Hemodynamic mechanisms of adaptation to chronic high sodium intake in normal humans.

Sullivan, Jay M.; Ratts, Thomas E.

doi:10.1161/01.hyp.5.6.814

Cited by 46 publications

(40 citation statements)

References 36 publications

(22 reference statements)

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“…This prevented salt-dependent hypertension in dogs that were infused with a subpressor dose of ANG II (18). A second possibility is that clamping ANG II levels at normal or high levels interferes with a vasodilatory response to volume expansion that has been reported to occur in normal animals (15,19) and humans (13,24,25) that consume a high-salt diet. Indeed, in a companion study to the servo control experiment in dogs (18), it was reported that a chronic Na ϩ load increased cardiac output in normal dogs but also resulted in a simultaneous decrease of vascular resistance such that arterial pressure did not change (19).…”

Section: Discussionmentioning

confidence: 99%

Responsiveness vs. basal activity of plasma ANG II as a determinant of arterial pressure salt sensitivity

Osborn¹,

Ariza-Nieto²,

Collister³

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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.-Infusion of angiotensin II (ANG II) causes salt-sensitive hypertension. It is unclear whether this is due to the body's inability to suppress ANG II during increased salt intake or, rather, an elevated basal level of plasma ANG II itself. To distinguish between these mechanisms, SpragueDawley rats were instrumented with arterial and venous catheters for measurement of arterial pressure and infusion of drugs, respectively. The sensitivity of arterial pressure to salt was measured in four groups with the following treatments: 1) saline control (Con, n ϭ 12); 2) administration of the angiotensin-converting enzyme inhibitor enalapril to block endogenous ANG II (ANG-Lo, n ϭ 10); 3) administration of enalapril and 5 ng ⅐ kg Ϫ1 ⅐ min Ϫ1 ANG II to clamp plasma ANG II at normal levels (ANG-Norm, n ϭ 10); and 4) administration of enalapril and 20 ng ⅐ kg Ϫ1 ⅐ min Ϫ1 ANG II to clamp ANG II at high levels (ANG-Hi, n ϭ 10). Rats ingested a 0.4% NaCl diet for 3 days and then a 4.0% NaCl diet for 11 days. Arterial pressure of rats fed the 0.4% NaCl diet was lower in ANG-Lo (84 Ϯ 2 mmHg) compared with Con (101 Ϯ 3 mmHg) and ANG-Norm (98 Ϯ 4 mmHg) groups, whereas ANG-Hi rats were hypertensive (145 Ϯ 4 mmHg). Salt sensitivity was expressed as the change in arterial pressure divided by the change in sodium intake on the last day of the 4.0% NaCl diet. Salt sensitivity (in mmHg/meq Na) was lowest in Con rats (0.0 Ϯ 0.1) and progressed from ANG-Lo (0.8 Ϯ 0.2) to ANG-Norm (1.5 Ϯ 0.5) to ANG-Hi (3.5 Ϯ 0.5) rats. We conclude that the major determinant of salt sensitivity of arterial pressure is the basal level of plasma ANG II rather than the responsiveness of the renin-angiotensin system.renin-angiotensin system; sympathetic nervous system LONG-TERM SALT SENSITIVITY of arterial pressure is a significant clinical problem in both the normotensive and hypertensive human populations. It is currently estimated that 25% of the normotensive population is "salt sensitive" in that their arterial pressures are abnormally sensitive to changes in dietary NaCl intake (29). This is clinically significant, because the salt sensitivity of arterial pressure may be a more accurate predictor of future cardiovascular disease and morbidity than the basal level of arterial pressure (29). Salt sensitivity is more prevalent in humans with essential hypertension; estimates are that 50-75% of these patients exhibit increased salt sensitivity of arterial pressure (28). Despite the clinical importance of salt-dependent hypertension, its pathogenesis is poorly understood.Previous studies support the idea that impaired regulation of the renin-angiotensin-aldosterone system (RAAS) increases the salt sensitivity of arterial pressure. For example, several studies show that long-term infusion of angiotensin II (ANG II) causes salt-dependent hypertension in experimental animals (1,7,9,11,12,16). However, the precise nature of the relationship between plasma ANG II and long-term salt sensitivity of arterial pressure remains unclear. It is logical to conclude that the ...

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Section: Discussionmentioning

confidence: 99%

Responsiveness vs. basal activity of plasma ANG II as a determinant of arterial pressure salt sensitivity

Osborn¹,

Ariza-Nieto²,

Collister³

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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show abstract

“…Thus, during periods of high sodium intake, sodium-resistant subjects accommodate increases in cardiac index by a proportionate fall in total peripheral resistance that our previous studies indicate can be maintained for at least 1 year. 29 Omvik and Lund-Johansen 30 have found that decreased blood pressure during long-term sodium depletion (9 months) was due to a sustained fall in cardiac output and an increase in vascular resistance. Our earlier data 13 also indicated that forearm vascular resistance was significantly higher in a mixed group of normotensive and borderline hypertensive sodium-sensitive subjects than in sodium-resistant subjects.…”

Section: Discussionmentioning

confidence: 99%

Sodium sensitivity in human subjects. Hemodynamic and hormonal correlates.

Sullivan

Ratts

1988

Hypertension

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SUMMARY To investigate factors associated with sodium sensitivity, 157 subjects were studied while receiving 10 and 200 mEq sodium diets. Measurements included blood pressure (BP), forearm vascular resistance, plasma renin activity (PRA), and plasma aldosterone. Sodium repletion was associated with a greater than 5% increase in mean BP in 16% of the normotensive subjects and 29% of the borderline hypertensive subjects. Sodium-sensitive subjects were compared with sodiumresistant subjects in both the normotensive (n = 92) and borderline hypertensive (n = 65) groups. Forearm vascular resistance was significantly higher (p<0.05) during sodium loading in the sodiumsensitive subgroups of both the normotensive and borderline hypertensive groups (35.8 ± 29 vs 23.8 ± 20 [SD] and 37.5 ± 29 vs 22.5 ± 14 mm Hg/ml/min/100 g, respectively. Venous capacitance was lower in the sodium-sensitive than in the sodium-resistant borderline hypertensive subjects (0.8 ± 0.21 vs 1.69 ± 0.24 ml/100 g). During sodium restriction, PRA was significantly lower (p<0.01) in the sodium-sensitive subsets (2.56 ± 1.6 vs 4.04 ± 2.6; 2.65 ± 2.1 vs 3.88 ± 2.6 ng angiotensin I/ml/hr). Aldosterone was lower (p<0.01) during sodium depletion in the sodium-sensitive subsets (17.3 ± 12 vs 26.3 ± 16; 18.5 ± 18 vs 27.9 ± 17 ng/ml). A significant inverse correlation existed between change in BP with sodium repletion and change in PRA or level of PRA during sodium depletion (p<0.003). We conclude that both normotensive and borderline hypertensive sodiumsensitive subjects are characterized by an increase in forearm vascular resistance during high sodium intake and that this characteristic is associated with decreased responsiveness of the renin-aldosterone system during sodium depletion. (Hypertension 11: 717-723, 1988) KEY WORDS * hypertension • sodium • vascular resistance • hemodynamics renin • aldosterone A LTHOUGH considerable evidence links dietary / \ sodium intake with high blood pressure, sev-A. \ . eral observations suggest that all persons are not affected equally by the hypertensive effects of sodium. By selective inbreeding, Dahl et al.1 have developed strains of rats that become hypertensive when fed a high sodium diet and others that are resistant to the hypertensive effects of sodium. Worldwide studies of sodium intake in various human populations have shown a direct relationship between sodium intake and the prevalence of hypertension, 2 yet in certain populations, the majority of persons remain normotensive despite high sodium intake.3 Over the past several years, a number of investigators have demonstrated

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“…In 10,20, and 30 mmol/L NaCl, the Phe-and caffeine-induced contractions were significantly reduced (Table).…”

Section: Effect Of Increases In [Namentioning

confidence: 99%

“…11,18 During high dietary Na ϩ intake, several adaptive mechanisms are activated to cope with the large Na ϩ overload. These mechanisms include expansion of extracellular fluid volume, 19 increased cardiac output, 20 and increased renal blood flow. 21 These adaptive mechanisms make Na ϩ excretion as equivalent as possible to Na ϩ intake and thus maintain the body Na ϩ and the extracellular fluid volume within normal levels.…”

mentioning

confidence: 99%

Gender Differences in Vascular Smooth Muscle Reactivity to Increases in Extracellular Sodium Salt

2002

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Hemodynamic mechanisms of adaptation to chronic high sodium intake in normal humans.

Cited by 46 publications

References 36 publications

Responsiveness vs. basal activity of plasma ANG II as a determinant of arterial pressure salt sensitivity

Responsiveness vs. basal activity of plasma ANG II as a determinant of arterial pressure salt sensitivity

Sodium sensitivity in human subjects. Hemodynamic and hormonal correlates.

Gender Differences in Vascular Smooth Muscle Reactivity to Increases in Extracellular Sodium Salt

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