URINE VOLUME AND TOTAL RENAL SODIUM EXCRETION DURING WATER DIURESIS

1948 ◽  
Vol 28 (1) ◽  
pp. 28 ◽  
2001 ◽  
Vol 29 (2) ◽  
pp. 131-139 ◽  
Author(s):  
H Schierok ◽  
M Pairet ◽  
N Hauel ◽  
W Wienen

The present study investigated the effects of telmisartan, a selective AT1 receptor antagonist, on renal function in dogs. Conscious female dogs were treated with (i) vehicle (controls) and three doses of telmisartan (0.03 mg/kg, 0.1 mg/kg and 0.3 mg/kg) administered intravenously; (ii) vehicle and three doses of telmisartan (0.3 mg/kg, 1.0 mg/kg and 3.0 mg/kg) administered orally; or (iii) 1.0 mg/kg per day telmisartan orally for 12 days. Eight dogs were used for each experiment. Each of the four treatments in (i) and (ii) was administered 7 days apart. During the 6 h after intravenous administration, urine volume was significantly higher in dogs treated with telmisartan 0.1 mg/kg (8.5 ± 1.6 ml/kg) and 0.3 mg/kg (7.0 ± 0.9 ml/kg) than controls (2.7 ± 0.3 ml/kg; P < 0.05), and renal sodium excretion was increased significantly with telmisartan 0.03 mg/kg (803 ± 124 μmol/kg), 0.1 mg/kg (1039 ± 213 μmol/kg) and 0.3 mg/kg (966 ± 161 μmol/kg) versus controls (159 ± 21 μmol/kg; P < 0.05). Oral telmisartan at doses of 1.0 mg/kg and 3.0 mg/kg also produced significant increases in urine volume (7.2 ± 1.1 ml/kg and 6.6 ± 1.2 ml/kg, respectively) and renal sodium excretion (599 ± 146 μmol/kg and 555 ± 131 μmol/kg, respectively) compared with controls (2.8 ± 0.5 ml/kg and 80 ± 33 μmol/kg; P < 0.05) over the 6-h post-dose period. Telmisartan at all intravenous doses and at 3.0 mg/kg orally increased the urinary excretion of chloride significantly over the 6-h post-dose period compared with vehicle alone. The excretion of potassium and creatinine were unchanged by any treatment. Telmisartan 1.0 mg/kg administered orally for 12 days produced similar results. In conclusion, acute intravenous or oral as well as subchronic oral administration of telmisartan to conscious dogs promotes diuresis and natriuresis without affecting potassium or creatinine excretion.


Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Weili Wang ◽  
Wei-Qing Han ◽  
Qing Zhu ◽  
Imad Damaj ◽  
Pin-Lan Li ◽  
...  

Although there are extensive studies on the regulation of renal sodium excretion by adrenergic pathway, the role of cholinergic pathway in the renal sodium excretion is largely unknown. The present study characterized the expression of α7 nicotinic acetylcholine receptor (nAChR) in the kidneys and determined the functional role of this nAChR subtype in urinary sodium excretion in Sprague Dawley rats. RT-PCR and Western blot analyses showed that α7 nAChR was present in the kidneys. Immunohistochemistry analysis demonstrated that the strongest immunostaining of α7 nAChR was observed in the distal tubules and collecting ducts in the kidneys. Infusion of an α7 nAChR agonist PNU-282987 (2.7 μM, 10 μl/min) into the renal medulla dramatically increased the urine volume (from 15.4 ± 2.1 to 42.5 ± 3.9 μl/min/g kwt) and sodium excretion (from 1.26 ± 0.18 to 4.15 ± 0.60 μmole/min/g kwt), which was blocked by an α7 nAChR antagonist methyllycaconitine (MLA, 5 μM, 10 μl/min), in anesthetized rats. Infusion of PNU-282987 did not cause any change in renal medullary blood flow as measured by Laser Doppler flowmeter. In addition, intra-renal medullary infusion of MLA (5 μM, 10 μl/min) significantly inhibited the volume expansion-induced increase of urine volume and sodium excretion by 25%. These data suggest that activation of renal medullary α7 nAChR produces a natriuretic effect through its tubular action in rats. (Supported by NIH grant HL89563 and HL106042)


Hypertension ◽  
1992 ◽  
Vol 19 (1_Suppl) ◽  
pp. I78-I78 ◽  
Author(s):  
A. K. Gupta ◽  
R. V. Clark ◽  
K. A. Kirchner

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Edwin K Jackson ◽  
Zaichuan Mi

We previously reported that 8-aminoguanosine and 8-aminoguanine are potent and efficacious K + -sparing diuretics/natriuretics that may represent a new class of antihypertensive drugs. Moreover, because these compounds are endogenous, they may have physiological roles. It is possible that the diuretic/natriuretic activity of 8-aminoguanosine is mediated mostly via conversion to 8-aminoguanine. To test this concept, we conducted 3 protocols in anesthetized rats. The 1 st protocol demonstrated that at 85 to 115 min post intravenous administration, both 8-aminoguanosine and 8-aminoguanine (33.5 μmol/kg) significantly increased urine volume [ml/min: 8-aminoguanosine from 0.3 ± 0.1 to 0.9 ± 0.1 (mean ± SEM; n=7); 8-aminoguanine from 0.3 ± 0.1 to 1.5 ± 0.2 (n=8)] and sodium excretion (μmol/min: 8-aminoguanosine from 12 ± 6 to 109 ± 21; 8-aminoguanine from 18 ± 8 to 216 ± 31). The 2 nd protocol showed that intrarenal artery infusions of 8-aminoguanosine (from 0.1 to 1 μmol/kg/min) did not affect urine volume or sodium excretion in either the ipsilateral or contralateral kidney. In contrast, intrarenal artery infusions of 8-aminoguanine significantly increased ipsilateral (but not contralateral) urine volume [at 1 μmol/kg/min from 0.2 ± 0.02 to 0.7 ± 0.1 (n=17)] and sodium excretion (from 24 ± 4 to 216 ± 31). In a 3 rd protocol we administered 8-aminoguanosine and 8-aminoguanine intravenously (33.5 μmol/kg) and measured renal interstitial (medulla) levels of 8-aminoguanosine and 8-aminoguanine using microdialysis combined with ultraperformance liquid chromatography-tandem mass spectrometry. Intravenous administration of 8-aminoguanosine and 8-aminoguanine similarly increased renal interstitial levels of 8-aminoguanine [ng/ml; 8-aminoguanosine from 4 ± 1 to 1025 ± 393 (n=6), and 8-aminoguanine from 2 ± 1 to 1069 ± 407 (n=6)]. Neither 8-aminoguanosine nor 8-aminoguanine affected renal interstitial levels of 8-aminoguanosine. Together these data clearly show that the renal effects of 8-aminoguanosine are not direct, but require conversion in the systemic circulation to 8-aminoguanine. If 8-aminoguanosine is physiologically important it should be viewed as a “pro-hormone.” As a pharmacological agent, it is best described as a “pro-drug.”


1987 ◽  
Vol 252 (5) ◽  
pp. R1009-R1014 ◽  
Author(s):  
K. Matsui ◽  
T. Kimura ◽  
K. Ota ◽  
M. Shoji ◽  
M. Inoue ◽  
...  

A quantitative bioassay for the detection and quantification of atrial natriuretic polypeptides (ANPs) was developed in a pentobarbital-anesthetized rat. Ten percent mannitol in 0.9% saline was infused to achieve stable diuresis. The conductivity of the urine, urine flow, and blood pressure were continuously recorded. A bolus injection of synthetic alpha-human atrial natriuretic polypeptide (alpha-hANP) elicited dose-dependent increases in the urine conductivity, sodium excretion, and urine volume. Changes in the urine conductivity correlated significantly with the increase in sodium excretion. By use of changes in urine conductivity, biological ANP activity of crude rat atrial extract was determined. Atrial contents of ANP in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) were 25.5 +/- 1.2 microgram per atrium (n = 4) and 25.1 +/- 0.8 (n = 5) in euhydration. They were increased to 27.0 +/- 1.1 micrograms (n = 4) and 29.3 +/- 1.3 (n = 5, P less than 0.05), after 5-day water deprivation, respectively. This assay procedure provides a good tool for rapid and quantitative determination of ANPs.


1989 ◽  
Vol 77 (5) ◽  
pp. 509-514 ◽  
Author(s):  
J. S. Milledge ◽  
J. M. Beeley ◽  
S. McArthur ◽  
A. H. Morice

1. To investigate the mechanisms of acute mountain sickness, 22 subjects travelled to 3100 m by road and the following day walked to 4300 m on Mount Kenya. Control measurements were made over 2 days at 1300 m before ascent and for 2 days after arrival at 4300 m. These included body weight, 24 h urine volume, 24 h sodium and potassium excretion, blood haemoglobin, packed cell volume, and symptom score for acute mountain sickness. In 15 subjects blood samples were taken for assay of plasma aldosterone and atrial natriuretic peptide. 2. Altitude and the exercise in ascent resulted in a marked decrease in 24 h urine volume and sodium excretion. Aldosterone levels were elevated on the first day and atrial natriuretic peptide levels were higher on both altitude days compared with control. 3. Acute mountain sickness symptom scores showed a significant negative correlation with 24 h urinary sodium excretion on the first altitude day. Aldosterone levels tended to be lowest in subjects with low symptom scores and higher sodium excretion. No correlation was found between changes in haemoglobin concentration, packed cell volume, 24 h urine volume or body weight and acute mountain sickness symptom score. 4. Atrial natriuretic peptide levels at low altitude showed a significant inverse correlation with acute mountain sickness symptom scores on ascent.


1993 ◽  
Vol 75 (1) ◽  
pp. 349-356 ◽  
Author(s):  
P. Norsk ◽  
C. Stadeager ◽  
L. B. Johansen ◽  
J. Warberg ◽  
P. Bie ◽  
...  

On one day six male subjects underwent an upright seated (SEAT) study, and on another day they were subjected to a head-down tilt of 3 degrees (HDT). Compared with SEAT, HDT induced prompt increases in central venous pressure (CVP) from -0.5 +/- 0.8 to 8.3 +/- 0.3 mmHg (P < 0.001) and in arterial pulse pressure of 8–18 mmHg (P < 0.001). CVP stabilized after 6 h at levels 2.4–2.8 mmHg below the peak value. Simultaneously, renal sodium excretion gradually increased over the initial 5 h of HDT and stabilized at a level approximately 125 mumol/min over that of SEAT (P < 0.001). Urine flow rate and solute free water clearance increased during the initial 2–6 h of HDT (P < 0.001) but returned to the level of SEAT thereafter. We concluded that CVP is slightly reduced over 12 h of HDT and that a clear temporal dissociation exists between renal sodium and water handling. We suggest that the combined effect of the sustained suppressions of plasma renin activity and plasma aldosterone and norepinephrine concentrations constitutes a mechanism of the increase in renal sodium excretion.


2020 ◽  
Vol 9 (8) ◽  
pp. 2532
Author(s):  
Upeksha S. Alwis ◽  
Joris Delanghe ◽  
Lien Dossche ◽  
Johan Vande Walle ◽  
John Van Camp ◽  
...  

Urea is the most abundant and the largest contributing factor for urine osmolality. Urinary urea excretion is highly interrelated with dietary protein intake. Accordingly, an increase of urinary urea excretion due to high protein diet may lead to urea-induced osmotic diuresis. This study aims to explore the association between nocturnal polyuria (NP) and urea. This is a post hoc analysis of a prospective observational study of subjects who completed a renal function profile between October 2011 and February 2015 (n = 170). Each subject underwent a 24 h urine collection, which included 8 urine samples collected at 3 h intervals. Urine volume, osmolality, creatinine, urea and sodium were determined. Urinary urea excretion was used to estimate dietary protein intake. Compared to the control group, subjects with NP exhibited significantly higher nighttime urea and sodium excretion. Estimated evening dietary protein intake was correspondingly significantly higher amongst the NP subgroup. Nighttime diuresis rate was positively associated with age and nighttime free water clearance, creatinine clearance, sodium excretion, and urea excretion in NP subjects. Therefore, increased nocturnal urinary urea excretion may reflect an additional important mediator of nocturia owing to excess nocturnal urine production.


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