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The Selfish Brain And The Barker Hypothesis
SUMMARY 1. Brain sparing is a feature of intra‐uterine growth retardation (IUGR). This implies that there is a redistribution of metabolic supply so that body growth slows to a greater extent than brain growth. 2. Intra‐uterine growth retardation, as evidenced by a low birthweight for gestational ag...
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Published in: | Clinical and Experimental Pharmacology and Physiology 2001-11, Vol.28 (11), p.942-947 |
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container_title | Clinical and Experimental Pharmacology and Physiology |
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creator | Lumbers, Eugenie R Yu, Ze-Yan Gibson, Karen J |
description | SUMMARY
1. Brain sparing is a feature of intra‐uterine growth retardation (IUGR). This implies that there is a redistribution of metabolic supply so that body growth slows to a greater extent than brain growth.
2. Intra‐uterine growth retardation, as evidenced by a low birthweight for gestational age is a predisposing factor for hypertension, cardiovascular disease and diabetes mellitus in adult life.
3. In species like humans, nephrogenesis is complete before birth. In the rat, it is completed shortly after birth. In both species, it can be shown that either undernutrition or IUGR is associated with reduced nephron number.
4. It has been proposed that oligonephropathy results in hyperfiltration, which ultimately leads to glomerulosclerosis and hypertension. The renin–angiotensin system (RAS) is necessary for normal renal development and fetal renal function. In the rat, blockade of the RAS in the first weeks of life by pharmacological agents reduces glomerular number and has been shown to cause hypertension in adult life. Renal denervation reduces the activity of the fetal RAS and also causes abnormal development of the renin‐secreting cells.
5. There is tonic renal sympathetic nerve activity in the late gestation fetal sheep. The level of renal sympathetic nerve activity (RSNA) is influenced by the fetal behavioural state.
6. However, interactions between the developing kidney and the developing sympathetic nervous system are poorly understood. On the one hand, renal innervation may be important in the provision of neurotrophic factors that stimulate the development of the RAS and kidney. On the other, high levels of RSNA associated with circulating catecholamines and vasopressin may cause vasoconstriction and limit nephrogenesis. This latter effect could be a predisposing factor to adult hypertension and cardiovascular disease. |
doi_str_mv | 10.1046/j.1440-1681.2001.03554.x |
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1. Brain sparing is a feature of intra‐uterine growth retardation (IUGR). This implies that there is a redistribution of metabolic supply so that body growth slows to a greater extent than brain growth.
2. Intra‐uterine growth retardation, as evidenced by a low birthweight for gestational age is a predisposing factor for hypertension, cardiovascular disease and diabetes mellitus in adult life.
3. In species like humans, nephrogenesis is complete before birth. In the rat, it is completed shortly after birth. In both species, it can be shown that either undernutrition or IUGR is associated with reduced nephron number.
4. It has been proposed that oligonephropathy results in hyperfiltration, which ultimately leads to glomerulosclerosis and hypertension. The renin–angiotensin system (RAS) is necessary for normal renal development and fetal renal function. In the rat, blockade of the RAS in the first weeks of life by pharmacological agents reduces glomerular number and has been shown to cause hypertension in adult life. Renal denervation reduces the activity of the fetal RAS and also causes abnormal development of the renin‐secreting cells.
5. There is tonic renal sympathetic nerve activity in the late gestation fetal sheep. The level of renal sympathetic nerve activity (RSNA) is influenced by the fetal behavioural state.
6. However, interactions between the developing kidney and the developing sympathetic nervous system are poorly understood. On the one hand, renal innervation may be important in the provision of neurotrophic factors that stimulate the development of the RAS and kidney. On the other, high levels of RSNA associated with circulating catecholamines and vasopressin may cause vasoconstriction and limit nephrogenesis. This latter effect could be a predisposing factor to adult hypertension and cardiovascular disease.</description><identifier>ISSN: 0305-1870</identifier><identifier>EISSN: 1440-1681</identifier><identifier>DOI: 10.1046/j.1440-1681.2001.03554.x</identifier><identifier>PMID: 11703402</identifier><language>eng</language><publisher>Melbourne, Australia: Blackwell Science Pty</publisher><subject>Barker hypothesis ; Fetal Growth Retardation - pathology ; Fetal Growth Retardation - physiopathology ; fetus ; Humans ; Kidney - abnormalities ; Kidney - blood supply ; Kidney - growth & development ; Kidney - innervation ; Regional Blood Flow ; renal sympathetic nerves ; renin-angiotensin system ; Renin-Angiotensin System - physiology ; Sympathetic Nervous System - physiology</subject><ispartof>Clinical and Experimental Pharmacology and Physiology, 2001-11, Vol.28 (11), p.942-947</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4034-a53f7896de07e7a95444f529d425b25ed136000988e73b7837f07e7b4d53e5423</citedby><cites>FETCH-LOGICAL-c4034-a53f7896de07e7a95444f529d425b25ed136000988e73b7837f07e7b4d53e5423</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>309,310,314,776,780,785,786,23909,23910,25118,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11703402$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lumbers, Eugenie R</creatorcontrib><creatorcontrib>Yu, Ze-Yan</creatorcontrib><creatorcontrib>Gibson, Karen J</creatorcontrib><title>The Selfish Brain And The Barker Hypothesis</title><title>Clinical and Experimental Pharmacology and Physiology</title><addtitle>Clin Exp Pharmacol Physiol</addtitle><description>SUMMARY
1. Brain sparing is a feature of intra‐uterine growth retardation (IUGR). This implies that there is a redistribution of metabolic supply so that body growth slows to a greater extent than brain growth.
2. Intra‐uterine growth retardation, as evidenced by a low birthweight for gestational age is a predisposing factor for hypertension, cardiovascular disease and diabetes mellitus in adult life.
3. In species like humans, nephrogenesis is complete before birth. In the rat, it is completed shortly after birth. In both species, it can be shown that either undernutrition or IUGR is associated with reduced nephron number.
4. It has been proposed that oligonephropathy results in hyperfiltration, which ultimately leads to glomerulosclerosis and hypertension. The renin–angiotensin system (RAS) is necessary for normal renal development and fetal renal function. In the rat, blockade of the RAS in the first weeks of life by pharmacological agents reduces glomerular number and has been shown to cause hypertension in adult life. Renal denervation reduces the activity of the fetal RAS and also causes abnormal development of the renin‐secreting cells.
5. There is tonic renal sympathetic nerve activity in the late gestation fetal sheep. The level of renal sympathetic nerve activity (RSNA) is influenced by the fetal behavioural state.
6. However, interactions between the developing kidney and the developing sympathetic nervous system are poorly understood. On the one hand, renal innervation may be important in the provision of neurotrophic factors that stimulate the development of the RAS and kidney. On the other, high levels of RSNA associated with circulating catecholamines and vasopressin may cause vasoconstriction and limit nephrogenesis. This latter effect could be a predisposing factor to adult hypertension and cardiovascular disease.</description><subject>Barker hypothesis</subject><subject>Fetal Growth Retardation - pathology</subject><subject>Fetal Growth Retardation - physiopathology</subject><subject>fetus</subject><subject>Humans</subject><subject>Kidney - abnormalities</subject><subject>Kidney - blood supply</subject><subject>Kidney - growth & development</subject><subject>Kidney - innervation</subject><subject>Regional Blood Flow</subject><subject>renal sympathetic nerves</subject><subject>renin-angiotensin system</subject><subject>Renin-Angiotensin System - physiology</subject><subject>Sympathetic Nervous System - physiology</subject><issn>0305-1870</issn><issn>1440-1681</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><recordid>eNqNkMtOwzAQRS0EoqXwCygrNihh_IqTBYs29AGqChJFLK2kmagp6QO7Fe3fE5MKtqw88px7bR1CPAoBBRHeLQIqBPg0jGjAAGgAXEoR7E9I-3dxStrAQfo0UtAiF9YuAEBCyM9Ji1IFXABrk9vpHL1XrIrSzr2eScuV113lnrvtpeYDjTc6bNbbOdrSXpKzIq0sXh3PDnkb9KfJyB8_Dx-T7tifibrVTyUvVBSHOYJClcZSCFFIFueCyYxJzCkP66_EUYSKZyriqnBgJnLJUQrGO-Sm6d2Y9ecO7VYvSzvDqkpXuN5ZrRhTKgYHRg04M2trDRZ6Y8plag6agnai9EI7H9r50E6U_hGl93X0-vjGLlti_hc8mqmB-wb4Kis8_LtYJ_0XN9V5v8mXdov733ztVIeKK6nfJ0Od0OEkehpM9AP_BjDbgic</recordid><startdate>200111</startdate><enddate>200111</enddate><creator>Lumbers, Eugenie R</creator><creator>Yu, Ze-Yan</creator><creator>Gibson, Karen J</creator><general>Blackwell Science Pty</general><scope>BSCLL</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>7X8</scope></search><sort><creationdate>200111</creationdate><title>The Selfish Brain And The Barker Hypothesis</title><author>Lumbers, Eugenie R ; Yu, Ze-Yan ; Gibson, Karen J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4034-a53f7896de07e7a95444f529d425b25ed136000988e73b7837f07e7b4d53e5423</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Barker hypothesis</topic><topic>Fetal Growth Retardation - pathology</topic><topic>Fetal Growth Retardation - physiopathology</topic><topic>fetus</topic><topic>Humans</topic><topic>Kidney - abnormalities</topic><topic>Kidney - blood supply</topic><topic>Kidney - growth & development</topic><topic>Kidney - innervation</topic><topic>Regional Blood Flow</topic><topic>renal sympathetic nerves</topic><topic>renin-angiotensin system</topic><topic>Renin-Angiotensin System - physiology</topic><topic>Sympathetic Nervous System - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lumbers, Eugenie R</creatorcontrib><creatorcontrib>Yu, Ze-Yan</creatorcontrib><creatorcontrib>Gibson, Karen J</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical and Experimental Pharmacology and Physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lumbers, Eugenie R</au><au>Yu, Ze-Yan</au><au>Gibson, Karen J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Selfish Brain And The Barker Hypothesis</atitle><jtitle>Clinical and Experimental Pharmacology and Physiology</jtitle><addtitle>Clin Exp Pharmacol Physiol</addtitle><date>2001-11</date><risdate>2001</risdate><volume>28</volume><issue>11</issue><spage>942</spage><epage>947</epage><pages>942-947</pages><issn>0305-1870</issn><eissn>1440-1681</eissn><abstract>SUMMARY
1. Brain sparing is a feature of intra‐uterine growth retardation (IUGR). This implies that there is a redistribution of metabolic supply so that body growth slows to a greater extent than brain growth.
2. Intra‐uterine growth retardation, as evidenced by a low birthweight for gestational age is a predisposing factor for hypertension, cardiovascular disease and diabetes mellitus in adult life.
3. In species like humans, nephrogenesis is complete before birth. In the rat, it is completed shortly after birth. In both species, it can be shown that either undernutrition or IUGR is associated with reduced nephron number.
4. It has been proposed that oligonephropathy results in hyperfiltration, which ultimately leads to glomerulosclerosis and hypertension. The renin–angiotensin system (RAS) is necessary for normal renal development and fetal renal function. In the rat, blockade of the RAS in the first weeks of life by pharmacological agents reduces glomerular number and has been shown to cause hypertension in adult life. Renal denervation reduces the activity of the fetal RAS and also causes abnormal development of the renin‐secreting cells.
5. There is tonic renal sympathetic nerve activity in the late gestation fetal sheep. The level of renal sympathetic nerve activity (RSNA) is influenced by the fetal behavioural state.
6. However, interactions between the developing kidney and the developing sympathetic nervous system are poorly understood. On the one hand, renal innervation may be important in the provision of neurotrophic factors that stimulate the development of the RAS and kidney. On the other, high levels of RSNA associated with circulating catecholamines and vasopressin may cause vasoconstriction and limit nephrogenesis. This latter effect could be a predisposing factor to adult hypertension and cardiovascular disease.</abstract><cop>Melbourne, Australia</cop><pub>Blackwell Science Pty</pub><pmid>11703402</pmid><doi>10.1046/j.1440-1681.2001.03554.x</doi><tpages>6</tpages></addata></record> |
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subjects | Barker hypothesis Fetal Growth Retardation - pathology Fetal Growth Retardation - physiopathology fetus Humans Kidney - abnormalities Kidney - blood supply Kidney - growth & development Kidney - innervation Regional Blood Flow renal sympathetic nerves renin-angiotensin system Renin-Angiotensin System - physiology Sympathetic Nervous System - physiology |
title | The Selfish Brain And The Barker Hypothesis |
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