Salt and hypertension: a phylogenetic perspective

Lev-Ran, Arye; Porta, Massimo

doi:10.1002/dmrr.539

Cited by 36 publications

(33 citation statements)

References 102 publications

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“…Of note, numerous epidemiological and experimental studies have demonstrated a link between dietary salt intake and hypertension (9). Interestingly, there is now emerging evidence that salt can directly influence immune cell function.…”

Section: Introductionmentioning

confidence: 99%

A salt-sensing kinase in T lymphocytes, SGK1, drives hypertension and hypertensive end-organ damage

et al. 2017

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Section: Introductionmentioning

confidence: 99%

A salt-sensing kinase in T lymphocytes, SGK1, drives hypertension and hypertensive end-organ damage

et al. 2017

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“…In the context of our evolutionary history, the addition of large quantities of salt to the diet is a recent phenomenon (approximately the last 5000 years). It appears that evolution has rendered us best adapted to handle far less sodium than we now consume, perhaps less than one-tenth as was the case with our hunter-gatherer ancestors [7,31,33,34,38]. A strictly vegetarian diet contains about 750 mg of salt per day [34].…”

Section: Daily Sodium Requirementmentioning

confidence: 99%

Salt craving: The psychobiology of pathogenic sodium intake

Morris

Johnson

2008

Physiology & Behavior

110

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Ionic sodium, obtained from dietary sources usually in the form of sodium chloride (NaCl, common table salt) is essential to physiological function, and in humans salt is generally regarded as highly palatable. This marriage of pleasant taste and physiological utility might appear fortunate -an appealing taste helps to ensure that such a vital substance is ingested. However, the powerful mechanisms governing sodium retention and sodium balance are unfortunately best adapted for an environment in which few humans still exist. Our physiological and behavioral means for maintaining body sodium and fluid homeostasis evolved in hot climates where sources of dietary sodium were scarce. For many reasons, contemporary diets are high in salt and daily sodium intakes are excessive. High sodium consumption can have pathological consequences. Although there are a number of obstacles to limiting salt ingestion, high sodium intake, like smoking, is a modifiable behavioral risk factor for many cardiovascular diseases. This review discusses the psychobiological mechanisms that promote and maintain excessive dietary sodium intake. Of particular importance are experiencedependent processes including the sensitization of the neural systems underlying sodium appetite and the effects of sodium balance on hedonic state and mood. Accumulating evidence suggests that plasticity within the central nervous system as a result of experience with high salt intake, sodium depletion, or a chronic unresolved sodium appetite fosters enduring changes in sodium related appetitive and consummatory behaviors.

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“…Na povećani unos natrijuma bubrezi odgovaraju povećanjem krvnog pritiska u cilju povećanja filtracije u bubregu i oslobađanja natrijuma preko tubula. Genetski polimorfizam povezan sa tubulskom retencijom natrijuma uključuje određene gene, odnosno polimorfizam gena [11,12]. Tabela 1 prikazuje opisane genetske polimorfizme povezane sa esencijalnom hipertenzijom.…”

Section: Mehanizmi Esencijalne Hipertenzijeunclassified

Kidney and hypertension

Jovanović¹

2014

Biomedicinska istraž.

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Kratak sadržajHipertenzija može biti uzrok i posledica bolesti bubrega. U današnjem društvu su i hipertenzija i bolest bubrega postale epidemijske i udružene sa povećanim rizikom od kardiovaskularnih bolesti. Poslednjih dekada brojne kliničke, eksperimentalne i genetske studije pokazuju da bubreg igra važnu ulogu u esencijalnoj hipertenziji. Međutim, malo se zna o direktnom mehanizmu na koji bubreg indukuje hipertenziju ili zašto krvni pritisak raste kod bolesnika sa bolestima bubrega. U ovom radu je opisana patofiziologija esencijalne hipertenzije i njena veza sa hroničnim bolestima bubrega i kardiovaskularnim bolestima. Posebno je opisan uticaj natrijuma, renin angiotenzin aldosteron sistema, simpatikusa kao i medijatora vazokonstrikcije i vazodilatacije na razvitak hipertenzije uzrokovane bubrezima. Sem toga, opisani su i medijatori koji započinju i održavaju progresiju hroničnih bolesti bubrega kao i njihov uticaj na hipertenziju. UvodHipertenzija je uz dijabetes jedna od najčešćih bolesti današnjice i moglo bi se reći da se javlja gotovo epidemijski. Preko 65 miliona ljudi u Sjedinjenim Američkim Državama (SAD) ima hipertenziju, a svake godine se dijagnostikuje oko 2 miliona novih bolesnika [1,2]. Najčešća je esencijalna hipertenzija koja nastaje kao posledica kompleksnih interakcija multiplih sistema bez jasne etiologije i predstavlja jedan od kardiovaskularnih (KV) faktora rizika. The Seventh Report of the Joint National Committee (JNC 7) definiše dva stadijuma hipertenzije: stadijum 1 hipertenzije -sistolni krvni pritisak 140-159 mmHg i dijastolni krvni pritisak 90-99 mmHg, i stadijum 2 hipertenzije -sistolni krvni pritisak ≥ 160 mmHg i dijastolni krvni pritisak ≥ 100 mmHg [2]. Adekvatna kontrola krvnog pritiska je potrebna u cilju prevencije KV komplikacija (infarkta miokarda, srčane insuficijencije), ali i moždanog udara i bolesti bubrega. Hroničnu insuficijenciju bubrega (HIB) ima 25 miliona stanovnika u SAD, a u terminalnoj fazi insuficijencije bubrega je preko 500 000. Hipertenzija je, pored dijabetesa, vodeći uzrok HIB koja se definiše kao smanjenje izračunate jačine glomerulske filtracije (JGF) ispod 60 ml/ min/1,73 m 2 . Ovo smanjenje JGF je udruženo sa KV komplikacijama, povećanim brojem hospitalizacija, ali i povećanim mortalitetom [3]. The National Kidney Faundation KDOQI vodiči preporučuju skrining svih bolesnika sa HIB na hipertenziju. Visina krvnog pritiska kod ovih bolesnika mora biti bolje kontrolisana i njihove vrednosti moraju biti niže nego u opštoj populaciji: ispod 130/80 mmHg kod bolesnika bez proteinurije i ispod 125/75 mmHg kod bolesnika sa proteinurijom [4].Najnovijim ispitivanjima utvrđeno je da su hronične bolesti bubrega i hipertenzija dve bolesti predodređene još u detinjstvu. Podaci iz "The National Health and Nutrition Examination Survey" potvrđuju da krvni pritisak kod dece i adolescenata u SAD raste i to sa prevalencijom hipertenzije oko 4% i pre-hipertenzije oko 10% [5]. Približno 50% dece sa HIB ima hipertenziju koja uzrokuje bržu progresiju bolesti [6]. Rani znak ošte...

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Salt and hypertension: a phylogenetic perspective

Cited by 36 publications

References 102 publications

A salt-sensing kinase in T lymphocytes, SGK1, drives hypertension and hypertensive end-organ damage

A salt-sensing kinase in T lymphocytes, SGK1, drives hypertension and hypertensive end-organ damage

Salt craving: The psychobiology of pathogenic sodium intake

Kidney and hypertension

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