Left Ventricular Hypertrophy Is More Marked in Salt-Sensitive Than in Salt-Resistant Hypertensive Patients

Heimann, Joel Cláudio; Drumond, Soraia; Tadeu, Artur; Alves, Rodrigues; Julio, Alfonso; Barbato, Guedes; Dichtchekenian, Varujan; Marcondes, M

doi:10.1097/00005344-199117002-00028

Cited by 41 publications

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“…SS hypertensive patients have a higher incidence of left ventricular hypertrophy, 19,20 endothelial dysfunction, 21 hyperlipidemia, 22,23 and microalbuminuria [22][23][24] compared with salt-resistant hypertensive patients. In addition, an association between insulin resistance and SS in nondiabetic, nonobese, essential hypertensive subjects has been reported.…”

Section: Discussionmentioning

confidence: 99%

Surgical Menopause Increases Salt Sensitivity of Blood Pressure

et al. 2006

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Abstract-Salt sensitivity of blood pressure is associated with an elevated risk of developing hypertension (HTN) and is an independent risk factor for cardiovascular disease. The prevalence of HTN increases after menopause. The aim of this study was to investigate prospectively whether the loss of ovarian hormones increases the occurrence of salt sensitivity among healthy premenopausal women. We enrolled 40 normotensive, nondiabetic women (age 47.2Ϯ3.5), undergoing hysterectomy-oophorectomy for nonneoplastic processes and not on hormone replacement, to determine the effect of changes in sodium intake on blood pressure the day before and subsequently 4 months after surgical menopause. Salt loading was achieved using a 2-L normal saline infusion and salt depletion produced by 40 mg of intravenous furosemide. A decrease Ͼ10 mm Hg in systolic blood pressure between salt loading and salt depletion was used to define salt sensitivity. Before and after menopause, salt-sensitive women exhibited higher waist/hip and waist/thigh ratios (PϽ0.01). Although all of the women remained normotensive, the prevalence of salt sensitivity was significantly higher after surgical menopause (21 women; 52.5%) than before (9 women; 22.5%; Pϭ0.01), because 12 (38.7%) salt-resistant women developed salt sensitivity after menopause. In summary, we demonstrated that the prevalence of salt sensitivity doubled as early as 4 months after surgical menopause, without an associated increase in blood pressure. Epidemiological studies indicate that development of HTN may not occur until 5 to 10 years after menopause. The loss of ovarian hormones may unmask a population of women prone to salt sensitivity who, with aging, would be at higher risk for the subsequent development of HTN and cardiovascular disease.

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Section: Discussionmentioning

confidence: 99%

Surgical Menopause Increases Salt Sensitivity of Blood Pressure

et al. 2006

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“…However, Na þ sensitivity has been linked to a number of metabolic and physiologic abnormalities such as albumin excretion, 16,17 left ventricular hypertrophy 18,19 and dyslipidaemia. 20 In a crosssectional study in Japanese hypertensives, cardiovascular events were found to be twice as common among Na þ sensitive hypertensives as among Na þ resistant hypertensives.…”

Section: Discussionmentioning

confidence: 99%

Effect of aerobic exercise training on blood pressure sensitivity to dietary sodium in older hypertensives

et al. 2006

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Although aerobic exercise training has been shown to lower blood pressure (BP) in older adults, its effect on BP sensitivity to dietary sodium (Na þ ) is unknown. Therefore, the present study was undertaken to examine the effect of aerobic exercise training on BP sensitivity to dietary Na þ in older hypertensive individuals. Blood pressure was measured after 8 days of low (20 mEq) and high (200 mEq) Na þ diets in 31 older (6377 years, mean7standard deviation), hypertensive (152711/ 8875 mm Hg) individuals at baseline and following 6 months of aerobic exercise training (at 75% VO 2 max, 3 times/week, 40 min/session). Subjects were grouped on the basis of the difference in mean arterial BP (MAP) between diets (Na þ sensitive: X5 mm Hg increase in MAP on high Na þ , n ¼ 20; Na þ resistant: o5 mm Hg increase in MAP on the high Na þ diet, n ¼ 11). Following 6 months of aerobic exercise training, there was a significant increase in maximal aerobic capacity (VO 2 max: 18.373.8 vs 20.774.2 ml/kg/min, Po0.017). Aerobic exercise training had a significant (P ¼ 0.02) effect on Na þ sensitivity status, with the proportion of Na þ -resistant individuals increasing from 35% at baseline to 61% following the 6-month aerobic exercise training programme. This study demonstrates the importance of physical activity on BP sensitivity to dietary Na þ .

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“…Consistent with our findings, a higher incidence of LVH in saltsensitive hypertensive patients than in salt-resistant hypertensive patients has been reported. 27 Three large studies of patients with essential hypertension demonstrated that patients who were salt-sensitive more often had LVH, cardiovascular events, and/or endothelial dysfunction than non-saltsensitive hypertensive patients. 28 -30 These findings highlight the important link between salt-sensitive hypertension and cardiovascular injury.…”

Section: Discussionmentioning

confidence: 99%

“…[27][28][29][30] After menopause, the loss of the ovarian hormones may unmask a population of women prone to salt-sensitive hypertension that would be at higher risk for cardiovascular morbidity and mortality. Clinically, we infer that after menopause, estrogen deficiency promotes an overexpression of renal AT 1 receptors resulting in oxidative stress, 41 disturbed renal sodium handling, 42 and hypertension, particularly in women genetically prone to salt sensitivity.…”

Section: Discussionmentioning

confidence: 99%

Postovariectomy Hypertension Is Linked to Increased Renal AT ₁ Receptor and Salt Sensitivity

2003

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Abstract-The functional balance between angiotensin II (Ang II) and nitric oxide (NO) plays a key role in modulating salt sensitivity. Estrogen has been shown to downregulate angiotensin type 1 (AT 1 ) receptor expression and to increase the bioavailability of endothelium-derived NO, which decreases AT 1 receptor expression. The present study tests the hypothesis that in the presence of genetic salt sensitivity, deficiency of endogenous estrogens after ovariectomy (OVX) fosters an upregulation of Ang II. Female Dahl salt-resistant (DR), Dahl salt-sensitive (DS), Wistar-Kyoto (WKY), and spontaneously hypertensive (SHR) rats underwent bilateral OVX or sham surgery (SHX) and were fed a normal salt diet (0.5% NaCl) for 14 weeks. Systolic blood pressures were measured every 2 weeks and were not significantly different between OVX and SHX for DR, WKY, and SHR groups. However, at the end of 14 weeks of normal salt diet, hypertension developed in DS OVX but not SHX rats (160Ϯ3 versus 136Ϯ3 mm Hg; PϽ0.05). Hypertension also developed in DS OVX rats pair-fed a normal salt diet (166Ϯ7 mm Hg). Development of hypertension in DS OVX rats was prevented by estrogen replacement (132Ϯ3 mm Hg), AT 1 receptor blockade (119Ϯ3 mm Hg), or feeding a very low salt diet (0.1% NaCl; 129Ϯ4 mm Hg). Renal AT 1 receptor protein expression was significantly elevated 2-fold in DS OVX relative to SHX rats and was prevented by estrogen replacement. These data strongly suggest that after OVX in salt-sensitive rats there is a lower threshold for the hypertensinogenic effect of salt that is linked to an activation of Ang II. Key Words: rats, Dahl Ⅲ rats, spontaneously hypertensive Ⅲ sodium, dietary Ⅲ angiotensin II Ⅲ estrogen Ⅲ receptors, angiotensin C ardiovascular diseases are the leading cause of death in women and claim the lives of more than half a million women every year. The incidence of cardiovascular disease is 4-fold higher in postmenopausal women than in women of the same age who are premenopausal. 1 Hypertension is a major risk factor for cardiovascular disease. It has been shown that after adjustment for age and body mass index, postmenopausal women are more than twice as likely to be hypertensive as premenopausal women. 2 Thus, after menopause, hypertension may contribute to the increase in cardiovascular risk of postmenopausal women. 3 Accumulating evidence also suggests that postmenopausal women are more salt-sensitive than premenopausal women. 4 A study conducted in postmenopausal Japanese women showed that salt sensitivity correlated inversely with levels of circulating hormones, 5 suggesting that decreases in ovarian hormone levels and increased sensitivity to dietary sodium may be important factors in the genesis of postmenopausal hypertension. Moreover, it has been recently reported that in contrast to women studied during the different phases of the menstrual cycle, menopausal women are characterized by a blunted suppression of renin by salt, which could contribute to the development of salt-sensitive hypertension. 6 These fin...

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Left Ventricular Hypertrophy Is More Marked in Salt-Sensitive Than in Salt-Resistant Hypertensive Patients

Cited by 41 publications

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Surgical Menopause Increases Salt Sensitivity of Blood Pressure

Surgical Menopause Increases Salt Sensitivity of Blood Pressure

Effect of aerobic exercise training on blood pressure sensitivity to dietary sodium in older hypertensives

Postovariectomy Hypertension Is Linked to Increased Renal AT ₁ Receptor and Salt Sensitivity

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Left Ventricular Hypertrophy Is More Marked in Salt-Sensitive Than in Salt-Resistant Hypertensive Patients

Cited by 41 publications

References 0 publications

Surgical Menopause Increases Salt Sensitivity of Blood Pressure

Surgical Menopause Increases Salt Sensitivity of Blood Pressure

Effect of aerobic exercise training on blood pressure sensitivity to dietary sodium in older hypertensives

Postovariectomy Hypertension Is Linked to Increased Renal AT 1 Receptor and Salt Sensitivity

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Postovariectomy Hypertension Is Linked to Increased Renal AT ₁ Receptor and Salt Sensitivity