Studies on the Mechanism of Sodium Excretion in Uraemia

1972 ◽  
Vol 42 (6) ◽  
pp. 711-723 ◽  
Author(s):  
R. Wilkinson ◽  
J. A. Luetscher ◽  
A. J. Dowdy ◽  
C. Gonzales ◽  
G. W. Nokes
Keyword(s):  
Blood Pressure ◽  
Glomerular Filtration Rate ◽  
Creatinine Clearance ◽  
Glomerular Filtration ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Plasma Renin ◽  
Sodium Depletion ◽  
Sodium Loading ◽  
Arteriolar Tone

1. A group of eight patients with advanced renal failure, and a creatinine clearance of 3·8–24 ml/min, were subjected to sodium loading and sodium depletion. 2. With sodium loading there was a consistent increase in blood pressure (0·01 < P <0·02), an increase in creatinine clearance that was significantly related to changes in mean arterial pressure (r = +0·3, 001 < P < 0·02); an increase in urinary sodium excretion that was closely correlated with changes in creatinine clearance (r = +0·82, P < 0·001); a decrease in fractional reabsorption of filtered sodium that was inversely proportional to creatinine clearance (r = −0·63, 0·05< P < 0·1). 3. Fractional reabsorption of filtered sodium was proportional to creatinine clearance both in the sodium-loaded (r = +0·86, 0·001 < P < 0·01) and sodium-depleted states (r = +0·92, 0·001 < P < 0·01). 4. Urinary aldosterone excretion and plasma renin activity consistently increased with sodium depletion, the percentage increases of the two being significantly related (r = +0·95, P < 0·001). 5. The results suggest that excretion of a sodium load in uraemia may be effected in part as the result of a raised blood pressure that elevates the glomerular filtration rate; by increasing the peritubular capillary pressure this may be responsible for the observed decrease in reabsorption of filtered sodium. The responsiveness of glomerular filtration rate to blood pressure changes suggests a decrease in afferent arteriolar tone that may account for the increased sodium excretion per nephron which occurs even in uraemic patients without hypertension. 6. It is suggested that aldosterone may continue to play an important regulatory role in sodium homeostasis in uraemia and that renin concentrations are the major determinants of aldosterone production in uraemia.

CNS-induced natriuresis and renal hemodynamics in conscious rats

1983 ◽  
Vol 245 (6) ◽  
pp. F763-F771 ◽  
Author(s):  
D. Beasley ◽  
R. L. Malvin ◽  
D. R. Mouw
Keyword(s):  
Blood Pressure ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Antidiuretic Hormone ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Plasma Renin ◽  
Renal Nerve ◽  
Natriuretic Hormone ◽  
Renal Nerve Activity

Sodium excretion was studied following experimental elevation of cerebrospinal fluid (CSF) sodium in heterozygous and homozygous (DI) Brattleboro rats given exogeneous antidiuretic hormone. Sodium excretion increased 4.5-fold in heterozygous and 3.5-fold in DI rats. The natriuresis in both groups was rapid in onset and occurred with a simultaneous kaliuresis. Blood pressure increased approximately 10 mmHg in the heterozygous but not in the DI rats. Accordingly, increased blood pressure may contribute to the natriuresis but is not the sole mechanism. Plasma renin concentration did not change in the DI rats during high Na CSF infusion, and chronic bilateral renal denervation did not abolish the natriuresis. Glomerular filtration rate increased during the high Na period in both the intact and renally denervated rats. These data provide evidence that a natriuretic mechanism exists that is not mediated by changes in antidiuretic hormone, renal nerve activity, mean arterial pressure, aldosterone, or angiotensin II, and thus may be due to another circulating substance or natriuretic hormone. This hormone may act totally or in part by increasing glomerular filtration rate.

Short-term analysis of the relationship between blood pressure and urinary sodium excretion in normotensive subjects

2000 ◽  
Vol 98 (4) ◽  
pp. 495-500 ◽  
Author(s):  
Leonardo CENTONZA ◽  
Giovanna CASTOLDI ◽  
Roberto CHIANCA ◽  
Giuseppe BUSCA ◽  
Raffaello GOLIN ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Short Term ◽  
Quiet Wakefulness ◽  
Normotensive Subjects

The aim of this study was to investigate whether, in the short term, physiological blood pressure changes are coupled with changes in urinary sodium excretion in normotensive subjects, maintained at fixed sodium intake and under controlled postural and behavioural conditions. Twelve normotensive subjects were recruited. For each subject, seven urine samples were collected at fixed time intervals during an overall 26 h period: late afternoon (16.00–20.00 hours), evening (20.00–24.00 hours), night (24.00–06.00 hours), quiet wakefulness (06.00–09.00 hours), morning (09.00–12.00 hours), post-prandial (12.00–15.00 hours) and afternoon (15.00–18.00 hours). Blood pressure was monitored by an ambulatory blood pressure device during the whole 26 h period. Each urine sample was used to measure urinary sodium excretion and glomerular filtration rate (creatinine clearance). Blood pressure, heart rate, urinary sodium excretion and glomerular filtration rate recorded in the daytime were higher than those measured during the night-time. A significant positive correlation between mean blood pressure and urinary sodium excretion was found during the night, over the whole 26 h period, and during two subperiods of the daytime: quiet wakefulness and the post-prandial period. The coefficient of the pressure–natriuresis curve was significantly decreased by postural changes. We conclude that, in normotensive subjects, blood pressure and urinary sodium excretion are coupled in the short term. The assumption of an upright posture can mask this relationship, presumably by activating neurohumoral factors.

Endothelin Excretion in Hypertensive Pregnancy: Relationship to Glomerular Filtration Rate, Blood Pressure, and Sodium Excretion

1994 ◽  
Vol 7 (4 Pt 1) ◽  
pp. 308-313 ◽  
Author(s):  
M.-X. Wang ◽  
M. A. Brown ◽  
M. L. Buddie ◽  
M. A. Carlton ◽  
G. M. Cario ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Hypertensive Pregnancy

Abstract P047: Relation of Body Mass Index to Creatinine Clearance and Glomerular Filtration Rate in Japanese Population Samples in Japan and Hawaii

Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Naomi Kitano ◽  
Katsuyuki Miura ◽  
Akira Okayama ◽  
Hideaki Nakagawa ◽  
Kiyomi Sakata ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Body Mass Index ◽  
Glomerular Filtration Rate ◽  
Creatinine Clearance ◽  
Glomerular Filtration ◽  
Body Mass ◽  
Filtration Rate ◽  
Urine Volume ◽  
Total Serum ◽  
Central Laboratory

Background: Obesity is an established risk factor for hypertension and end stage kidney disease. There is little information on how obesity relates to risk of impaired renal function in apparently healthy individuals. We investigated associations of body mass index (BMI) with timed 24-hour creatinine clearance (Ccr) and glomerular filtration rate (GFR) in the cross-sectional population-based INTERLIPID Study, ancillary study of the International Study on Macro- and Micro-Nutrients and Blood Pressure (INTERMAP). Methods: INTERLIPID participants ages 40-59 y from 5 INTERMAP research samples (4 Japanese and 1 Hawaiian) were investigated. Participants were ethnically all Japanese. Two timed 24-hour urine specimens were collected by each participant and analyses were performed in a central laboratory. Values of serum creatinine (Scr) were assayed by Jaffe’s method in a Japanese central laboratory. Data were analyzed from 1,338 Japanese, 570 men and 563 women in Japan, 100 men and 105 women in Hawaii. Measures of kidney function were 24-hour Ccr (ml/min) and GFR (ml/min/1.73m 2 ). Ccr was calculated by equation (urine creatinine х urine volume)/(Scr х 1440); GFR was calculated as Ccr х (1.73/body surface area (BSA)). BSA was estimated by the DuBois formula. In addition, estimated GFR (eGFR) was calculated by use of the Modification of Diet in Renal Disease (MDRD) Study equation, 186 х Scr -1.154 х age -0.203 х 0.742 (if female). All statistical analyses were stratified by gender. Adjusted mean values of Ccr, GFR, and eGFR in quartiles of BMI were estimated using analysis of covariance. Model 1 was adjusted for age; model 2, for age and urine volume; model 3 for variables in model 2 plus blood pressure, pulse rate, physical activity, smoking habit, alcohol consumption, urinary sodium excretion, HbA1c, and total serum cholesterol. Results: Ccr (mean (SD)) were 107.5 (18.9) in men in Japan, 91.9 (17.0) in women in Japan, 123.4 (25.1) in men in Hawaii, and 98.5 (20.3) in women in Hawaii. BMI quartile ranges were in men Q1 16.8-22.3, Q2 22.3-24.1, Q3 24.1-26.1, and Q4 26.1-42.9; in women Q1 15.9-21.2, Q2 21.2-23.0, Q3 23.0-25.1, and Q4 25.1-47.0. In men, BMI was positively related to multivariate-adjusted Ccr and GFR ( P for trend across BMI quartiles <0.001 and <0.001, respectively), however, multivariate-adjusted eGFR was inversely associated with BMI ( P for trend 0.001). In women, BMI was positively related to multivariate-adjusted Ccr ( P for trend across BMI quartiles <0.001); multivariate-adjusted GFR and eGFR were not significantly associated with BMI. Interactions between age and BMI were not significant in men or women. Conclusions: These results indicate that excess BMI may lead to higher Ccr, and that the MDRD equation may underestimate GFR in middle-aged overweight or obese Japanese men.

Natriuresis Following Fourth Ventricle Perfusion with High-sodium Artificial CSF

1975 ◽  
Vol 53 (3) ◽  
pp. 363-367 ◽  
Author(s):  
S. S. Passo ◽  
J. R. Thornborough ◽  
A. B. Rothballer
Keyword(s):  
Blood Pressure ◽  
Cerebrospinal Fluid ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Sodium Excretion ◽  
Fourth Ventricle ◽  
Filtration Rate ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
High Sodium

Perfusion of the fourth cerebral ventricle with high-sodium artificial cerebrospinal fluid was found to result in an increase in urinary sodium excretion in anesthetized cats. The natriuresis was accompanied by an increase in blood pressure and glomerular filtration rate. However, in animals with the changes in blood pressure and glomerular filtration rate prevented by alpha-adrenergic blockade (phenoxybenzamine), the increase in urinary sodium excretion persisted. The data suggest the presence of a neural mechanism in the vicinity of the fourth ventricle sensitive to cerebrospinal fluid sodium levels and capable of affecting urinary sodium excretion independent of changes in blood pressure or glomerular filtration rate. The possible role of the area postrema and adjacent medulla is considered.

Effect of a kinin antagonist on renal function and haemodynamics during alterations in sodium balance in conscious normotensive rats

1990 ◽  
Vol 78 (2) ◽  
pp. 165-168 ◽  
Author(s):  
Paolo Madeddu ◽  
Nicola Glorioso ◽  
Aldo Soro ◽  
Paolo Manunta ◽  
Chiara Troffa ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Sodium Intake ◽  
Urinary Sodium Excretion

1. To evaluate whether sodium intake can modulate the action of endogenous kinins on renal function and haemodynamics, a receptor antagonist of bradykinin was infused in conscious normotensive rats maintained on either a normal or a low sodium diet. 2. The antagonist inhibited the hypotensive effect of exogenously administered bradykinin. It did not change the vasodepressor effect of acetylcholine, dopamine or prostaglandin E2. 3. The antagonist did not affect mean blood pressure, glomerular filtration rate, renal blood flow or urinary sodium excretion, in rats on sodium restriction. It did not change mean blood pressure, glomerular filtration rate or urinary sodium excretion, but decreased renal blood flow, in rats on a normal sodium intake. 4. The kallikrein–kinin system has a role in the regulation of renal blood flow in rats on a normal sodium diet.

Studies on the Mechanism of Hypernatriuresis in Essential Hypertension in Relation to Measurements of Plasma Renin Concentration, Body Fluid Compartments and Renal Function

1971 ◽  
Vol 41 (3) ◽  
pp. 219-231 ◽  
Author(s):  
M. A. D. H. Schalekamp ◽  
X. H. Krauss ◽  
M. P. A. Schalekamp-Kuyken ◽  
G. Kolsters ◽  
W. H. Birkenhäger
Keyword(s):  
Cardiac Output ◽  
Glomerular Filtration Rate ◽  
Essential Hypertension ◽  
Arterial Pressure ◽  
Glomerular Filtration ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Plasma Renin ◽  
Plasma Renin Concentration ◽  
Intrarenal Pressure

1. In twenty-two patients representing different stages of benign essential hypertension, hyperosmotic saline was administered intravenously. Determinations of intra-arterial pressure, renal plasma flow, glomerular filtration rate and plasma renin concentration were carried out before and, in the majority, also during and after saline infusion. Changes in cardiac output were followed in ten patients. Plasma volume and extracellular volume were determined in the control period only, although haemodilution was assessed by haematocrit readings. 2. Excess of sodium excretion showed a wide range and was related to the patient's age, as well as to a set of parameters reflecting intrarenal pressure patterns; hypernatriuresis consistently occurred in older patients, in whom renal vascular resistance and nitration fraction were elevated and plasma renin was suppressed. It could not be clarified whether hypernatriuresis together with renin suppression were determined by intrarenal pressure relationships or by an independent age-related factor in the hypertensive patient. 3. Excess of sodium excretion was not related to increments in arterial pressure, cardiac output, renal blood flow or glomerular filtration rate. 4. Plasma renin concentration failed to show consistent changes after hyperosmotic saline infusion. 5. It is concluded that natriuresis is not mediated by changes in the activity of the renin-angiotensin system. Hypernatriuresis appears to be a feature of progressive benign hypertension.

Effects of small C-ANF receptor ligands on plasma levels of atrial natriuretic factor, blood pressure, and renal function in the rat

1991 ◽  
Vol 69 (10) ◽  
pp. 1561-1566 ◽  
Author(s):  
Juraj Okolicany ◽  
Glenn A. McEnroe ◽  
Lisa C. Gregory ◽  
John A. Lewicki ◽  
Thomas Maack
Keyword(s):  
Blood Pressure ◽  
Amino Acids ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Plasma Levels ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Recovery Period ◽  
Receptor Ligands ◽  
Arterial Blood

In this article, after a very brief review on ANF receptors, we report our study on the effects of small C-ANF receptor ligands in the rat. Two small ligands were synthesized: 2-napthoxyacetyl-isonipecotyl-rANF 11–15-NH2 (5 aa), containing 5 amino acids; and Ala7-rANF 8–17-NH2 (10 aa), containing 10 amino acids from the ring structure of ANF 1–28. After control periods, 5 aa or 10 aa were infused i.v. at a dose of 10 μg∙min−1∙kg−1 body weight for 70 min in anesthetized rats, followed by a 60-min recovery period. The 5 aa and 10 aa peptides significantly and reversibly increased plasma levels of endogenous immunoreactive ANF by 106 ± 29 and 52 ± 24 pg/mL, respectively. Infusion of the 5 aa peptide significantly decreased mean arterial blood pressure from 113 ± 1 to 100 ± 3 mmHg (1 mmHg = 133.32 Pa) and increased glomerular filtration rate from 1.6 ± 0.2 to 2.3 ± 0.2 mL/min, sodium excretion from 0.6 ± 0.3 to 3.4 ± 0.4 μmol/min, and potassium excretion from 0.5 ± 0.2 to 1.2 ± 0.2 μmol/min. Similar results were obtained with the 10 aa peptide. The effects of both peptides on blood pressure and sodium excretion persisted throughout the recovery period. The results confirm and extend previous observations showing that C-ANF receptors mediate the removal of ANF from the circulation. The shortening of the minimal peptide length necessary to bind to C-ANF receptors markedly enhances the possibility of developing orally active C-ANF receptor ligands for the treatment of cardiovascular and renal diseases.Key words: C-ANF receptors, linear atrial peptides, glomerular filtration rate, natriuresis, kaliuresis.

scholarly journals Knockout of Macula Densa Neuronal Nitric Oxide Synthase Increases Blood Pressure in db/db Mice

Hypertension ◽  
2021 ◽  
Author(s):  
Jie Zhang ◽  
Ximing Wang ◽  
Yu Cui ◽  
Shan Jiang ◽  
Jin Wei ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Leptin Receptor ◽  
Macula Densa ◽  
Glomerular Hyperfiltration ◽  
No Production

Hypertension is a common comorbid condition in patients with diabetes. The pathogenesis of hypertension in diabetes has not been fully clarified. Primary tubular hyperreabsorption may contribute, which may be counteracted by glomerular hyperfiltration in the early diabetic kidney. In this study, we hypothesize that in early diabetes, the macula densa neuronal nitric oxide synthase (NOS1)-derived nitric oxide (NO) production is enhanced, which blunts tubuloglomerular feedback (TGF) response, promotes glomerular hyperfiltration, and maintains normal blood pressure; conversely, insufficient NO generation by the macula densa induces hypertension by lowering glomerular filtration rate and thus inhibiting natriuresis. To test this hypothesis, we examined the changes of macula densa NOS1 expression and phosphorylation as well as NO production, TGF response, glomerular filtration rate, sodium excretion, and blood pressure in a murine model of leptin receptor-deficient (db/db) diabetes with or without macula densa-specific NOS1 deletion. We found that db/db mice presented reduced fractional renal sodium excretion and only a small increase in blood pressure, associated with upregulated expression and activity of macula densa NOS1, inhibited TGF response, and glomerular hyperfiltration. Genetic knockout of macula densa NOS1 restored the TGF response and attenuated glomerular hyperfiltration in db/db mice but also further reduced fractional renal sodium excretion and substantially increased blood pressure. In conclusion, the present study demonstrates that in the early stage of leptin receptor-deficient diabetes, the upregulation of macula densa NOS1 inhibits TGF and increases glomerular filtration rate, which counteracts renal sodium retention and limits the rise in blood pressure.

Effect of brain-stem stimulation on renal function

1960 ◽  
Vol 198 (6) ◽  
pp. 1291-1295 ◽  
Author(s):  
Burton L. Wise ◽  
William F. Ganong
Keyword(s):  
Blood Pressure ◽  
Glomerular Filtration Rate ◽  
Creatinine Clearance ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Renal Denervation ◽  
Area Postrema ◽  
Urine Volume ◽  
Systemic Blood Pressure ◽  
Stimulation Of

The effect of stimulation of the hypothalamus, midbrain, pons and medulla oblongata on renal excretion of water, sodium and potassium and on glomerular filtration rate has been determined in 26 pentobarbital anesthetized dogs with chronically implanted electrodes. The effect of renal denervation on the stimulation responses has been determined in 12 animals. Stimulation of 15 points in the dorsal medulla just lateral to the mid-line led to a rise in blood pressure and an associated fall in creatinine clearance and urine volume. The renal changes were blocked by renal denervation. Stimulation of six points located in and near the area postrema led to a rise in creatinine clearance and urine volume without a significant change in systemic blood pressure. Stimulation of two points in the pons led to increases in sodium excretion without a detectable change in glomerular filtration rate. Stimulation of three points in the midbrain led to a decrease in creatinine clearance, but stimulation of 39 points elsewhere in the medulla, pons, midbrain and posterior hypothalamus had no effect on glomerular filtration rate and water and electrolyte excretion, even though changes in blood pressure did occur with some of these stimuli.

Sign in / Sign up

Export Citation Format

Share Document