[Sodium chloride and hypertension (an additional, temporary hypothesis)].
Around the turn of the century it was observed that low dietary salt consumption is frequently associated with reduction in blood pressure in essential hypertension. It has not been established whether this is a specific effect of NaCl or whether it is an unspecific consequence of the weight loss frequently accompanying low salt intake. Changes of the Renin-Angiotension-Aldosterone system do not seem overly important for the understanding of the original lesion in essential hypertension. Hemodynamic studies demonstrate that increased peripheral (arterial) resistance is characteristic for the disease. It was possible to breed a rat strain with an "anlage" for hypertension which could be unmasked by salt supplements. In humans, essential hypertension is associated with increased salt preference suggesting a genetic factor. This increased desire for salt induces a high salt content of the body including the arterial wall. The hypothesis is being discussed that the stimulating effect of NaCl leads to contraction of the arterial wall inducing increased peripheral resistance - the hallmark of essential hypertension.
D000450:Aldosterone; D000809:Angiotensins / Q000502:physiology; D000818:Animals; D001835:Body Weight; D004039:Diet, Sodium-Restricted; D004195:Disease Models, Animal; D006801:Humans; D006973:Hypertension / Q000178:diet therapy / Q000503:physiopathology*; D051381:Rats; D012083:Renin / Q000502:physiology
D000809:Angiotensins; D000450:Aldosterone; D012083:Renin
Kochsalz und Hypertonie. (Eine weitere, vorläufige Hypothese).