The Volhard lecture. Potassium and sodium in hypertension.
For the first 98.5% of mankind's existence, prehistoric people all ate low-sodium high-potassium, low-fat diets. With evolutionary forces working all this while, humans became very well adapted to the low-sodium, high-potassium, low-fat diet. In modern times, man has deserted his ancient cuisine and now favours a high-sodium, low-potassium, high-fat diet, which has produced several 'diseases of civilization', including hypertension. Many studies indicate that a 'normal'-potassium diet encourages arterial thickening and lesions in hypertensive arteries and kidneys, whereas a high-potassium diet can prevent many of these arterial and renal lesions, even though the blood pressure remains equally hypertensive. The high-potassium diet also tends to retard the development of hypertension. In susceptible people and rats, a high-NaCl diet leads to hypertension. This susceptibility is probably brought about by kidneys that have a sluggish sodium excretion in response to a NaCl load. This type of kidney combined with a high-NaCl diet tends to produce NaCl retention. Evidence is presented that this NaCl signal may be perceived by structures in the wall of the third brain ventricle. In susceptible men or rats, this can lead to a hypertensive rise in blood pressure, which over time can become partially irreversible, even though a low-NaCl diet is reinstituted.
Tobian
L
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University of Minnesota Hospital, Minneapolis 55455.
D000818:Animals; D002561:Cerebrovascular Disorders / Q000209:etiology; D004032:Diet; D004730:Endothelium, Vascular / Q000187:drug effects / Q000473:pathology; D005110:Extracellular Space / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000473:pathology / Q000503:physiopathology* / Q000517:prevention & control; D011188:Potassium / Q000494:pharmacology / Q000502:physiology*; D051381:Rats; D011922:Rats, Mutant Strains / Q000502:physiology; D012964:Sodium / Q000494:pharmacology / Q000502:physiology*
D012964:Sodium; D011188:Potassium