Sodium sensitivity in human subjects. Hemodynamic and hormonal correlates.

Sullivan, Jay M.; Ratts, Thomas E.

doi:10.1161/01.hyp.11.6.717

Cited by 74 publications

(39 citation statements)

References 47 publications

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“…The current finding that FBF increased profoundly and FVR decreased with salt loading in the SS patients is consistent with the result of a recent study 35 using a sodium loading period of 4 days and a modest increase in sodium intake (200 meq/day). These findings are opposite to those reported earlier: Takeshita et al 36 and Koolen and Van Brummelen 12 observed that SS patients responded to a high salt intake with a decrease in FBF and an increase in FVR.…”

supporting

confidence: 92%

Systemic and regional hemodynamics in patients with salt-sensitive hypertension.

1990

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Twenty-two patients with normal plasma renln and essential hypertension were classified as "salt-sensitive" (SS) (n=9) or "non-salt-sensitive" (NSS) (n=13) from an increase in mean blood pressure with changes in sodium intake from 25 to 250 meq/day. With the high sodium diet, the SS patients gained more weight (/?<0.05), retained more sodium (/><0.05), and had a greater increase in cardiac output (/?<0.05). Despite the markedly increased cardiac output, systemic vascular resistance did not change with sodium loads in the SS patients, whereas the NSS patients had a significant decrease in systemic vascular resistance. Thus, the greater increase in blood pressure with sodium loads in SS patients can be attributed not only to an increase in cardiac output, possibly resulting from greater sodium retention, but also to inappropriately elevated systemic vascular resistance. Concomitant with a greater increase in cardiac output, the SS patients had a greater increase in forearm blood flow with sodium loading than the NSS patients (p<0.02). In contrast, blood flow to the kidney and the liver was not significantly changed in either group; renal (p<0.05) and hepatic (/><0.01) vascular resistance increased significantly in SS patients but remained unchanged in NSS patients. Thus, evidence presented suggests that the greater increase in blood pressure with sodium loads seems to be characterized by a very inhomogenous distribution of local flow and resistance in SS patients; renal and hepatic blood flow remains essentially unchanged and skeletal muscle blood flow receives almost all of the increase in cardiac output Moreover, systemic vascular resistance changes did not reflect the resistance of individual beds because vasoconstriction appeared in the kidney and the splanchnic area but was masked by prominent vasodilation in the skeletal muscle. Because this hemodynamic pattern is similar to the pattern evoked during defense reaction, it is suggested that sympathetic overactivity on a selective basis might be involved in the impaired renal function for sodium excretion and the increase in blood pressure with sodium loads in SS patients. (Hypertension 1990,16:235-244)

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supporting

confidence: 92%

Systemic and regional hemodynamics in patients with salt-sensitive hypertension.

1990

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“…In salt-sensitive patients, calculated renal afferent resistance increased from 5231 ±624 to 7379+533 (dyne/s)/cm~5 (P<.0l), renal efferent resistance increased from 4567±541 to 6539±586 (dyne/s)/cnT 5 (P<.01), and glomerular pressure increased from 58±2.6 to 64±4.3 mm Hg (P<.01) during the high NaCl intake. However, these parameters did not change in salt-resistant patients.…”

Section: Urinary Albumin Excretionmentioning

confidence: 94%

Microalbuminuria in salt-sensitive patients. A marker for renal and cardiovascular risk factors.

Bigazzi¹,

Bianchi²,

Baldari³

et al. 1994

Hypertension

237

133

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We previously showed that a high salt diet increases glomerular capillary pressure in salt-sensitive hypertensive patients and suggested that this may underlie the greater propensity of these patients to develop renal failure. Because microalbuminuria is considered an initial sign of renal damage, we have tested whether salt-sensitive patients display greater urinary albumin excretion than salt-resistant hypertensive patients. Twenty-two patients were placed on a low sodium intake (20 mEq/d) for 7 days followed by a high sodium diet (250 mEq/d) for 7 more days. Twelve patients were classified as salt sensitive and 10 as salt resistant. Urinary albumin excretion was greater in salt-sensitive than saltresistant patients (54±11 versus 22±5 mg/24 h, P<.01). During the low sodium diet, glomerular filtration rate, renal plasma flow, and filtration fraction were similar between the two groups. During the high sodium intake, glomerular filtration, renal plasma flow, filtration fraction, and calculated intraglomerular pressure did not change in salt-resistant patients; in salt-sensitive patients, however, renal plasma flow decreased, and filtration fraction and intraglomerular pressure increased, whereas glomerular filtration rate did not change. Urinary albumin excretion was significantly correlated with glomerular capillary pressure. Salt-sensitive patients displayed higher serum levels of low-density lipoprotein cholesterol and lipoprotein(a) and lower levels of high-density lipoprotein cholesterol than salt-resistant patients. These studies have shown greater urinary albumin excretion and serum concentrations of atherogenic lipoproteins in salt-sensitive than in salt-resistant hypertensive patients, suggesting that salt sensitivity may be a marker for greater risk of renal and cardiovascular complications. (Hypertension. 1994;23:195-199.)

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“…The methods used in these studies have been reported in detail elsewhere. 34 ' 35 We have now studied 183 volunteers, 111 normal subjects and 72 patients with labile, borderline hypertension. Analysis of the blood pressure change with sodium loading yielded a normal distribution of responses ( Figure 1).…”

Section: Human Studiesmentioning

confidence: 99%

Salt sensitivity. Definition, conception, methodology, and long-term issues.

1991

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Several laboratories have examined the relation between salt intake and blood pressure in both experimental animals and humans. The human studies have used widely varying methodologies and different criteria for sodium sensitivity. Nonetheless, these studies have produced convincing data that the blood pressure of some individuals is far more sensitive to the effects of sodium depletion or loading than that of others. Furthermore, a minority of the population appears to comprise acutely salt-sensitive individuals. Some studies have shown that sodiumsensitive individuals share several characteristics. They include increased forearm vascular resistance, decreased venous compliance, suppressed plasma renln activity, and lower circulating aldosterone concentration. These findings have also been described in the Dahl salt-sensitive rat, which suggest a genetic link in humans as well as the rat Long-term follow-up of sodium-sensitive and sodium-resistant groups has shown that although blood pressure levels are approximately equal in the two groups during sodium depletion, resumption of a daily sodium intake of about 150 meq results in significantly higher levels of blood pressure and forearm vascular resistance in the sodium-sensitive group. This difference persists for at least 12 months.

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Sodium sensitivity in human subjects. Hemodynamic and hormonal correlates.

Cited by 74 publications

References 47 publications

Systemic and regional hemodynamics in patients with salt-sensitive hypertension.

Systemic and regional hemodynamics in patients with salt-sensitive hypertension.

Microalbuminuria in salt-sensitive patients. A marker for renal and cardiovascular risk factors.

Salt sensitivity. Definition, conception, methodology, and long-term issues.

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