin resistance with a suppressed biologic activity of natriuretic peptide, which contributes to sodium retention with concomitant expanded cardiopulmonary volume and increased cardiac output. The cellular metabolism of cations may be altered in obesity and may lead to changes in vascular responsiveness and increased vascular resistance. These changes lead to structural adaptations in the heart characterized by concentric–eccentric left ventricular hypertrophy. The hypertrophic condition provides the basis for the development of congestive heart failure and cardiac arrhythmias that may explain the higher rates of cardiac sudden death in those patients. In the kidneys, obesity hypertension may initiate a derangement of renal function. The increased deposit of interstitial cells and of extracellular matrix between the tubules induces higher interstitial hydrostatic pressure and tubular sodium reabsorption. The consequent increase in renal flow and glomerular filtration enhances albuminuria excretion and the susceptibility to the development of renal damage. In summary, the hemodynamic and structural adaptations related to obesity hypertension is the cause of greater risk for adverse cardiovascular and renal events. |
doi_str_mv | 10.1016/S0895-7061(00)01254-1 |
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This association causes the following changes: insulin and leptin resistance with a suppressed biologic activity of natriuretic peptide, which contributes to sodium retention with concomitant expanded cardiopulmonary volume and increased cardiac output. The cellular metabolism of cations may be altered in obesity and may lead to changes in vascular responsiveness and increased vascular resistance. These changes lead to structural adaptations in the heart characterized by concentric–eccentric left ventricular hypertrophy. The hypertrophic condition provides the basis for the development of congestive heart failure and cardiac arrhythmias that may explain the higher rates of cardiac sudden death in those patients. In the kidneys, obesity hypertension may initiate a derangement of renal function. The increased deposit of interstitial cells and of extracellular matrix between the tubules induces higher interstitial hydrostatic pressure and tubular sodium reabsorption. 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The consequent increase in renal flow and glomerular filtration enhances albuminuria excretion and the susceptibility to the development of renal damage. In summary, the hemodynamic and structural adaptations related to obesity hypertension is the cause of greater risk for adverse cardiovascular and renal events.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>blood pressure</subject><subject>cardiovascular disease</subject><subject>Cardiovascular System - drug effects</subject><subject>Cardiovascular System - physiopathology</subject><subject>Humans</subject><subject>Hypertension - complications</subject><subject>Hypertension - physiopathology</subject><subject>Kidney - drug effects</subject><subject>Kidney - pathology</subject><subject>Kidney - physiopathology</subject><subject>Leptin - pharmacology</subject><subject>Leptin - physiology</subject><subject>Medical sciences</subject><subject>Metabolic diseases</subject><subject>Natriuretic Agents - physiology</subject><subject>Obesity</subject><subject>Obesity - complications</subject><subject>Obesity - pathology</subject><subject>Obesity - physiopathology</subject><subject>renal hemodynamics</subject><issn>0895-7061</issn><issn>1879-1905</issn><issn>1941-7225</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><recordid>eNqFkVFr1TAUx4Mo7m76EZSCMPQh86RpktYXkW3eCdMJUxBfQpqessze5i5ph_fbm66XqxPBp7z8_v9z8juEPGNwxIDJ15dQVoIqkOwlwCtguSgoe0AWrFQVZRWIh2SxQ_bIfozXAFBIyR6TPcYYB6Xkgpxe1BjdsKFXmzWGAfvofP8mG64ww7ZFO8TM95k1oXH-1kQ7diZkpm-ygL3psriJA67iE_KoNV3Ep9v3gHx9f_rl-IyeXyw_HL87p1ZUYqAtV3XdcMklGitRmEIBcFOJqgAQqlamsVKJqmYW6rZIdCvEtAaayjZQ8gNyOPeug78ZMQ565aLFrjM9-jFqlQtWlBwS-OIv8NqPIW0cNYNcSshVWSRKzJQNPsaArV4HtzJhkyA9WdZ3lvWkUAPoO8uapdzzbftYr7D5ndpq_WN8Uma6NpjeurjjSlayfKqBmfLj-t-T6b3JdIrQOeKS95-7kAk_tFRcCX327bsuP39c8k_LS32S-Lczj-kqtw6DjtZhb7FxIR1XN97956-_AIUbtTs</recordid><startdate>20001201</startdate><enddate>20001201</enddate><creator>Zhang, Rubin</creator><creator>Reisin, Efrain</creator><general>Elsevier Inc</general><general>Oxford University Press</general><general>Elsevier Science</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope></search><sort><creationdate>20001201</creationdate><title>Obesity-hypertension: the effects on cardiovascular and renal systems</title><author>Zhang, Rubin ; 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This association causes the following changes: insulin and leptin resistance with a suppressed biologic activity of natriuretic peptide, which contributes to sodium retention with concomitant expanded cardiopulmonary volume and increased cardiac output. The cellular metabolism of cations may be altered in obesity and may lead to changes in vascular responsiveness and increased vascular resistance. These changes lead to structural adaptations in the heart characterized by concentric–eccentric left ventricular hypertrophy. The hypertrophic condition provides the basis for the development of congestive heart failure and cardiac arrhythmias that may explain the higher rates of cardiac sudden death in those patients. In the kidneys, obesity hypertension may initiate a derangement of renal function. The increased deposit of interstitial cells and of extracellular matrix between the tubules induces higher interstitial hydrostatic pressure and tubular sodium reabsorption. 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source | Oxford Journals Online |
subjects | Animals Biological and medical sciences blood pressure cardiovascular disease Cardiovascular System - drug effects Cardiovascular System - physiopathology Humans Hypertension - complications Hypertension - physiopathology Kidney - drug effects Kidney - pathology Kidney - physiopathology Leptin - pharmacology Leptin - physiology Medical sciences Metabolic diseases Natriuretic Agents - physiology Obesity Obesity - complications Obesity - pathology Obesity - physiopathology renal hemodynamics |
title | Obesity-hypertension: the effects on cardiovascular and renal systems |
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