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.

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.

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

2000 ◽  
Vol 98 (4) ◽  
pp. 495 ◽  
Author(s):  
Leonardo CENTONZA ◽  
Giovanna CASTOLDI ◽  
Roberto CHIANCA ◽  
Giuseppe BUSCA ◽  
Raffaello GOLIN ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Short Term ◽  
Normotensive Subjects ◽  
The Relationship ◽  
Term Analysis

Effect of Urodilatin Infusion on Renal Haemodynamics, Tubular Function and Vasoactive Hormones

1997 ◽  
Vol 92 (4) ◽  
pp. 397-407 ◽  
Author(s):  
JAN Carstens ◽  
Kaare T. Jensen ◽  
Erling B. Pedersen
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Distal Part ◽  
Renal Haemodynamics ◽  
Sodium Reabsorption ◽  
Lithium Clearance ◽  
Short Term

1. The renal efficacy of urodilatin in humans has only been partly investigated. It is unknown whether intravenously infused urodilatin has an effect on sodium reabsorption in both the proximal and distal part of the nephron. 2. Twelve healthy subjects participated in this double-blind, placebo-controlled study in a crossover design. They received, in a randomized order, a short term (60 min) infusion of urodilatin in three different doses (10, 20 and 40 ng min−1 kg−1 of body weight) and placebo. Renal haemodynamics were estimated by clearance technique with radioactive tracers, and proximal tubular handling of sodium was evaluated by lithium clearance. 3. The 20 ng min−1 kg−1 dose increased the urinary sodium excretion and urinary flow rate compared with the effects of placebo. It increased the glomerular filtration rate and decreased the effective renal plasma flow. In addition, the dose increased the lithium clearance compared with placebo, but did not significantly change the fractional excretion of lithium. On the other hand, it markedly decreased the distal fractional reabsorption of sodium. It also had a suppressive effect on renin secretion. The systemic arterial blood pressure was unchanged, but the dose increased the pulse rate and the haematocrit. The highest dose (40 ng min−1 kg−1) induced a wide variation in the natriuretic and diuretic responses, probably due to a blood-pressure-lowering effect. 4. We conclude, that the urodilatin dose of 20 ng min−1 kg−1 of body weight was most efficacious in this short-term infusion study, and that it had potent natriuretic and diuretic qualities, probably due to stimulation of the glomerular filtration rate and inhibition of sodium reabsorption in the distal part of the nephron.

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 386: A Novel Aquaretic and Glomerular Filtration Rate Enhancing Peptide Without Vascular Vasodilatory Actions in Experimental CHF.

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Horng H Chen ◽  
ShuChong Pan ◽  
John C Burnett ◽  
Robert D Simari
Keyword(s):  
Blood Pressure ◽  
Amino Acids ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Urinary Sodium Excretion ◽  
Sodium Concentration ◽  
Water Excretion ◽  
Arterial Blood ◽  
Change In Mean

BACKGROUND: BNP is a cardiac peptide with vasodilatory, natriuretic and diuretic properties. Recent studies have suggested that its vasodilatory hypotensive properties may limit the renal actions of BNP, especially in patients with borderline low blood pressure. We have recently identified an alternatively spliced transcript for BNP (ASBNP) that includes a unique and distinct longer carboxyl-terminus consisting of 34 amino acids. Based upon preliminary studies, we generated a truncated form (ASBNP2.1) that contains the first 16 amino acids of the C-terminal of ASBNP. METHODS: We determined the cardiorenal and humoral actions of intravenous infusion of ASBNP2.1 at 2 pmol/Kg/min, 10 pmol/Kg/min and 100 pmol/Kg /min in 10 dogs with rapid ventricular pacing induced overt CHF (240 bpm for 10 days). * p<0.05 RESULTS: IV infusion of ASBNP 2.1 increased aquaresis (from 0.19±0.04 to 0.32±0.07, 0.46±0.11 and 0.39±0.09 ml/min*) without a significant change in urinary sodium excretion. Importantly, ASBNP 2.1 enhanced glomerular filtration rate (GFR), from 31±4 to 47±8, 69±10 and 56±9 ml/min*. These renal actions were associated with increases in urinary BNP*, ANP* and cGMP* excretion. BNP 2.1 did not have any systemic vasodilatory action resulting in no change in mean arterial blood pressure or cardiac-filling pressures even at the highest dose. There was not change in serum sodium concentration. CONCLUSION: We report for the first time that this novel peptide based upon ASBNP has potent aquaretic and GFR enhancing actions without the vasodilatory hypotensive properties in an experimental model of overt CHF. The lack of vasodilatation but with renal actions also suggest that the C-terminus plays a key role in the vascular actions of this peptide offering new insights into vascular-renal structure function of BNP and related peptides. This renal specific peptide may have potential therapeutic benefit in states of renal dysfunction with volume overload to enhance GFR and water excretion without the detrimental side effect of hypotension.

scholarly journals Cardiorenal Effects of Long‐Term Phosphodiesterase V Inhibition in Pre–Heart Failure

2022 ◽  
Author(s):  
Scott A. Hubers ◽  
Siu‐Hin Wan ◽  
Fadi W. Adel ◽  
Sherry L. Benike ◽  
John C. Burnett ◽  
...  
Keyword(s):  
Heart Failure ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Clearance ◽  
Filtration Rate ◽  
Urinary Sodium ◽  
Short Term ◽  
Renal Response ◽  
Clearance Study

Background Phosphodiesterase V (PDEV) is upregulated in heart failure, leading to increased degradation of cGMP and impaired natriuresis. PDEV inhibition improves the renal response to B‐type natriuretic peptide in animal models. We tested the hypothesis that long‐term PDEV inhibition would improve renal function and cardiorenal response after short‐term volume load in subjects with pre–heart failure. Methods and Results A total of 20 subjects with pre–heart failure (defined as an ejection fraction ≤45% without previous diagnosis of heart failure) and renal impairment were randomized in a 2:1 manner to tadalafil or placebo. Baseline echocardiography and renal clearance study were performed, followed by a short‐term saline load and repeated echocardiography and renal clearance study. Subjects then received either tadalafil at a goal dose of 20 mg daily or placebo, and the study day was repeated after 12 weeks. Long‐term tadalafil did not improve glomerular filtration rate (median increase of 2.0 mL/min in the tadalafil group versus 13.5 mL/min in the placebo group; P =0.54). There was no difference in urinary sodium or cGMP excretion with PDEV inhibition following short‐term saline loading. Conclusions Glomerular filtration rate and urinary sodium/cGMP excretion were not significantly different after 12 weeks of tadalafil compared with placebo. These results do not support the use of PDEV inhibition to improve renal response in patients with pre–heart failure. Registration URL: https://www.clinicaltrials.gov ; Unique identifier: NCT01970176.

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