Rodríguez CFE

Language: Spanish
References: 11
Page: 161-163
PDF size: 71.71 Kb.

ABSTRACT

Individuals with elevated blood pressure are at increased risk for cardiovascular events and death. Almost 50% of essential hypertension is salt-sensitive, this characteristic increases and becomes more prevalent with age. Salt sensitivity has been linked to an increased risk for the development of left ventricular hypertrophy, proteinuria, and a blunted nocturnal decline in blood pressure (“non-dipping”). Salt sensitivity implies an alteration in the relation between arterial pressure and sodium excretion or “pressure natriuresis”. The development of salt-sensitive hypertension is proposed to occur in three phases. In the first phase, the kidney is structurally normal, and sodium is excreted normally. However, the kidney may be exposed to various stimuli that result in renal vasoconstriction. In the second phase, subtle renal injury develops, impairing sodium excretion and leading to an increase in blood pressure. In the third phase, the kidneys equilibrate at a higher blood pressure, allowing them to resume normal sodium handling. Other mechanisms, such as primary tubulointerstitial disease, genetic alterations in sodium regulation and excretion, or a congenital reduction in nephron number that limits sodium filtration are important in the development of salt-sensitive hypertension.

REFERENCES

1. WEINBERGER MH, FINEBERG NS, FINEBERG SE, WEINBERGER M: Salt Sensitivity, Pulse Pressure, and Death in Normal and Hypertensive Humans. Hypertension 2001; 37[part 2]: 429-432.

2. WEINBERGER MH: Salt sensitivity of blood pressure in humans. Hypertension 1996; 27(pt 2): 481-490.

3. HERRERA JA: Hipertensión arterial dependiente de sal. Arch Cardiol Mex 2001; 71 Supl. 1: S76-S80.

4. JOHNSON R, HERRERA JA, SCHREINER G, RODRÍGUEZ BI: Subtle Acquired Renal Injury As A Mechanism Of Salt-Sensitive Hypertension. N Engl J Med 2002; 346: 913-923.

5. ARDILES LG, FIGUEROA CD, MEZZANO SA: Renal kallikrein-kinin system damage and salt sensitivity: Insights from experimental models. Kidney Int 2003; 64: S2-S8.

6. ZEWDE T, MATTSON DL: Inhibition of Cyclooxygenase-2 in the Rat Renal Medulla Leads to Sodium-Sensitive Hypertension. Hypertension 2004; 44: 424-428.

7. RODRIGUEZ F, LINAS MT, GONZALEZ JD, RIVERA J, SALAZAR FJ: Renal changes induced by a cyclooxygenase-2 inhibitor during normal and low sodium intake. Hypertension. 2000; 36: 276-281.

8. BEIERWALTES WH: COX-2 products compensate for inhibition of nitric oxide regulation of renal perfusion. Am J Physiol 2002; 283: F68-F72.

9. GRO ML, AMANN K, RITZ E: Nephron Number and Renal Risk in Hypertension and Diabetes. J Am Soc Nephrol 2005; 16: S27-S29.

10. WOODS LL, WEEKS DA, RASCH R: Programming of adult blood pressure by maternal protein restriction: Role of nephrogenesis. Kidney Int 2004; 65: 1339-1348.

11. FROHLICH ED AND VARAGIC J: Sodium directly impairs target organ function in hypertension. Curr Opin Cardiol 2005; 20: 424-429.