Sodium and obesity in the pathogenesis of hypertension.
In the present work I focus on the pathophysiological mechanisms that may explain the association between high sodium intake, obesity and high blood pressure. Despite epidemiological and etiological controversies on the link between excess sodium in the diet and elevated arterial pressure, the association could be explained on the basis of three different pathophysiological mechanisms: (1) abnormal electrolyte transport across cell membranes, a defect that alters sodium/potassium exchange and also sodium/calcium exchanges, increasing the concentration of intracellular calcium ions that heightens vessel wall tension and the smooth muscle process, (2) increased sympathetic nervous system activity and (3) altered cellular sodium concentration that induces waterlogging in the peripheral arteriolar walls. These mechanisms increase peripheral resistance and enhance arterial pressure. Early epidemiological studies documented a strong association between obesity and hypertension; and a greater incidence of high blood pressure and diabetes was reported in persons with upper body obesity (high waist/hip ratio). Researchers have explained obesity-related hypertension accordingly with various mechanisms. Hyperinsulinemia and vascular resistance may trigger the metabolic and adrenergic changes described in obese hypertensive patients in several ways. Insulin may increase absorption of sodium in the diluting segment of the distal nephron with consequent water retention. Alternatively, insulin might alter sodium/potassium distribution thus causing increased vascular peripheral resistance. The increased sodium stimulates adrenergic activity. The water retention in obese subjects increases absolute volume that is predominantly redistributed in the cardiopulmonary area, leading to augmented venous return and cardiac output. These changes in association with a total peripheral resistance considered inappropriately normal, are the main hemodynamic characteristics of obesity-related hypertension.
Reisin
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Department of Medicine, Louisiana State University, New Orleans 70112.
D001794:Blood Pressure; D001810:Blood Volume; D004573:Electrolytes / Q000378:metabolism; D006439:Hemodynamics; D006801:Humans; D006946:Hyperinsulinism / Q000150:complications / Q000503:physiopathology; D006973:Hypertension / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D007333:Insulin Resistance; D009765:Obesity / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D012084:Renin-Angiotensin System; D012964:Sodium / Q000378:metabolism; D012982:Sodium, Dietary / Q000009:adverse effects*; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D013564:Sympathetic Nervous System / Q000503:physiopathology; D014655:Vascular Resistance
D004573:Electrolytes; D012982:Sodium, Dietary; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase