title: Sodium metabolism and hypertension: how are they linked?
abstract: Some of the critical links between sodium metabolism and vascular smooth muscle (VSM) contraction have been examined in an effort to explain the role of sodium in the etiology of hypertension. We found that the Na electrochemical gradient across the sarcolemma plays a critical role in the control of contractility in rat aorta and bovine tail artery. Reducing external Na and/or increasing internal Na increases vascular reactivity to norepinephrine (NE), to K and (in rat aorta) to caffeine, and slows relaxation; marked reduction in the Na gradient induces contraction. These effects appear to be the results of Ca movements mediated by Na/Ca exchange. Studies with Ca channel blockers and with alpha-adrenoceptor antagonists (except when NE was used) indicate that these effects cannot be attributed to Ca entry through Ca channels or to release of endogenous alpha-agonists. There is increasing evidence that individuals with essential hypertension have kidneys with an impaired ability to excrete Na. The retained Na (Cl) and attendant (slight) volume expansion may be compensated by the secretion of a (natriuretic) hormone which inhibits Na pumps. Inhibition of the Na pump in kidney tubules would be expected to induce a natriuresis (and net negative Na balance). Inhibition of the Na pump in VSM should increase intracellular Na, and thus enhance contractility via Na/Ca exchange. These mechanisms may explain the increased vascular reactivity and vascular tone that are the hallmark of essential hypertension and many other types of hypertension. The direct natriuretic action of the hormone, as well as the pressure natriuresis that results from its action on VSM, may help to protect these hypertensive individuals against the tendency to extracellular fluid volume expansion at the expense of the elevated blood pressure.
mesh_terms: D000818:Animals; D001810:Blood Volume; D002118:Calcium / Q000378:metabolism / Q000494:pharmacology; D002316:Cardiotonic Agents / Q000037:antagonists & inhibitors; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000139:chemically induced / Q000188:drug therapy / Q000378:metabolism*; D007473:Ion Channels / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D045283:Natriuretic Agents / Q000502:physiology; D012964:Sodium / Q000378:metabolism*; D012965:Sodium Chloride / Q000378:metabolism; D013327:Strophanthidin / Q000494:pharmacology; D014661:Vasoconstriction / Q000187:drug effects
chemical_list: D002316:Cardiotonic Agents; D007473:Ion Channels; D045283:Natriuretic Agents; D012965:Sodium Chloride; D013327:Strophanthidin; D012964:Sodium; D002118:Calcium