Blood pressure and arterial stiffness in patients with high sodium intake in relation to sodium handling and left ventricular diastolic dysfunction status

Abstract

In a population with high sodium consumption, we assessed relation between brachial and central blood pressures, elastic properties of large arteries, echocardiographic left ventricular diastolic function and sodium reabsorption as fractional urinary lithium excretion in proximal (FELi) and fractional sodium reabsorption in distal tubules assessed using the endogenous lithium clearance. Mean±s.d. age of 131 treated hypertensive patients (66 men and 65 women) was 61.9±7.5 years. We found significant interaction between left ventricular diastolic function and FELi with respect to the values of brachial blood pressure: systolic (SBP), diastolic (DBP) and mean blood pressure (MBP) (all PINT<0.03). In patients with FELi below the median value and impaired left ventricular diastolic function, the values of SBP (149.3 vs 132.5 mm Hg; P=0.005), DBP (85.1 vs 76.1 mm Hg; P=0.001), MBP (106.5 vs 94.9 mm Hg; P=0.001), central SBP (SBPC) (137.4 vs 122.0 mm Hg; P=0.01), central DBP (DBPC) (84.8 vs 76.0 mm Hg; P=0.003), central MBP (MBPC) (106.9 vs 95.9 mm Hg; P=0.007), aortic pulse wave augmentation (18.0 vs 13.5 mm Hg; P=0.03), pulse wave velocity (14.6 vs 12.5 m s(-1); P=0.02) and central aortic pulse wave augmentation index (155.7% vs 140.9%; P=0.01) were significantly higher than in patients with normal left ventricular diastolic function. Such relationships were not observed in the entire group and patients with FELi above the median value. In the hypertensive population with high sodium intake, increased sodium reabsorption in proximal tubules may affect blood pressure parameters and arterial wall damage, thus contributing to the development of left ventricular diastolic function impairment.

Increased urinary sodium excretion is associated with systolic blood pressure in first degree relatives of hypertensive patients in Ibadan, Southwestern Nigeria

“…For increased salt intake to result in permanent changes in arterial pressure, renal function must be altered [25]. An increase in salt intake would lead to an increase in blood pressure and vice-versa, increased sodium reabsorption in the proximal tubule, and damage to the vascular wall as documented in previous studies [22, 26, 27].…”

“…Consistent with this hypothesis, diminished capacity for sodium and water excretion has been observed in models of hypertension. In those who develop hypertension, the blood pressure does not return to normal, possibly due to vascular damage and diastolic dysfunction [26]. Chronic but mild hypervolemia and hypertension could be the long-term consequences of reduced sodium excretion [29], and this may explain the comparatively higher systolic blood pressure in normotensive patients with positive family history of hypertension who are at a higher risk of developing high blood pressure.…”

Arterial Stiffness, Central Pulsatile Hemodynamic Load, and Orthostatic Hypotension

“…First, patients with OH have a higher risk of heart failure with preserved ejection fraction compared with patients without OH (HR, 1.32; 95% CI, 1.07–1.48; P =.033) . Second, Cwynar and colleagues found that hypertension patients with diastolic LV dysfunction have near‐significantly higher values of CSBP than patients without diastolic LV dysfunction (135.1±20.3 mm Hg vs 127.3±19.7 mm Hg, P =.049). Third, Borlaug and colleagues showed that LV diastolic and systolic tissue velocities vary inversely with arterial afterload, with late systolic load having the greatest influence on early diastolic velocity.…”

Blood pressure, arterial stiffness and endogenous lithium clearance in relation to AGTR1 A1166C and AGTR2 G1675A gene polymorphisms

“…The study design has been described in detail elsewhere. 14 Briefly, all patients were requested to complete a standard epidemiologic questionnaire including detailed medical history, antihypertensive medications, and socioeconomic and demographic characteristics. The patients provided written informed consent to participate in the study.…”