The kidney in the pathogenesis of hypertension: the role of sodium.
In this review, we first summarize the evidence which indicates that the inability of the kidney to excrete salt and water normally, particularly when combined with increased salt intake, is frequently associated with hypertension. We then concentrate on the link between sodium and water retention and hypertension. The increase in blood pressure probably results from the increase in volume rather than from the increase in salt. Recent evidence suggests that an increase in volume in the lesser circulation stimulates the release of a sodium pump inhibitor, probably the putative natriuretic hormone, from the hypothalamus. This agent appears to affect cardiac and vascular smooth muscle by suppressing Na+,K+-ATPase, and hence Na+-K+ pump activity in both muscle cells and adrenergic nerve terminals. The sodium pump inhibitor is a heat stable small molecule but its chemical structure is still unknown. It is clearly different from atrial natriuretic factor. We conclude the review with speculations on the possible role of renotropin and various growth and growth inhibitory factors in the vascular structural changes.
Haddy
F J
FJ
Pamnani
M B
MB
D000251:Adenosine Triphosphatases / Q000378:metabolism / Q000502:physiology; D000328:Adult; D000818:Animals; D004039:Diet, Sodium-Restricted; D006321:Heart / Q000503:physiopathology; D006801:Humans; D006977:Hypertension, Renal / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D007031:Hypothalamus / Q000378:metabolism / Q000503:physiopathology; D007473:Ion Channels / Q000502:physiology; D007668:Kidney / Q000378:metabolism / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism; D009318:Natriuresis; D011188:Potassium / Q000378:metabolism / Q000502:physiology; D051381:Rats; D012964:Sodium / Q000378:metabolism / Q000502:physiology*; D014883:Water-Electrolyte Imbalance
D007473:Ion Channels; D012964:Sodium; D000251:Adenosine Triphosphatases; D011188:Potassium