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    "titulo" => "Genetic predisposition for essential hypertension&#44; based on studies of genetic polymorphisms in modern global human populations&#58; The perspective of evolutionary biology"
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">The article by Sousa et al&#46; in this issue of the <span class="elsevierStyleItalic">Journal</span><a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">1</span></a> raises several interesting questions related to the association of the C825T polymorphism of the <span class="elsevierStyleItalic">GNB3</span> gene&#44; which codes for the beta 3 subunit of G proteins &#40;responsible for the transduction of messages resulting from activation of G protein-coupled receptors&#41;&#44; with hypertension and cardiovascular risk&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">The first question concerns differences in susceptibility to essential hypertension in modern human populations that result from the natural selection of genes over the last 30<span class="elsevierStyleHsp" style=""></span>000 years associated with environmental factors during the global expansion of humanity after ancestral populations left Africa&#44; as described in an important article by Young et al&#46;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">2</span></a> The factors acting at that time were temperature and humidity&#44; inversely related to latitude in Africa&#44; which activated compensatory adaptive hypertensive mechanisms secondary to decreased volume-dependent blood pressure associated with severe loss of sodium chloride by sweating&#46; Young et al&#46;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">2</span></a> identified several polymorphic variants of five genes encoding proteins involved in these compensatory mechanisms of volume change and vascular reactivity secondary to salt loss&#46; The genetic variant most strongly associated with current global variation in susceptibility to hypertension is the C825T polymorphism of the <span class="elsevierStyleItalic">GNB3</span> gene&#46; The frequency distribution of genetic variants associated with adaptive mechanisms&#44; especially the one analyzed by Sousa et al&#46;&#44; is independent of the continent where they occur&#44; as shown by the similarity of their distribution in Native Americans of the equatorial zones to that of modern African populations&#46; We performed a study<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">3</span></a> of the Hp1 polymorphic variant &#40;only found in humans&#41; of haptoglobin&#44; an acute phase protein that for more than 30 years has been associated with higher blood pressure sensitivity to sodium&#46; In this work we found very similar allelic frequencies of the <span class="elsevierStyleItalic">HP</span> gene in Honduras &#40;Central America&#41; and in Mozambique &#40;Africa&#41;&#46; These countries are at similar latitudes&#44; although in the case of Native American populations the adaptations occurred over the course of less than 20<span class="elsevierStyleHsp" style=""></span>000 years&#46; This is the result of movements in Eurasia&#44; in the opposite direction &#40;north to south&#41; to the initial movement subsequent to the departure from Africa of the original populations in which these gene variants were initially fixed&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">With regard to the same Hp allele&#44; we published a paper in the <span class="elsevierStyleItalic">Journal</span> in 2000&#44;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">4</span></a> the results of which showed a different nocturnal blood pressure response in salt-sensitive hypertensive individuals&#44; compared to normotensive and non-sensitive individuals&#44; after a change of diet from low to high sodium&#46; The Hp1-1 allele was found in 100&#37; of both normotensive and hypertensive salt-sensitive subjects&#46; In this study we also showed that in urban settings in modern African populations&#44; these individuals have increased cardiovascular risk&#44; even compared to those in the current African diaspora&#44; which confirms the epidemiological transition of these populations with respect to the original ones 50 years ago&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">As further evidence of the effect of these ancestral gene variants&#44; the work by Sousa et al&#46; shows that the risk for obesity conferred by the 825T allele of the <span class="elsevierStyleItalic">GNB3</span> gene in Madeira&#44; also demonstrated in other populations&#44; is associated with a higher risk of essential hypertension&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">5</span></a> The frequency of this morbid allele is higher in hypertensive patients than in controls in the population of the Madeira archipelago&#44; in contrast to those found in a larger population &#40;the PHYSA study&#41; on the mainland&#46;<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">6&#44;7</span></a> Regardless of the differences in sampling methods between these two studies&#44; the explanation for the association of this variant with hypertension on this Portuguese island&#44; which is not observed on the mainland&#44; probably lies in the fact that the Madeira population is a genetic isolate in which the effect of stratification of these genes is likely to be maximized&#44; despite its common ethnic origins with mainland populations&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">8</span></a></p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0025" class="elsevierStylePara elsevierViewall">The author has no conflicts of interest to declare&#46;</p></span></span>"
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Genetic predisposition for essential hypertension, based on studies of genetic polymorphisms in modern global human populations: The perspective of evolutionary biology
Perspetivas de biologia evolutiva da predisposição genética para hipertensão arterial essencial, estudada com base em polimorfismos genéticos nas atuais populações humanas globais
Manuel Bicho
Laboratório de Genética e Instituto de Saúde Ambiental (ISAMB) da Faculdade de Medicina da Universidade de Lisboa, Lisboa, Portugal
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    "titulo" => "Genetic predisposition for essential hypertension&#44; based on studies of genetic polymorphisms in modern global human populations&#58; The perspective of evolutionary biology"
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        "titulo" => "Perspetivas de biologia evolutiva da predisposi&#231;&#227;o gen&#233;tica para hipertens&#227;o arterial essencial&#44; estudada com base em polimorfismos gen&#233;ticos nas atuais popula&#231;&#245;es humanas globais"
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">The article by Sousa et al&#46; in this issue of the <span class="elsevierStyleItalic">Journal</span><a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">1</span></a> raises several interesting questions related to the association of the C825T polymorphism of the <span class="elsevierStyleItalic">GNB3</span> gene&#44; which codes for the beta 3 subunit of G proteins &#40;responsible for the transduction of messages resulting from activation of G protein-coupled receptors&#41;&#44; with hypertension and cardiovascular risk&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">The first question concerns differences in susceptibility to essential hypertension in modern human populations that result from the natural selection of genes over the last 30<span class="elsevierStyleHsp" style=""></span>000 years associated with environmental factors during the global expansion of humanity after ancestral populations left Africa&#44; as described in an important article by Young et al&#46;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">2</span></a> The factors acting at that time were temperature and humidity&#44; inversely related to latitude in Africa&#44; which activated compensatory adaptive hypertensive mechanisms secondary to decreased volume-dependent blood pressure associated with severe loss of sodium chloride by sweating&#46; Young et al&#46;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">2</span></a> identified several polymorphic variants of five genes encoding proteins involved in these compensatory mechanisms of volume change and vascular reactivity secondary to salt loss&#46; The genetic variant most strongly associated with current global variation in susceptibility to hypertension is the C825T polymorphism of the <span class="elsevierStyleItalic">GNB3</span> gene&#46; The frequency distribution of genetic variants associated with adaptive mechanisms&#44; especially the one analyzed by Sousa et al&#46;&#44; is independent of the continent where they occur&#44; as shown by the similarity of their distribution in Native Americans of the equatorial zones to that of modern African populations&#46; We performed a study<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">3</span></a> of the Hp1 polymorphic variant &#40;only found in humans&#41; of haptoglobin&#44; an acute phase protein that for more than 30 years has been associated with higher blood pressure sensitivity to sodium&#46; In this work we found very similar allelic frequencies of the <span class="elsevierStyleItalic">HP</span> gene in Honduras &#40;Central America&#41; and in Mozambique &#40;Africa&#41;&#46; These countries are at similar latitudes&#44; although in the case of Native American populations the adaptations occurred over the course of less than 20<span class="elsevierStyleHsp" style=""></span>000 years&#46; This is the result of movements in Eurasia&#44; in the opposite direction &#40;north to south&#41; to the initial movement subsequent to the departure from Africa of the original populations in which these gene variants were initially fixed&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">With regard to the same Hp allele&#44; we published a paper in the <span class="elsevierStyleItalic">Journal</span> in 2000&#44;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">4</span></a> the results of which showed a different nocturnal blood pressure response in salt-sensitive hypertensive individuals&#44; compared to normotensive and non-sensitive individuals&#44; after a change of diet from low to high sodium&#46; The Hp1-1 allele was found in 100&#37; of both normotensive and hypertensive salt-sensitive subjects&#46; In this study we also showed that in urban settings in modern African populations&#44; these individuals have increased cardiovascular risk&#44; even compared to those in the current African diaspora&#44; which confirms the epidemiological transition of these populations with respect to the original ones 50 years ago&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">As further evidence of the effect of these ancestral gene variants&#44; the work by Sousa et al&#46; shows that the risk for obesity conferred by the 825T allele of the <span class="elsevierStyleItalic">GNB3</span> gene in Madeira&#44; also demonstrated in other populations&#44; is associated with a higher risk of essential hypertension&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">5</span></a> The frequency of this morbid allele is higher in hypertensive patients than in controls in the population of the Madeira archipelago&#44; in contrast to those found in a larger population &#40;the PHYSA study&#41; on the mainland&#46;<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">6&#44;7</span></a> Regardless of the differences in sampling methods between these two studies&#44; the explanation for the association of this variant with hypertension on this Portuguese island&#44; which is not observed on the mainland&#44; probably lies in the fact that the Madeira population is a genetic isolate in which the effect of stratification of these genes is likely to be maximized&#44; despite its common ethnic origins with mainland populations&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">8</span></a></p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0025" class="elsevierStylePara elsevierViewall">The author has no conflicts of interest to declare&#46;</p></span></span>"
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Revista Portuguesa de Cardiologia (English edition)
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