Abnormal diurnal urinary sodium and water excretion in diabetic autonomic neuropathy

1987 ◽  
Vol 73 (3) ◽  
pp. 259-265 ◽  
Author(s):  
G. M. Bell ◽  
W. Reid ◽  
D. J. Ewing ◽  
A. D. Cumming ◽  
M. L. Watson ◽  
...  
Keyword(s):  
Autonomic Neuropathy ◽  
Sodium Excretion ◽  
Urine Output ◽  
Urine Volume ◽  
Urinary Sodium ◽  
Diabetic Patients ◽  
Urinary Kallikrein ◽  
Diurnal Patterns ◽  
Urinary Kallikrein Excretion ◽  
Sodium And Potassium

1. Diurnal patterns of urine output and sodium and potassium excretion were studied in 10 diabetic patients with and 10 without autonomic neuropathy, and in 10 normal subjects. 2. The diurnal patterns of excretion in the diabetic patients with autonomic neuropathy differed significantly from the two other groups, as a smaller proportion of the 24 h output of urine, sodium and potassium was excreted during the day and a larger proportion was excreted at night. 3. Similar changes were noted in the diurnal patterns of urinary kallikrein excretion in diabetic patients with autonomic neuropathy, and urinary kallikrein output correlated significantly with urine volume but not with urinary sodium excretion. 4. The diurnal patterns of excretion of urinary prostaglandin E2 and 6-keto-PGF1α were not significantly different in diabetic patients with autonomic neuropathy. 5. Nocturia was a common complaint in this group, and the number of nocturnal voidings correlated with night urine volume. There was no evidence of premature bladder emptying. 6. The changes observed in the day/night urine output and sodium excretion could not be explained by glycosuria, insulin regimens, impaired renal function or abnormal diurnal prostaglandin excretion; their possible relevance to the diurnal changes of urinary kallikrein excretion is discussed.

Amiloride inhibits the rise of urinary kallikrein excretion induced by frusemide administration in the rat

1987 ◽  
Vol 72 (4) ◽  
pp. 449-454 ◽  
Author(s):  
L. F. O. Obika ◽  
M. MARIN-GREZ
Keyword(s):  
Continuous Infusion ◽  
Sodium Excretion ◽  
Regression Line ◽  
Urine Volume ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Urinary Kallikrein ◽  
Sprague Dawley ◽  
Urinary Kallikrein Excretion ◽  
Urinary Potassium

1. The effect of amiloride administration on the urinary kallikrein response to the injection or continuous infusion of frusemide in normal Sprague–Dawley rats was investigated. 2. Injections of frusemide induced repeatedly an increase in urinary kallikrein excretion. This effect was suppressed by amiloride. Amiloride also blocked the response to mannitol injection. A continuous infusion of frusemide lasting 100 min also induced an increase in urinary kallikrein excretion which persisted throughout the experiment. This response was completely blocked by the injection of amiloride. 3. Urinary kallikrein excretion was directly and positively related to urine volume and urinary sodium excretion before and after amiloride injection. The regression lines had markedly decreased slopes after amiloride administration. The urinary kallikrein excretion was also positively related to the urine volume and urinary sodium excretion when frusemide was continuously infused. However, these relationships were abolished after amiloride injection. 4. In both the injection and the infusion experiments, there was a direct relationship of urinary kallikrein excretion to urinary potassium excretion. Although this relationship persisted after amiloride injection, the regression line was shifted to the left. 5. The suppression of the kallikrein stimulating effect of frusemide by the sodium channel blocker amiloride indicates that distal tubule sodium re-absorption is the triggering factor in urinary kallikrein excretion. The study suggests that the mechanism involved in the release of kallikrein by the distal tubular cells is linked to the renal mechanism affected by amiloride.

Urinary kallikrein response to repeated frusemide injections in rats: Effect of adrenalectomy and deoxycorticosterone acetate treatment

1986 ◽  
Vol 71 (5) ◽  
pp. 497-503 ◽  
Author(s):  
L. F. O. Obika ◽  
M. Marin-Grez
Keyword(s):  
Urine Volume ◽  
Urinary Kallikrein ◽  
Deoxycorticosterone Acetate ◽  
Intravenous Injections ◽  
Urinary Kallikrein Excretion ◽  
Mineralocorticoid Activity ◽  
Sodium And Potassium ◽  
Adrenalectomized Rats

1. The effect of repeated intravenous injections of frusemide (0.17 mg/kg) on the urinary kallikrein excretion of normal, adrenalectomized and deoxycorticosterone acetate (D0CA)-treated adrenalectomized rats was studied. 2. Adrenalectomy decreased baseline urinary kallikrein excretion, while DOCA treatment restored it to normal. 3. Frusemide injections repeatedly increased urinary kallikrein excretion in the three groups of rats studied. Compared with control and DOCA-treated animals, adrenalectomized rats were less responsive. 4. The excretion of urinary kallikrein was positively correlated with urine volume and with the excretion of sodium and potassium in all groups. The regression lines were shifted to the left in DOCA-treated adrenalectomized rats showing that mineralocorticoids enhance the effect of frusemide on urinary kallikrein excretion. The regression lines between urinary kallikrein excretion and the measured variables in adrenalectomized rats did not differ from those of control animals. 5. We conclude that the response of urinary kallikrein to frusemide is influenced by the level of mineralocorticoid activity. The effect of frusemide on urinary kallikrein excretion does not appear to be a ‘wash-out’ of the enzyme since its influence did not subside after repeated injections.

scholarly journals Association between 24-h urinary sodium and potassium excretion and blood pressure among Chinese adults aged 18–69 years

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Xiaofu Du ◽  
Le Fang ◽  
Jianwei Xu ◽  
Xiangyu Chen ◽  
Yamin Bai ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Inverse Association ◽  
Potassium Excretion ◽  
Chinese Adults ◽  
Potassium Intake ◽  
Sodium And Potassium

AbstractThe direction and magnitude of the association between sodium and potassium excretion and blood pressure (BP) may differ depending on the characteristics of the study participant or the intake assessment method. Our objective was to assess the relationship between BP, hypertension and 24-h urinary sodium and potassium excretion among Chinese adults. A total of 1424 provincially representative Chinese residents aged 18 to 69 years participated in a cross-sectional survey in 2017 that included demographic data, physical measurements and 24-h urine collection. In this study, the average 24-h urinary sodium and potassium excretion and sodium-to-potassium ratio were 3811.4 mg/day, 1449.3 mg/day, and 4.9, respectively. After multivariable adjustment, each 1000 mg difference in 24-h urinary sodium excretion was significantly associated with systolic BP (0.64 mm Hg; 95% confidence interval [CI] 0.05–1.24) and diastolic BP (0.45 mm Hg; 95% CI 0.08–0.81), and each 1000 mg difference in 24-h urinary potassium excretion was inversely associated with systolic BP (− 3.07 mm Hg; 95% CI − 4.57 to − 1.57) and diastolic BP (− 0.94 mm Hg; 95% CI − 1.87 to − 0.02). The sodium-to-potassium ratio was significantly associated with systolic BP (0.78 mm Hg; 95% CI 0.42–1.13) and diastolic BP (0.31 mm Hg; 95% CI 0.10–0.53) per 1-unit increase. These associations were mainly driven by the hypertensive group. Those with a sodium intake above about 4900 mg/24 h or with a potassium intake below about 1000 mg/24 h had a higher risk of hypertension. At higher but not lower levels of 24-h urinary sodium excretion, potassium can better blunt the sodium-BP relationship. The adjusted odds ratios (ORs) of hypertension in the highest quartile compared with the lowest quartile of excretion were 0.54 (95% CI 0.35–0.84) for potassium and 1.71 (95% CI 1.16–2.51) for the sodium-to-potassium ratio, while the corresponding OR for sodium was not significant (OR, 1.28; 95% CI 0.83–1.98). Our results showed that the sodium intake was significantly associated with BP among hypertensive patients and the inverse association between potassium intake and BP was stronger and involved a larger fraction of the population, especially those with a potassium intake below 1000 mg/24 h should probably increase their potassium intake.

scholarly journals Joint association of urinary sodium and potassium excretion with cardiovascular events and mortality: prospective cohort study

BMJ ◽  
2019 ◽  
pp. l772 ◽  
Author(s):  
Martin O’Donnell ◽  
Andrew Mente ◽  
Sumathy Rangarajan ◽  
Matthew J McQueen ◽  
Neil O’Leary ◽  
...  
Keyword(s):  
Urinary Excretion ◽  
Sodium Excretion ◽  
Cardiovascular Events ◽  
Sodium Intake ◽  
Urinary Sodium ◽  
Potassium Excretion ◽  
High Potassium ◽  
High Sodium ◽  
Low Sodium ◽  
Sodium And Potassium

AbstractObjectiveTo evaluate the joint association of sodium and potassium urinary excretion (as surrogate measures of intake) with cardiovascular events and mortality, in the context of current World Health Organization recommendations for daily intake (<2.0 g sodium, >3.5 g potassium) in adults.DesignInternational prospective cohort study.Setting18 high, middle, and low income countries, sampled from urban and rural communities.Participants103 570 people who provided morning fasting urine samples.Main outcome measuresAssociation of estimated 24 hour urinary sodium and potassium excretion (surrogates for intake) with all cause mortality and major cardiovascular events, using multivariable Cox regression. A six category variable for joint sodium and potassium was generated: sodium excretion (low (<3 g/day), moderate (3-5 g/day), and high (>5 g/day) sodium intakes) by potassium excretion (greater/equal or less than median 2.1 g/day).ResultsMean estimated sodium and potassium urinary excretion were 4.93 g/day and 2.12 g/day, respectively. After a median follow-up of 8.2 years, 7884 (6.1%) participants had died or experienced a major cardiovascular event. Increasing urinary sodium excretion was positively associated with increasing potassium excretion (unadjusted r=0.34), and only 0.002% had a concomitant urinary excretion of <2.0 g/day of sodium and >3.5 g/day of potassium. A J-shaped association was observed of sodium excretion and inverse association of potassium excretion with death and cardiovascular events. For joint sodium and potassium excretion categories, the lowest risk of death and cardiovascular events occurred in the group with moderate sodium excretion (3-5 g/day) and higher potassium excretion (21.9% of cohort). Compared with this reference group, the combinations of low potassium with low sodium excretion (hazard ratio 1.23, 1.11 to 1.37; 7.4% of cohort) and low potassium with high sodium excretion (1.21, 1.11 to 1.32; 13.8% of cohort) were associated with the highest risk, followed by low sodium excretion (1.19, 1.02 to 1.38; 3.3% of cohort) and high sodium excretion (1.10, 1.02 to 1.18; 29.6% of cohort) among those with potassium excretion greater than the median. Higher potassium excretion attenuated the increased cardiovascular risk associated with high sodium excretion (P for interaction=0.007).ConclusionsThese findings suggest that the simultaneous target of low sodium intake (<2 g/day) with high potassium intake (>3.5 g/day) is extremely uncommon. Combined moderate sodium intake (3-5 g/day) with high potassium intake is associated with the lowest risk of mortality and cardiovascular events.

Effects of the Fab fragment of digoxin antibody on the natriuresis and increase in blood pressure induced by intracerebroventricular infusion of hypertonic saline solution in rats

1992 ◽  
Vol 82 (6) ◽  
pp. 625-630 ◽  
Author(s):  
Kaoru YAMADA ◽  
Atsuo GOTO ◽  
Chen HUI ◽  
Noriko YAGI ◽  
Tsuneaki SUGIMOTO
Keyword(s):  
Blood Pressure ◽  
Cerebrospinal Fluid ◽  
Sodium Excretion ◽  
Urine Volume ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Minor Role ◽  
Fab Fragment ◽  
High Sodium ◽  
Intracerebroventricular Infusion

1. The effects of intravenous injection of Fab fragments of anti-digoxin IgG (Digibind) on the changes in blood pressure, urine volume and urinary sodium excretion after intracerebroventricular infusion of artificial cerebrospinal fluid with normal or high sodium concentration were examined in anaesthetized rats. 2. The biological efficacy of Digibind was confirmed by experiments in vitro and in vivo, which showed that pre-treatment with Digibind completely abolished or significantly attenuated the aortic contractile response or pressor response to digoxin in guinea-pigs. 3. Infusion of high-sodium cerebrospinal fluid, but not normal-sodium cerebrospinal fluid, into the lateral brain ventricle of rats caused marked increases in blood pressure, urine volume and urinary sodium excretion. 4. Digibind did not significantly affect the increases in blood pressure, urine volume and urinary sodium excretion caused by intracerebroventricular infusion of high-sodium cerebrospinal fluid. 5. Digoxin-like immunoreactive factor may play a minor role, if any, in central nervous system-induced natriuresis in rats.

Rhythmic changes in renal function in the rat

1965 ◽  
Vol 209 (6) ◽  
pp. 1187-1192 ◽  
Author(s):  
George A. Bray
Keyword(s):  
Renal Function ◽  
Cold Exposure ◽  
Sodium Excretion ◽  
Urine Output ◽  
Sodium Intake ◽  
Urine Volume ◽  
Potassium Excretion ◽  
Electrolyte Excretion ◽  
Threefold Increase ◽  
Electrolyte Intake

Cold exposure causes rats to increase their urine output. This increase in urine output was found to occur in 5- to 8-day cycles with peak urine volumes three or more times the volumes prior to exposure to the cold. Cycles in urine volume occurred on a constant electrolyte intake and in animals receiving exogenous Pitressin. The peaks in urine volume were accompanied by a threefold increase in the variability of sodium excretion but not potassium excretion. The increase in urine volume which occurred at the same time in all rats in a group began at night and continued through the following day. These data have been discussed in the light of a possible mechanism controlling sodium intake with water intake and electrolyte excretion.

scholarly journals Role of epoxyeicosatrienoic acids (EETs) in mediation of dopamine's effects in the kidney

2013 ◽  
Vol 305 (12) ◽  
pp. F1680-F1686 ◽  
Author(s):  
Ming-Zhi Zhang ◽  
Yinqiu Wang ◽  
Bing Yao ◽  
Leslie Gewin ◽  
Shouzuo Wei ◽  
...  
Keyword(s):  
Sodium Excretion ◽  
Urine Volume ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
High Salt ◽  
Epoxyeicosatrienoic Acids ◽  
Wild Type ◽  
Salt Diet ◽  
Low Salt ◽  
Renal Dopamine

We have recently demonstrated that intrarenal dopamine plays an important role in preventing the development of systemic hypertension. Similarly, renal cytochrome P-450 (CYP)-epoxygenase-derived arachidonic acid metabolites, epoxyeicosatrienoic acids (EETs), also are antihypertensive through inhibiting sodium reabsorption and vasodilation. The potential interaction between renal dopamine and epoxygenase systems was investigated. Catechol- O-methyl-transferase (COMT)−/− mice with increased intrarenal dopamine levels and proximal tubule deletion of aromatic amino acid decarboxylase (ptAADC−/−) mice with renal dopamine deficiency were treated with a low-salt diet or high-salt diet for 2 wk. Wild-type or Cyp2c44−/− mice were treated with gludopa, which selectively increased renal dopamine levels. In low salt-treated mice, urinary EET levels were related to renal dopamine levels, being highest in COMT−/− mice and lowest in ptAADC−/− mice. In high salt-treated mice, total EET and individual EET levels in both the kidney and urine were also highest in COMT−/− mice and lowest in ptAADC−/− mice. Selective increases in renal dopamine in response to gludopa administration led to marked increases in both total and all individual EET levels in the kidney without any changes in blood levels. qRT-PCR and immunoblotting indicated that gludopa increased renal Cyp2c44 mRNA and protein levels. Gludopa induced marked increases in urine volume and urinary sodium excretion in wild-type mice. In contrast, gludopa did not induce significant increases in urine volume or urinary sodium excretion in Cyp2c44−/− mice. These studies demonstrate that renal EET levels are maintained by intrarenal dopamine, and Cyp2c44-derived EETs play an important role in intrarenal dopamine-induced natriuresis and diuresis.

Altered expression of renal aquaporins and Na+ transporters in rats treated with L-type calcium blocker

2001 ◽  
Vol 280 (6) ◽  
pp. R1632-R1641 ◽  
Author(s):  
Weidong Wang ◽  
Tae-Hwan Kwon ◽  
Chunling Li ◽  
Allan Flyvbjerg ◽  
Mark A. Knepper ◽  
...  
Keyword(s):  
Proximal Tubule ◽  
Sodium Excretion ◽  
Urine Output ◽  
Collecting Duct ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Compensatory Mechanism ◽  
Thick Ascending Limb ◽  
Water Reabsorption ◽  
Altered Expression

Nifedipine, a calcium antagonist, has diuretic and natriuretic properties. However, the molecular mechanisms by which these effects are produced are poorly understood. We examined kidney abundance of aquaporins (AQP1, AQP2, and AQP3) and major sodium transporters [type 3 Na/H exchanger (NHE-3); type 2 Na-Pi cotransporter (NaPi-2); Na-K-ATPase; type 1 bumetanide-sensitive cotransporter (BSC-1); and thiazide-sensitive Na-Cl cotransporter (TSC)] as well as inner medullary abundance of AQP2, phosphorylated-AQP2 (p-AQP2), AQP3, and calcium-sensing receptor (CaR). Rats treated with nifedipine orally (700 mg/kg) for 19 days had a significant increase in urine output, whereas urinary osmolality and solute-free water reabsorption were markedly reduced. Consistent with this, immunoblotting revealed a significant decrease in the abundance of whole kidney AQP2 (47 ± 7% of control rats, P< 0.05) and in inner medullary AQP2 (60 ± 7%) as well as in p-AQP2 abundance (17 ± 6%) in nifedipine-treated rats. In contrast, whole kidney AQP3 abundance was significantly increased (219 ± 28%). Of potential importance in modulating AQP2 levels, the abundance of CaR in the inner medulla was significantly increased (295 ± 25%) in nifedipine-treated rats. Nifedipine treatment was also associated with increased urinary sodium excretion. Consistent with this, semiquantitative immunoblotting revealed significant reductions in the abundance of proximal tubule Na+ transporters: NHE-3 (3 ± 1%), NaPi-2 (53 ± 12%), and Na-K-ATPase (74 ± 5%). In contrast, the abundance of the distal tubule Na-Cl cotransporter (TSC) was markedly increased (240 ± 29%), whereas BSC-1 in the thick ascending limb was not altered. In conclusion, 1) increased urine output and reduced urinary concentration in nifedipine-treated-rats may, in part, be due to downregulation of AQP2 and p-AQP2 levels; 2) CaR might be involved in the regulation of water reabsorption in the inner medulla collecting duct; 3) reduced expression of proximal tubule Na+ transporters (NHE-3, NaPi-2, and Na, K-ATPase) may be involved in the increased urinary sodium excretion; and 4) increase in TSC expression may occur as a compensatory mechanism.

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