Sodium Homeostasis in Patients with Autonomic Failure

1977 ◽  
Vol 53 (4) ◽  
pp. 321-328 ◽  
Author(s):  
C. S. Wilcox ◽  
M. J. Aminoff ◽  
J. D. H. Slater
Keyword(s):  
Blood Pressure ◽  
Sodium Excretion ◽  
Autonomic Failure ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Sodium Balance ◽  
Control Group ◽  
Salt Restriction ◽  
Control Subjects ◽  
Autonomic Reflexes

1. The renal excretion of sodium by five patients with autonomic failure (Shy—Drager syndrome) was compared with a matched control group who had normal autonomic reflexes (Parkinson's disease). For 8 or 9 days the daily sodium intake was reduced to 17 mmol, and for 5 subsequent days it was increased to 189 mmol. 2. The sodium excretion of the patients with autonomic failure was not significantly reduced during 7 days of restricted intake whereas that of the control group fell rapidly to values comparable with their sodium intake. Patients with autonomic failure had a larger fall in body body weight than the control subjects. 3. Both lying and standing values of mean blood pressure fell during salt restriction in the patients with autonomic failure, but not in the control subjects. 4. Values of plasma renin activity (PRA) were significantly depressed in patients with autonomic failure. However, PRA rose to values similar to those of control subjects while standing during the period of restricted sodium intake. At this time the patients with autonomic failure had a large orthostatic fall in blood pressure and creatinine clearance. 5. Aldosterone secretion rates were measured in three patients with autonomic failure at both levels of sodium intake and were considerably lower than the rates found in the control group. 6. A mineralocorticoid drug (9α-fludrocortisone; 2 mg/day), given on the last 2 days of restricted sodium intake, failed to correct fully the negative sodium balance of the patients with autonomic failure, since an excessive sodium excretion persisted during the period of recumbency at night. 7. These results demonstrate a severe defect in renal salt conservation in certain patients with autonomic failure. They suggest that the defect may not be entirely due to deficient secretion of mineralocorticoid hormones.

Comparison of the Renin Response to Dopamine and Noradrenaline in Normal Subjects and Patients with Autonomic Insufficiency

1974 ◽  
Vol 46 (4) ◽  
pp. 481-488 ◽  
Author(s):  
C. S. Wilcox ◽  
M. J. Aminoff ◽  
A. B. Kurtz ◽  
J. D. H. Slater
Keyword(s):  
Autonomic Failure ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Control Groups ◽  
Autonomic Reflexes ◽  
Fractional Increase ◽  
The Mean ◽  
Autonomic Insufficiency ◽  
Stimulation Of

1. The effect on plasma renin activity (PRA) of dopamine and noradrenaline infusions was studied in three patients with Shy—Drager syndrome, three patients with Parkinson's disease and normal autonomic reflexes, and three healthy volunteers. The patients with the Shy—Drager syndrome had functional evidence of a peripheral lesion of the sympathetic nervous system and subnormal PRA on a controlled sodium intake. 2. In all subjects catecholamines were infused step-wise for 4 min until a 30% rise in systolic blood pressure occurred. 3. In each subject, PRA fell after noradrenaline but rose after dopamine. The mean fractional increase in PRA after dopamine was no less in the Shy—Drager patients than in the control groups. 4. The results suggest, first, that stimulation of dopamine receptors can release renin, and secondly, that inadequate renin stores cannot explain the low PRA found in our patients with autonomic failure.

Effects of Nifedipine during Low, Normal and High Intakes of Sodium in Patients with Essential Hypertension

1982 ◽  
Vol 63 (s8) ◽  
pp. 447s-450s ◽  
Author(s):  
Gloria Valdés ◽  
M. Eugenia Soto ◽  
Hector R. Croxatto ◽  
Teresa Bellolio ◽  
Ramón Corbalán ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Hypotensive Effect ◽  
Sodium Balance ◽  
Hypotensive Action ◽  
High Sodium ◽  
High Sodium Intake ◽  
Low Sodium Diet

1. Nifedipine (20 mg) was given by mouth to seven patients with moderate essential hypertension receiving a low, normal or high sodium intake. The drug produced an important hypotensive effect. Normal sodium intake enhanced the hypotensive action of the drug compared with that during the low and high sodium regimens. Blood pressure remained significantly lower 3 h after drug ingestion. 2. Increases in heart rate and plasma renin activity under all conditions reflected enhanced adrenergic activity. 3. A short-term natriuresis followed nifedipine ingestion in spite of increased aldosterone excretion during the low sodium diet and a decrease in urinary kallikrein during the low and high sodium diets. 4. Nifedipine increased urinary volume only during the high sodium intake. 5. Apart from vasodilatation, nifedipine induces important changes in neurogenic, renal and adrenal mechanisms that regulate blood pressure homoeostasis. Different conditions of sodium balance modulate most of these effects.

Role of renal nerves in maintaining sodium balance in unrestrained conscious rats

1985 ◽  
Vol 249 (6) ◽  
pp. F819-F826 ◽  
Author(s):  
E. Fernandez-Repollet ◽  
C. R. Silva-Netto ◽  
R. E. Colindres ◽  
C. W. Gottschalk
Keyword(s):  
Blood Pressure ◽  
Renal Denervation ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Renal Nerves ◽  
Sodium Restriction ◽  
Low Sodium ◽  
Dietary Sodium Restriction

This study was designed to investigate the effects of bilateral renal denervation on sodium and water balance, the renin-angiotensin system, and systemic blood pressure in unrestrained conscious rats maintained on a normal- or low-sodium diet. Renal denervation was proven by chemical and functional tests. Both bilaterally denervated rats (n = 18) and sham-denervated rats (n = 15) maintained positive sodium balance while on a normal sodium intake. Both groups were in negative sodium balance for 1 day after dietary sodium restriction was instituted but were in positive sodium balance for the following 9 days. Systolic blood pressure was higher in sham-denervated (115 +/- 3 mmHg) than in denervated rats (102 +/- 3 mmHg) while on a normal diet (P less than 0.05) and remained so during sodium restriction. Plasma renin concentration (PRC) and plasma aldosterone concentration (PAC) were significantly diminished in the denervated rats during normal sodium intake (P less than 0.05). After dietary sodium restriction, PRC increased in both groups but remained significantly lower in the denervated rats (P less than 0.05). Following dietary sodium restriction, PAC also increased significantly to levels that were similar in both groups of rats. These results demonstrate that awake unrestrained growing rats can maintain positive sodium balance on a low sodium intake even in the absence of the renal nerves. However, efferent renal nerve activity influenced plasma renin activity in these animals.

Inhibition of cGMP-specific phosphodiesterase type 5 reduces sodium excretion and arterial blood pressure in patients with NaCl retention and ascites

2005 ◽  
Vol 288 (5) ◽  
pp. F1044-F1052 ◽  
Author(s):  
Helle C. Thiesson ◽  
Boye L. Jensen ◽  
Bente Jespersen ◽  
Ove B. Schaffalitzky de Muckadell ◽  
Claus Bistrup ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Sodium Excretion ◽  
Plasma Concentrations ◽  
Plasma Renin ◽  
Sodium Balance ◽  
Ang Ii ◽  
Double Blind ◽  
Arterial Blood ◽  
Phosphodiesterase Type

In the present study, we tested the hypothesis that inhibition of renal phosphodiesterase type 5 (PDE5) in patients with liver cirrhosis and ascites increases sodium excretion. The effect of sildenafil citrate was studied in a randomized double-blind. placebo-controlled crossover study. Diuretics were withdrawn, and a fixed sodium diet (100 mmol/day) was given to the patients for 5 days before both study days. After a 60-min basal period, eight patients received either oral sildenafil (50 mg) or placebo. Glomerular filtration rate (GFR) and renal blood flow (RBF) were determined by 99mTc-diethylenetriamine-pentaacetate and 131I-hippuran clearances. In human nephrectomy specimens, PDE5 mRNA was expressed at similar levels in the cortex ( n = 6) and inner medulla ( n = 4). Histochemical staining showed PDE5 immunoreactivity in collecting ducts and vascular smooth muscle. At baseline, cirrhotic patients exhibited elevated plasma concentrations of ANP, renin, ANG II, and aldosterone that did not differ on the 2 study days. Basal sodium excretion was similar at the 2 study days (median 17 and 18 mmol, respectively), and patients were in positive sodium balance. Sildenafil increased heart rate, plasma renin activity, plasma ANG II, and aldosterone concentrations significantly after 60 min. Plasma cGMP concentration was increased after 120 and 180 min, and urinary sodium excretion and mean arterial blood pressure were decreased significantly at 120 and 180 min. Plasma ANP concentration, GFR, and RBF did not change after sildenafil. In patients with ascites and cirrhosis, inhibition of PDE5 did not promote natriuresis but led to increased plasma levels of the renin-angiotensin-aldosterone system.

Evidence that intrarenal bradykinin plays a role in regulation of renal function

1993 ◽  
Vol 265 (4) ◽  
pp. E648-E654 ◽  
Author(s):  
H. M. Siragy
Keyword(s):  
Renal Function ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Sodium Balance ◽  
Kinin System ◽  
Plasma Aldosterone Concentration ◽  
Low Sodium

Bradykinin (BK) is produced by the kidney, but the role of the renal kallikrein-kinin system (KKS) in the control of renal function is not understood. We studied the effects of intrarenal infusion of the BK antagonist, D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-Phe-Thi-Arg-trifluoroacetic acid (BKA, n = 5) and BK (n = 4) alone or combined with antagonist (BKA 0.025 ng.kg-1 x min-1 + BK 0.25 ng.kg-1 x min-1, n = 4) in uninephrectomized conscious dogs in sodium balance at 10 and 80 meq/day. During low sodium intake, administration of BKA (infusions from 0.025 to 2.5 ng.kg-1 x min-1) caused a significant antidiuresis (P < 0.0001) and antinatriuresis (P < 0.0001) and a decrease in fractional sodium excretion (P < 0.0001). There were no changes in estimated renal plasma flow (RPF) or glomerular filtration rate during intrarenal administration of BKA at 0.025 and 0.25 ng.kg-1 x min-1. A dose of 2.5 ng.kg-1 x min-1 BKA caused a significant decrease in RPF. There were no changes in plasma aldosterone concentration, plasma renin activity, or systemic arterial pressure during intrarenal BKA administration. At 80 meq/day sodium balance (n = 5), intrarenal administration of BKA did not cause any systemic or renal effects. Intrarenal administration of BK at 0.25 ng.kg-1 x min-1 during low sodium balance caused an increase in urine flow rate and urinary sodium excretion. Coinfusion of BK with BKA completely abrogated the renal excretory changes induced by BKA. These data suggest that intrarenal KKS plays a role in control of renal function largely by a tubular mechanism during low sodium intake.

Renal Haemodynamics and Plasma Renin in Patients with Essential Hypertension

1976 ◽  
Vol 50 (5) ◽  
pp. 409-414 ◽  
Author(s):  
E. B. Pedersen ◽  
H. J. Kornerup
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Vascular Resistance ◽  
Plasma Renin ◽  
Renal Vascular Resistance ◽  
Control Group ◽  
Hypertensive Patients ◽  
Control Subjects ◽  
Hypertensive Group ◽  
Renal Vascular

1. Blood pressure, glomerular filtration rate (GFR) and renal plasma flow (RPF) were measured in twenty-three patients with essential hypertension and in twenty-one control subjects. Plasma renin concentration was measured in all the hypertensive patients and in fifteen control subjects. 2. GFR and RPF were similar in the hypertensive group and in the control group, whereas the renal vascular resistance was significantly higher in the hypertensive patients. GFR and RPF decreased with increasing blood pressure in both groups. Increasing age induced a further reduction in GFR and RPF in the control subjects but not in the hypertensive patients. 3. Plasma renin concentration in the hypertensive group did not differ from that in the control subjects. The concentration was not correlated to age in either the hypertensive or normal group. 4. Plasma renin index was positively correlated to GFR and RPF and inversely correlated to filtration fraction and renal vascular resistance. 5. It is concluded that GFR and RPF depend on blood pressure in both hypertensive patients and normotensive control subjects. In contrast to the control group, the age effect was negligible in the hypertensive group. It is suggested that renin release depends on changes in renal vascular resistance in the arterioles at the glomerulus and the results support the baroreceptor theory of renin release.

Natriuretic Response to Head-Out Immersion in Humans with Recent Kidney Transplants

1993 ◽  
Vol 85 (4) ◽  
pp. 471-477 ◽  
Author(s):  
Ton J. Rabelink ◽  
Karin A. van Tilborg ◽  
Ronald J. Hené ◽  
Hein A. Koomans
Keyword(s):  
Plasma Renin Activity ◽  
Vascular Resistance ◽  
Sodium Excretion ◽  
Water Immersion ◽  
Plasma Renin ◽  
Renal Vascular Resistance ◽  
Renin Activity ◽  
Control Group ◽  
Control Subjects ◽  
Renal Vascular

1. Recently implanted kidneys may have decreased flexibility to adjust sodium excretion to volume challenges, since modulation by renal sympathetic nerve activity is absent. To examine this hypothesis, we studied the natriuretic response to head-out water immersion in eight patients with well-functioning renal allografts of 37 days (range 24–56 days), at a time when renal re-innervation has probably not occurred. 2. By the third hour of head-out water immersion, sodium excretion had increased equally in the patients (from 120 +21 to 204 +37 μmol/min) and in eight healthy control subjects (from 105 +9 to 191+19 μmol/min). 3. Glomerular filtration rate was 60 + 6 ml/min in the patients and 113 +6 ml/min in the control subjects, and did not change upon head-out water immersion. Estimated renal plasma flow increased upon head-out water immersion in the control group but not in the patients. Blood pressure decreased similarly in both groups. The renal vascular resistance, calculated from these data, decreased in response to head-out water immersion in the control subjects but not in the renal transplant patients. 4. Head-out water immersion suppressed plasma renin activity only in the normal group, whereas the plasma aldosterone level was suppressed in both groups. The natriuretic response in patients was associated with about 3-fold elevated plasma levels of atrial natriuretic peptide. 5. Since renal re-innervation at 37 days after transplantation is very unlikely, these data suggest that inact renal innervation is not mandatory for a normal natriuretic response to head-out water immersion in humans. However, sympathetic modulation might be involved in the decrease in renal vascular resistance and plasma renin activity normally observed during immersion.

scholarly journals Natriuretic effect of 2 weeks of dapagliflozin treatment in patients with type 2 diabetes and preserved kidney function: results of the DAPASALT trial

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
R Scholtes ◽  
M.H.A Muskiet ◽  
M.J.B Van Baar ◽  
P.J Greasley ◽  
C Karlsson ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Type 2 Diabetes ◽  
Steady State ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Sodium Balance ◽  
Funding Source ◽  
Treatment Change ◽  
Glucose Excretion

Abstract Background Sodium glucose co-transporter 2 (SGLT2) inhibitors reduce the risk for heart failure hospitalization, potentially by inducing sodium excretion, osmotic diuresis and plasma volume contraction, leading to more favorable systemic hemodynamic function. However, this hypothesis has never been formally investigated as no studies have assessed cumulative sodium excretion with SGLT2 inhibition during standardized sodium intake. Methods We conducted a mechanistic open label study in patients with type 2 diabetes mellitus (T2D) with preserved kidney function, who were receiving a standardized sodium intake (150 mmol/day) to evaluate the acute effects (average day 2–4), effects at steady state (average day 12–14) and effects during three days wash-out of dapagliflozin on sodium balance and blood pressure. Primary outcome measure was 24-hr sodium excretion during the acute phase. Secondary outcomes included 24-hr glucose excretion and 24-hr blood pressure at each time period and sodium excretion at steady state and during follow-up. Results Seventeen patients with T2D were enrolled (64.7% male, mean ± SD age 64.24±7.33 years, weight 99.54±17.36 kg, eGFR 94.53±10.10 mL/min/1.73m2, HbA1c 7.20±0.63%). Average sodium excretion at baseline was 147±32 mmol/24 hr, which did not significantly change during treatment (Change at day 2–4 [95% CI]: −5.21 [19.54, 9.12] mmol/24 hr; Change at Day 12–14 [95% CI]: 3.69 [−24.82, 32.20] mmol/24 hr). However, sodium excretion was reduced following washout compared to end of treatment (Change at Day 15–17 [95% CI]: −16.72 [−34.11, 0.66] mmol/24 hr). Glucose excretion was significantly increased throughout the study. Systolic blood pressure was 127.0±10.3 mmHg at baseline and significantly reduced at Day 3 [95% CI]: −5.27 [−8.55, −1.99] mmHg and Day 14 [95% CI]: −7.10 [−10.04, −4.16] mmHg compared to baseline and remained lower following washout. Conclusions This study shows that, during a standardized sodium intake, the SGLT-2 inhibitor dapagliflozin acutely reduces blood pressure without altering sodium excretion, indicating possible direct vascular effects independent of sodium balance. Funding Acknowledgement Type of funding source: Other. Main funding source(s): Astra Zeneca

Effect of cyclosporin on blood pressure and renin-aldosterone axis in rats

1987 ◽  
Vol 253 (6) ◽  
pp. H1596-H1600 ◽  
Author(s):  
S. Lustig ◽  
N. Stern ◽  
P. Eggena ◽  
M. L. Tuck ◽  
D. B. Lee
Keyword(s):  
Blood Pressure ◽  
Creatinine Clearance ◽  
Plasma Renin ◽  
Sodium Balance ◽  
Control Group ◽  
High Dose ◽  
Ang Ii ◽  
Aldosterone Secretion ◽  
Renin Substrate

Although hypertension is a frequent complication of cyclosporin A (CSA) therapy in clinical practice, little experimental information is available on the nature and the mechanism of this form of hypertension. We studied the effect of currently recommended therapeutic dosages of CSA, i.e., 5 (CSA5) and 20 (CSA20) mg.kg-1.day-1, on blood pressure and the renin-aldosterone system (RAS) in spontaneously hypertensive rats (SHR). Influence of in vivo CSA treatment on in vitro angiotensin II (ANG II)-stimulated aldosterone secretion by isolated adrenal glomerulosa cells (AGC) was also measured. CSA treatment in SHR resulted in a consistent increase in systolic blood pressure. This increase in blood pressure occurred in the absence of significant changes in creatinine clearance in CSA5 rats, whereas in CSA20 rats a significant reduction in creatinine clearance was observed. Sodium balance and serum calcium and magnesium concentrations were not different between the control group and either of the two CSA-treated groups of rats. Plasma renin concentration (PRC) and inactive renin (IR) were markedly elevated, but plasma renin substrate remained unchanged with CSA administration. Despite the presence of hyperreninemia, plasma aldosterone was not elevated, suggesting that CSA may induce relative adrenal resistance to ANG II. This possibility was tested using AGC isolated from CSA-treated rats. ANG II-stimulated aldosterone secretion in AGC was diminished by low dose and aborted by high dose CSA-treatment. Thus CSA administration in SHR induces a predictable increase in blood pressure in association with "hyperreninemic hypoaldosteronism."

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