Possible mechanisms of sodium-dependent hypertension: volume expansion or vasoconstriction?
A series of experiments was designed to explore the mechanisms contributing to hypertension caused by an acute or chronic sodium load. Acute salt-loading in totally or subtotally nephrectomized animals caused hypertension mediated partly through stimulation of excessive vasopressin release and partly through adrenergic stimulation. Chronic high-salt diet in rats submitted to partial nephrectomy, mineralocorticoid excess or one-kidney-one-clip renovascular hypertension caused blood pressure elevation mediated through a central neurogenic mechanism that could be reversed by administration of an inhibitor of phenylethanolamine-N-methyltransferase, the enzyme catalyzing conversion of norepinephrine to epinephrine. Thus, two vasopressor mechanisms were stimulated by sodium excess: an acute, transient, partly vasopressin-mediated phase seemed to be followed by a chronic phase mediated through stimulation of central sympathetic neurons. In neither phase was blood pressure related to intravascular fluid volume expansion.
D000821:Animal Feed; D000818:Animals; D004039:Diet, Sodium-Restricted; D006973:Hypertension / Q000139:chemically induced*; D009392:Nephrectomy; D010625:Phenylethanolamine N-Methyltransferase / Q000378:metabolism; D010953:Plasma Volume; D051381:Rats; D012964:Sodium / Q000009:adverse effects*; D013564:Sympathetic Nervous System / Q000502:physiology*; D014667:Vasopressins / Q000502:physiology*
D014667:Vasopressins; D012964:Sodium; D010625:Phenylethanolamine N-Methyltransferase