塩と血圧の関係をしらべたパート２
Nutrients 2019, 11(9), 1970; https://doi.org/10.3390/nu11091970
Review
Sodium Intake and Hypertension
：よく分からなかったのでもう1本読んでみた。
Increased salt consumption may provoke water retention, thus leading to a condition of high flow in arterial vessels. The mechanism of pressure natriuresis has been proposed as a physiologic phenomenon where an increase in BP in the renal arteries causes increased salt and water excretion [10]. This hemodynamic load, as studies with animal models have shown [11,12], may lead to an adverse microvascular remodeling by the effects of increased BP levels.
：Na摂取→血管内volume増加→腎動脈血流増加→RAA系抑制→Na排泄亢進。うん。
●Naが低いことについて
High sodium intake and increased BP levels are linked by changes in vascular resistances, but the mechanisms controlling this phenomenon may not be only viewed as a reflex pressor response aimed at increasing sodium excretion. Excessive salt intake may induce several adverse effects, causing microvascular endothelial inflammation, anatomic remodeling, and functional abnormalities, even in normotensive subjects [13]. More recent studies have shown that changes in sodium plasma levels do not only exert their effects on small resistance arteries, but may also affect the function and structure of large elastic arteries.
Actually, in the analysis of this topic, several cohort studies [16,17,18] and meta-analyses [19,20] have shown that the relationship between sodium intake and poor patient prognosis have not a linear trend, but rather describe a J-shape curve.
：今日の一番びっくり。Jカーブ！
Mente et al. [19] reported that only patients with arterial hypertension have a high cardiovascular risk associated with high sodium intake, while this association was not confirmed in patients without hypertension [19].
：Na食べて心血管リスク上がるひとは、高血圧の人だけ。血圧高くない人はNaたべても心血管リスク上がらない。･･･うん、でも、Na食べたら血圧あがるのでは？
In experimental models, it is known that sodium restriction results in increased atherosclerosis [21]. In humans, the relationship between salt restriction and increased renin-angiotensin-aldosterone system activation has been described [22,23], as well as the relationship with increased sympathetic activity [24] and insulin resistance [25,26,27].
●Naが高いことについて
Nearly half a century ago, Guyton and Coleman proposed that whenever arterial pressure is elevated, the pressure natriuresis mechanism enhances the excretion of sodium and water until blood volume is reduced adequately in order to return BP to normal values [31]. According to this premise, hypertension may occur only when the ability of the kidney of excreting sodium is impaired.
：そうなのでした。
Recent studies have highlighted the genetic and metabolic background of salt-sensitivity, a phenomenon with remarkable variability among human subjects [33], as well as among animal models [42]. A number of genetic, hormonal, and neuro-endocrine factors are involved in the salt-sensitivity of BP [43]. The sympathetic nervous system, the renin-angiotensin-aldosterone system, natriuretic peptides, insulin, leptin, and several endothelial mediators with endocrine activity may modify BP response to salt [15].
：でしょうね。
Recent clinical research has highlighted that salt-sensitive and salt-resistant patients do not show any difference in circulating volumes, cardiac output, or sodium balance after salt loading [53]. This may be explained by non-osmolar storage of sodium, without considering the effect on water retention.
：salt-sensitiveな人もそうでない人も、Na負荷しても体液量そんなに変わらない→水以外(浸透圧以外)のNaのため方がある？？
Evidence has accumulated showing that impairment in vascular function may play a relevant role in salt-sensitive hypertension. In fact, abnormal responses of vascular resistance in the renal circulation are present after salt intake in salt-sensitive individuals, without an increase in sodium retention or cardiac output [46,54]. After acute or chronic increases in salt intake, salt-sensitive patients are not subject to an increase in sodium storage and do not increase the cardiac output, when compared to normal controls [55]. Then, the increase in BP induced by salt may be mediated by abnormalities in the vascular response to salt, in particular in peripheral and renal resistances, along with changes in sodium balance and in cardiac output [56].
：BP上昇が体液量にかかわってないってことは、血管がおかしいのでは。特に末梢の血管とか腎血管とか。
●Naと交感神経
Therefore, an increased dietary salt supply can induce a reflex reduction of sympathetic efferent activity if reflex cardiovascular regulation is physiologically preserved, activating cardiopulmonary receptors through an increase in plasma volume [63].
In conclusion, the increased BP associated with excessive sodium intake observed in hypertensive patients, characterized by high salt-sensitivity, may be due to the impairment of their baroreflex function or to their inability to increase baroreflex sensitivity and reduce sympathetic activity in response to the increase in plasma volume, determined by sodium loading.
●Naと血管障害
In experimental animal studies, salt intake was associated with microvascular rarefaction in normotensive and hypertensive rats, resulting from structural alterations and differing from the degenerative processes observed in experimental animals with chronic hypertension that are characterized by microvascular rarefaction [69]. Moreover, apart from microvessel rarefaction, a reduced arterial vasodilator capacity developed with high-salt diet has also been described in rats with hypertension induced by a reduced renal mass, which and was restored with low-salt diet [70]. Additional vascular effects of a high sodium intake include the potentiation of local vasoconstrictive effectors, such as alterations of endothelial Ca2+ signaling [71] or an abnormal high production of 20-hydroxyeicosatetraenoic acid [72].
：いろいろ。Na摂ると、血管が菲薄化したり、拡張できなくなっちゃったりする。
Impaired vasodilatation of the small vessels has been shown to occur in conditions of high salt intake [74]. In young, healthy normotensives, salt loading impaired vascular endothelial function along with left ventricular mechanical relaxation [75]. These results were confirmed in normotensive adults, where sodium-induced impairments in microvascular function were observed. The microvascular function was improved by the administration of the anti-oxidant ascorbic acid, suggesting a role of oxidative stress in this process [76].
：内皮がダメになっちゃう。アスコルビン酸とかの抗酸化物質でよくなる。へー。
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ここまで下書きに書いて2週間。
残りを読む気配を自分に感じないので、ここらで一旦シワにする。はい。
