Effects of Sodium Status on the Venous Response to Noradrenaline Infusion in Pre-Ascitic Cirrhosis

1995 ◽  
Vol 88 (5) ◽  
pp. 525-531 ◽  
Author(s):  
Florence Wong ◽  
Arieh Bomzon ◽  
Alexander Logan ◽  
Laurence Blendis
Keyword(s):  
Sodium Intake ◽  
High Sodium ◽  
Sodium Diet ◽  
High Sodium Intake ◽  
Control Subjects ◽  
Low Sodium ◽  
Dorsal Hand ◽  
Hand Vein ◽  
Cirrhotic Patients ◽  
Dorsal Hand Vein

1. This study assesses the effects of sodium status on venous responsiveness to noradrenaline and the neurohumoral profile in pre-ascitic cirrhotic patients. Eight cirrhotic patients and ten control subjects were studied after both a low (20 mmol/day) and a high (200 mmol/day) sodium diet. Venous responsiveness to increasing doses of noradrenaline in a dorsal hand vein and various plasma hormone levels were measured. Maximal response (Rmax.) and the dose of noradrenaline that yielded 50% of Rmax (ED50) were then calculated. 2. A significantly smaller dorsal hand vein diameter was observed in the control subjects on a low sodium (2.23 ± 0.14 mm) compared with a high sodium (2.57 ± 0.15 mm; P = 0.04) diet, but not in the cirrhotic patients. Rmax. was not significantly different in either group on both diets. With low sodium intake, ED50 was similar in the two groups. However, on high sodium intake, control subjects had a significantly higher ED50 (34.4 ± 7.4 ng/min) than the cirrhotic patients (5.03 ± 0.86 ng/min; P < 0.003). Plasma noradrenaline in the control subjects fell significantly with the change from a low (1.29 ± 0.11 nmol/l) to a high (0.68 ± 0.09 nmol/l; P < 0.001) sodium diet, but remained elevated in the cirrhotic patients. Cirrhotic patients had significantly higher atrial natriuretic factor levels and lower plasma renin activity than the control subjects on both diets. 3. In conclusion, pre-ascitic cirrhotic patients show no evidence of venodilatation. Their sympathetic nervous activity is not suppressible by volume expansion. Relative hyper-responsiveness of the peripheral venous circulation to adrenergic stimulation with high sodium intake is present.

Plasma Angiotensin II Concentration Regulates Vascular but Not Adrenal Responsiveness to Restriction of Sodium Intake in Normal Man

1981 ◽  
Vol 61 (5) ◽  
pp. 527-534 ◽  
Author(s):  
Bess F. Dawson-Hughes ◽  
T. J. Moore ◽  
R. G. Dluhy ◽  
N. K. Hollenberg ◽  
G. H. Williams
Keyword(s):  
Sodium Intake ◽  
Regression Line ◽  
Sodium Balance ◽  
Ang Ii ◽  
High Sodium ◽  
Sodium Diet ◽  
High Sodium Intake ◽  
Low Sodium ◽  
Vascular Responsiveness ◽  
High Sodium Diet

1. Sodium restriction increases adrenal and decreases vascular sensitivity to angiotensin II (ANG II). These responses may be mediated either by the circulating level of ANG II or other mechanisms also modified by a change in sodium balance. To assess the importance of the ANG II level, captopril, an oral converting enzyme inhibitor, was used to lower the plasma ANG II level to the sodium-loaded range while maintaining subjects in low sodium balance. 2. Normal volunteer subjects received an infusion of ANG II in increasing doses in three states: high sodium intake, low sodium intake and low sodium intake after pretreatment with captopril. 3. Basal levels of ANG II on high-sodium diet and low-sodium diet plus captopril were similar. In the ANG II infusion studies the slope of the aldosterone—ANG II regression line on low sodium intake was significantly steeper than that on high sodium intake. After the addition of captopril the slope was not decreased, indicating that the endogenous ANG II concentration is not necessary to maintain adrenal sensitivity during sodium restriction. 4. In the ANG II infusion studies the slope of the mean blood pressure—ANG II regression line on high sodium intake was significantly steeper than that on low sodium intake. The addition of captopril to sodium-restricted subjects caused the slope of the regression relationship to increase significantly, consistent with an enhanced vascular responsiveness when endogenous ANG II levels were lowered. However, the slope on low sodium plus captopril did not increase to the level of subjects on a high-sodium diet, suggesting that factors in addition to the circulating ANG II level are also important in regulating the vascular responsiveness to ANG II.

scholarly journals Sodium Sensitivity, Sodium Resistance, and Incidence of Hypertension

Hypertension ◽  
2021 ◽  
Author(s):  
Jiang He ◽  
Jian-Feng Huang ◽  
Changwei Li ◽  
Jing Chen ◽  
Xiangfeng Lu ◽  
...  
Keyword(s):  
Sodium Intake ◽  
Experimental Studies ◽  
Dietary Sodium ◽  
Cross Sectional ◽  
Incident Hypertension ◽  
High Sodium ◽  
Sodium Sensitivity ◽  
Sodium Diet ◽  
Low Sodium ◽  
Increased Risk

Cross-sectional studies have reported that high sodium sensitivity is more common among individuals with hypertension. Experimental studies have also reported various animal models with sodium-resistant hypertension. It is unknown, however, whether sodium sensitivity and resistance precede the development of hypertension. We conducted a feeding study, including a 7-day low-sodium diet (1180 mg/day) followed by a 7-day high-sodium diet (7081 mg/day), among 1718 Chinese adults with blood pressure (BP) <140/90 mm Hg. We longitudinally followed them over an average of 7.4 years. Three BP measurements and 24-hour urinary sodium excretion were obtained on each of 3 days during baseline observation, low-sodium and high-sodium interventions, and 2 follow-up studies. Three trajectories of BP responses to dietary sodium intake were identified using latent trajectory analysis. Mean (SD) changes in systolic BP were −13.7 (5.5), −4.9 (3.0), and 2.4 (3.0) mm Hg during the low-sodium intervention and 11.2 (5.3), 4.4 (4.1), and −0.2 (4.1) mm Hg during the high-sodium intervention ( P <0.001 for group differences) in high sodium-sensitive, moderate sodium-sensitive, and sodium-resistant groups, respectively. Compared with individuals with moderate sodium sensitivity, multiple-adjusted odds ratios (95% CIs) for incident hypertension were 1.43 (1.03–1.98) for those with high sodium sensitivity and 1.43 (1.03–1.99) for those with sodium resistance ( P =0.006 for nonlinear trend). Furthermore, a J-shaped association between systolic BP responses to sodium intake and incident hypertension was identified ( P <0.001). Similar results were observed for diastolic BP. Our study indicates that individuals with either high sodium sensitivity or sodium resistance are at an increased risk for developing hypertension.

Alterations in Cerebrospinal Fluid Angiotensin II by Sodium Intake in Patients with Essential Hypertension

1989 ◽  
Vol 77 (4) ◽  
pp. 389-394 ◽  
Author(s):  
Minoru Kawamura ◽  
Yuhei Kawano ◽  
Kaoru Yoshida ◽  
Masahito Imanishi ◽  
Satoshi Akabane ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Essential Hypertension ◽  
Sodium Intake ◽  
Ang Ii ◽  
Sodium Depletion ◽  
High Sodium ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium

1. Angiotensin (ANG) levels were measured in the cerebrospinal fluid of 15 patients with essential hypertension on a high sodium diet for 1 week and on a low sodium diet for a further week. ANGs were determined using a system of extraction by Sep-Pak cartridges followed by h.p.l.c. combined with radioimmunoassay. 2. Sodium depletion resulted in increases of ANG II in the cerebrospinal fluid from 1.16 ± 0.38 (sem) to 1.83 ± 0.43 fmol/ml (P < 0.01) and of ANG III from 0.65 ± 0.11 to 0.86 ± 0.15 fmol/ml (P < 0.01). 3. The ANG II level in the cerebrospinal fluid was found to be unchanged and recovery of added ANG II was approximately 90%, even after incubation for 3 h, on both diets. Thus, it is unlikely that ANG II is produced or degraded in the cerebrospinal fluid in vitro. 4. There was no significant correlation between the cerebrospinal fluid and the plasma ANG II concentration on the low sodium diet. 5. These results suggest that the cerebrospinal fluid ANG II level increases with sodium depletion, and that the effect of the level of ANG II on the activity of the angiotensin-forming system in the central nervous system may be assessed by determination of ANG II in the cerebrospinal fluid in patients with essential hypertension.

P4540Obesity in patients with heart failure and without diabetes mellitus is associated with longer event-free survival only among those with high dietary sodium intake

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
Z Saleh ◽  
T Lennie ◽  
D Moser
Keyword(s):  
Diabetes Mellitus ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Obese Patients ◽  
Event Free Survival ◽  
Free Survival ◽  
High Sodium ◽  
High Sodium Intake ◽  
Low Sodium ◽  
Patients With Heart Failure

Abstract Background Obesity is paradoxically associated with better short- and long-term outcomes in patients with heart failure (HF) and without diabetes mellitus (DM). While excessive dietary sodium intake is common among obese persons, its impact on the association between obesity and outcomes has not been considered. Aim To determine whether dietary sodium intake levels would affect the association between obesity and better outcomes in patients with HF and without DM. Method A sample of 129 patients (age 60±12.4 years; 30% female) provided a single 24-hour urine collection sample to estimate dietary sodium intake. Patients were divided into 4 groups based on body mass index (BMI) and the sodium intake recommendation for HF of 3g/day (obese with high sodium intake [n=41; 32%], obese with low sodium intake [n=16; 12%], non-obese with high sodium intake [n=35; 27%], and non-obese with low sodium intake [n=37; 29%]). Patients were followed-up during an average period of 395 days to determine time to first event of all-cause hospitalization or death. Cox regression was used to determine the association between obesity and outcomes in the context of sodium intake after controlling for age, gender, NYHA class (I II vs. III IV) and LVEF. Results There were 41 patients (31.8%) who had an event of all-cause hospitalization or death. Obese patients with high sodium intake had 61% lower risk for events than those non-obese with low dietary sodium intake (figure). There were no differences in the event-free survival among other groups. Conclusion These data suggest that dietary sodium intake may be particularly important for obese patients with HF and without DM.

scholarly journals Dietary sodium modulates the interaction between efferent and afferent renal nerve activity by altering activation of α2-adrenoceptors on renal sensory nerves

2011 ◽  
Vol 300 (2) ◽  
pp. R298-R310 ◽  
Author(s):  
Ulla C. Kopp ◽  
Michael Z. Cicha ◽  
Lori A. Smith ◽  
Saku Ruohonen ◽  
Mika Scheinin ◽  
...  
Keyword(s):  
Substance P ◽  
Sodium Intake ◽  
Sensory Nerves ◽  
Nerve Activity ◽  
Renal Nerve ◽  
High Sodium ◽  
Sodium Diet ◽  
Low Sodium ◽  
Renal Nerve Activity ◽  
High Sodium Diet

Activation of efferent renal sympathetic nerve activity (ERSNA) increases afferent renal nerve activity (ARNA), which then reflexively decreases ERSNA via activation of the renorenal reflexes to maintain low ERSNA. The ERSNA-ARNA interaction is mediated by norepinephrine (NE) that increases and decreases ARNA by activation of renal α1-and α2-adrenoceptors (AR), respectively. The ERSNA-induced increases in ARNA are suppressed during a low-sodium (2,470 ± 770% s) and enhanced during a high-sodium diet (5,670 ± 1,260% s). We examined the role of α2-AR in modulating the responsiveness of renal sensory nerves during low- and high-sodium diets. Immunohistochemical analysis suggested the presence of α2A-AR and α2C-AR subtypes on renal sensory nerves. During the low-sodium diet, renal pelvic administration of the α2-AR antagonist rauwolscine or the AT1 receptor antagonist losartan alone failed to alter the ARNA responses to reflex increases in ERSNA. Likewise, renal pelvic release of substance P produced by 250 pM NE (from 8.0 ± 1.3 to 8.5 ± 1.6 pg/min) was not affected by rauwolscine or losartan alone. However, rauwolscine+losartan enhanced the ARNA responses to reflex increases in ERSNA (4,680 ± 1,240%·s), and renal pelvic release of substance P by 250 pM NE, from 8.3 ± 0.6 to 14.2 ± 0.8 pg/min. During a high-sodium diet, rauwolscine had no effect on the ARNA response to reflex increases in ERSNA or renal pelvic release of substance P produced by NE. Losartan was not examined because of low endogenous ANG II levels in renal pelvic tissue during a high-sodium diet. Increased activation of α2-AR contributes to the reduced interaction between ERSNA and ARNA during low-sodium intake, whereas no/minimal activation of α2-AR contributes to the enhanced ERSNA-ARNA interaction under conditions of high sodium intake.

Dietary sodium intake modulates renal excretory responses to intrarenal angiotensin (1–7) administration in anesthetized rats

2013 ◽  
Vol 304 (3) ◽  
pp. R260-R266 ◽  
Author(s):  
Julie O'Neill ◽  
Alan Corbett ◽  
Edward J. Johns
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
High Sodium ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Renal Hemodynamic

Angiotensin II at the kidney regulates renal hemodynamic and excretory function, but the actions of an alternative metabolite, angiotensin (1–7), are less clear. This study investigated how manipulation of dietary sodium intake influenced the renal hemodynamic and excretory responses to intrarenal administration of angiotensin (1–7). Renal interstitial infusion of angiotensin (1–7) in anesthetized rats fed a normal salt intake had minimal effects on glomerular filtration rate but caused dose-related increases in urine flow and absolute and fractional sodium excretions ranging from 150 to 200%. In rats maintained for 2 wk on a low-sodium diet angiotensin (1–7) increased glomerular filtration rate by some 45%, but the diuretic and natriuretic responses were enhanced compared with those in rats on a normal sodium intake. By contrast, renal interstitial infusion of angiotensin (1–7) in rats maintained on a high-sodium intake had no effect on glomerular filtration rate, whereas the diuresis and natriuresis was markedly attenuated compared with those in rats fed either a normal or low-sodium diet. Plasma renin and angiotensin (1–7) were highest in the rats on the low-sodium diet and depressed in the rats on a high-sodium diet. These findings demonstrate that the renal hemodynamic and excretory responses to locally administered angiotensin (1–7) is dependent on the level of sodium intake and indirectly on the degree of activation of the renin-angiotensin system. The exact way in which angiotensin (1–7) exerts its effects may be dependent on the prevailing levels of angiotensin II and its receptor expression.

The Effect of Chronic Sodium Loading and Sodium Restriction on Plasma and Renal Concentrations of Prostaglandin a in Normal Wistar and Spontaneously Hypertensive Aoki Rats

1973 ◽  
Vol 45 (s1) ◽  
pp. 325s-329s ◽  
Author(s):  
R. M. Zusman ◽  
B. H. Forman ◽  
G. Schneider ◽  
B. V. Caldwell ◽  
L. Speroff ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Wistar Rats ◽  
Sodium Intake ◽  
Dietary Group ◽  
Sodium Restriction ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
High Sodium ◽  
High Sodium Intake ◽  
Low Sodium

1. In normal and hypertensive rats prostaglandin A (PGA) in plasma and kidney increased on low sodium intake and decreased on high sodium intake. 2. Plasma and renal concentrations of PGA were higher in spontaneously hypertensive rats than in normal Wistar rats in each dietary group.

Effects of sodium intake on cardiovascular variables in humans during posture changes and ambulatory conditions

2002 ◽  
Vol 283 (6) ◽  
pp. R1404-R1411 ◽  
Author(s):  
Morten Damgaard ◽  
Anders Gabrielsen ◽  
Martina Heer ◽  
Jørgen Warberg ◽  
Peter Bie ◽  
...  
Keyword(s):  
Supine Position ◽  
Sodium Intake ◽  
Arterial Baroreflex ◽  
High Sodium ◽  
High Sodium Intake ◽  
Laboratory Conditions ◽  
Low Sodium ◽  
The Difference ◽  
Cardiovascular Variables ◽  
Healthy Males

The hypothesis was tested that cardiac output (CO) and stroke volume (SV) are increased by a moderate physiological elevation in sodium intake with a more pronounced effect in the ambulatory upright seated than supine position. Fourteen healthy males were investigated during ambulatory and controlled laboratory conditions at the end of two consecutive 5-day periods with sodium intakes of 70 (low) and 250 (high) mmol/24 h or vice versa, respectively. Comparing high and low sodium intake, plasma volume and plasma protein concentrations were 9 and 8% higher in the seated and the supine position, respectively. When seated during laboratory conditions, CO was 5.3 ± 0.2 l/min on the high sodium intake vs. 4.8 ± 0.2 l/min on the low ( P < 0.05), and SV was 81 ± 3 vs. 68 ± 3 ml ( P< 0.05). In the supine position, SV was 107 ± 3 ml on the high vs. 99 ± 3 ml ( P < 0.05) on the low sodium intake, while CO remained unchanged. The difference in CO and SV induced by the change in sodium intake was significantly higher in the seated than in the supine position ( P < 0.05). During upright ambulatory conditions, CO was 5.9 ± 0.2 l/min during the high and 5.2 ± 0.2 l/min during the low sodium intake ( P < 0.05), and SV was 84 ± 3 and 69 ± 3 ml ( P < 0.05), respectively. Mean arterial pressure was unchanged by the variations in sodium intake. In conclusion, increments in sodium intake within the normal physiological range increase CO and SV and more so in the seated vs. the supine position. These changes are readily detectable during upright, ambulatory conditions. The results indicate that the higher SV and CO could constitute an arterial baroreflex stimulus for the augmented renal sodium excretion.

Dietary sodium affects systemic and renal hemodynamic response to NO inhibition in healthy humans

1998 ◽  
Vol 274 (5) ◽  
pp. F914-F923 ◽  
Author(s):  
J. N. Bech ◽  
C. B. Nielsen ◽  
P. Ivarsen ◽  
K. T. Jensen ◽  
E. B. Pedersen
Keyword(s):  
Sodium Excretion ◽  
Sodium Intake ◽  
Renal Hemodynamics ◽  
Dietary Sodium ◽  
High Sodium ◽  
High Sodium Intake ◽  
Healthy Humans ◽  
Low Sodium ◽  
Arterial Blood ◽  
Relative Decrease

Animal studies have indicated that increased nitric oxide (NO) synthesis plays a significant role in the renal adaptation to increased sodium intake. To investigate the role of NO during increased sodium intake in humans, we studied the effect of acute, systemic injection of N G-monomethyl-l-arginine (l-NMMA) on renal hemodynamics [glomerular filtration rate and renal plasma flow (GFR and RPF, respectively)], urinary sodium excretion (FENa), systemic hemodynamics [mean arterial blood pressure and heart rate (MAP and HR)], and plasma levels of several vasoactive hormones in 12 healthy subjects during high (250 mmol/day) and low (77 mmol/day) sodium intake in a crossover design. The sodium diets were administered for 5 days before the l-NMMA treatments, in randomized order, with a washout period of 9 days between each diet and l-NMMA treatment. GFR and RPF were measured using the renal clearance of51Cr-labeled EDTA and125I-labeled hippuran by the constant infusion technique in clearance periods of 30-min duration. Two baseline periods were obtained, after whichl-NMMA was given (3 mg/kg over 10 min), and the effect of treatment was followed over the next five clearance periods. During high sodium intake,l-NMMA induced a more pronounced relative decrease in RPF ( P = 0.0417, ANOVA), a more pronounced relative decrease in FENa( P = 0.0032, ANOVA), and a more pronounced relative increase in MAP ( P= 0.0231, ANOVA). During low sodium intake, the effect ofl-NMMA on FENa was abolished. During low sodium intake, l-NMMA induced a sustained drop in plasma renin (31 ± 5 vs. 25 ± 5 μU/ml, P < 0.001), which was not seen during high sodium intake. The data indicate that increased production of NO is an important part of the adaptation to increased dietary sodium intake in healthy humans, with respect to renal hemodynamics, sodium excretion, and the secretion of renin.

Hemodynamic and neuroendocrine responses to changes in sodium intake in compensated heart failure

2006 ◽  
Vol 290 (5) ◽  
pp. R1294-R1301 ◽  
Author(s):  
Morten Damgaard ◽  
Peter Norsk ◽  
Finn Gustafsson ◽  
Jørgen K. Kanters ◽  
Niels Juel Christensen ◽  
...  
Keyword(s):  
Heart Failure ◽  
Water Retention ◽  
Sodium Intake ◽  
Plasma Concentrations ◽  
Volume Index ◽  
Bicycle Exercise ◽  
High Sodium ◽  
Sodium Diet ◽  
High Sodium Intake ◽  
Neuroendocrine Responses

Patients with untreated heart failure (HF) exhibit a blunted hemodynamic and neuroendocrine response to a high sodium intake, leading to excessive sodium and water retention. However, it is not known whether this is the case for patients with compensated HF receiving angiotensin-converting enzyme inhibitors and β-adrenoreceptor blockers. Therefore, we determined the hemodynamic and neuroendocrine responses to 1 wk of a low-sodium diet (70 mmol/day) and 1 wk of a high-sodium diet (250 mmol/day) in 12 HF patients and 12 age-matched controls in a randomized, balanced fashion. During steady-state conditions, hemodynamic and neuroendocrine examinations were performed at rest and during bicycle exercise. In seated HF patients, high sodium intake increased body weight (1.6 ± 0.4%), plasma volume (9 ± 2%), cardiac index (14 ± 6%), and stroke volume index (21 ± 5%), whereas mean arterial pressure was unchanged. Therefore, the total peripheral resistance decreased by 10 ± 4%. Similar hemodynamic changes were observed during an incremental bicycle exercise test. Plasma concentrations of angiotensin II and norepinephrine were suppressed, whereas plasma pro-B-type natriuretic peptide remained unchanged. In conclusion, high sodium intake was tolerated without any excessive sodium and water retention in medically treated patients with compensated HF. The observation that high sodium intake improves cardiac performance, induces peripheral vasodilatation, and suppresses the release of vasoconstrictor hormones does not support the advice for HF patients to restrict dietary sodium.

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