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Sodium ions, calcium ions, blood pressure regulation, and hypertension: a reassessment and a hypothesis

American Journal of Physiology-Cell Physiology · 1977 · Vol. 232(5) · pp. C165–C173

Abstract

An attempt is made to elucidate the cellular mechanisms which may account for the well-documented correlation between sodium metabolism and peripheral vascular resistance. As a starting point, the evidence that the Na electrochemical gradient across the vascular smooth muscle cell plasma membrane (sarcolemma) plays an important role in cell calcium regulation is reviewed. Because there is significant resting tension ("tone") in most resistance vessels, the ionized Ca2+ level ([Ca2+]1) in the smooth muscle fibers in these vessels must be maintained above the contraction threshold. Consequently, the Ca transport system in the sarcolemma, presumably an Na-Ca exchange mechanism, must be set so as to hold [Ca2+]1 at this suprathreshold level. Any change in the Na gradient will then be reflected as a change in [Ca2+]1 and, therefore, in steady vessel wall tension and peripheral resistance. The correlation between Na metabolism and hypertension could then be accounted for if a circulating agent, perhaps the "natriuretic hormone," affects the Na gradient (across the sarcolemma) and, therefore, [Ca2+]1 and tension.

Ion channel regulation and functionElectrochemical sensors and biosensorsNitric Oxide and Endothelin EffectsSarcolemmaCalciumSodiumChemistryBiophysicsVascular smooth muscleEndocrinologyInternal medicineContraction (grammar)Calcium metabolism

MeSH terms

AnimalsBiological TransportBlood PressureBlood VesselsCalciumHumansHypertensionMuscle ContractionMuscle, SmoothSarcolemmaSarcoplasmic ReticulumSodiumVascular Resistance
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