Normotensive sodium loading in normal man: regulation of renin secretion during β-receptor blockade

2009 ◽  
Vol 296 (2) ◽  
pp. R436-R445 ◽  
Author(s):  
Simon Mølstrøm ◽  
Nils H. Larsen ◽  
Jane A. Simonsen ◽  
Remon Washington ◽  
Peter Bie
Keyword(s):  
Arterial Pressure ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Venous Pressure ◽  
Macula Densa ◽  
Renin Secretion ◽  
Sodium Reabsorption ◽  
Plasma Sodium ◽  
Adrenergic Blockade ◽  
Saline Loading

Saline administration may change renin-angiotensin-aldosterone system (RAAS) activity and sodium excretion at constant mean arterial pressure (MAP). We hypothesized that such responses are elicited mainly by renal sympathetic nerve activity by β1-receptors (β1-RSNA), and tested the hypothesis by studying RAAS and renal excretion during slow saline loading at constant plasma sodium concentration (Na+ loading; 12 μmol Na+·kg−1·min−1 for 4 h). Normal subjects were studied on low-sodium intake with and without β1-adrenergic blockade by metoprolol. Metoprolol per se reduced RAAS activity as expected. Na+ loading decreased plasma renin concentration (PRC) by one-third, plasma ANG II by one-half, and plasma aldosterone by two-thirds (all P < 0.05); surprisingly, these changes were found without, as well as during, acute metoprolol administration. Concomitantly, sodium excretion increased indistinguishably with and without metoprolol (16 ± 2 to 71 ± 14 μmol/min; 13 ± 2 to 55 ± 13 μmol/min, respectively). Na+ loading did not increase plasma atrial natriuretic peptide, glomerular filtration rate (GFR by 51Cr-EDTA), MAP, or cardiac output (CO by impedance cardiography), but increased central venous pressure (CVP) by ∼2.0 mmHg ( P < 0.05). During Na+ loading, sodium excretion increased with CVP at an average slope of 7 μmol·min−1·mmHg−1. Concomitantly, plasma vasopressin decreased by 30–40% ( P < 0.05). In conclusion, β1-adrenoceptor blockade affects neither the acute saline-mediated deactivation of RAAS nor the associated natriuretic response, and the RAAS response to modest saline loading seems independent of changes in MAP, CO, GFR, β1-mediated effects of norepinephrine, and ANP. Unexpectedly, the results do not allow assessment of the relative importance of RAAS-dependent and -independent regulation of renal sodium excretion. The results are compatible with the notion that at constant arterial pressure, a volume receptor elicited reduction in RSNA via receptors other than β1-adrenoceptors, decreases renal tubular sodium reabsorption proximal to the macula densa leading to increased NaCl concentration at the macula densa, and subsequent inhibition of renin secretion.

Osmoregulatory control of renal sodium excretion after sodium loading in humans

1998 ◽  
Vol 275 (6) ◽  
pp. R1833-R1842 ◽  
Author(s):  
Lars Juel Andersen ◽  
Peter Norsk ◽  
Lars Bo Johansen ◽  
Poul Christensen ◽  
Thomas Engstrøm ◽  
...  
Keyword(s):  
Central Venous Pressure ◽  
Sodium Excretion ◽  
Salt Intake ◽  
Sodium Intake ◽  
Venous Pressure ◽  
Sodium Balance ◽  
Plasma Sodium ◽  
Central Venous ◽  
Salt Loading ◽  
Significant Difference

The hypothesis that renal sodium handling is controlled by changes in plasma sodium concentration was tested in seated volunteers. A standard salt load (3.08 mmol/kg body wt over 120 min) was administered as 0.9% saline (Isot) or as 5% saline (Hypr) after 4 days of constant sodium intake of 75 (LoNa+) or 300 mmol/day (HiNa+). Hypr increased plasma sodium by ∼4 mmol/l but increased plasma volume and central venous pressure significantly less than Isot irrespective of diet. After LoNa+, Hypr induced a smaller increase in sodium excretion than Isot (48 ± 8 vs. 110 ± 17 μmol/min). However, after HiNa+the corresponding natriureses were identical (135 ± 33 vs. 139 ± 39 μmol/min), despite significant difference between the increases in central venous pressure. Decreases in plasma ANG II concentrations of 23–52% were inversely related to sodium excretion. Mean arterial pressure, plasma oxytocin and atrial natriuretic peptide concentrations, and urinary excretion rates of endothelin-1 and urodilatin remained unchanged. The results indicate that an increase in plasma sodium may contribute to the natriuresis of salt loading when salt intake is high, supporting the hypothesis that osmostimulated natriuresis is dependent on sodium balance in normal seated humans.

Effects of hypoproteinemia on renal hemodynamics, arterial pressure, and fluid volume

1987 ◽  
Vol 252 (1) ◽  
pp. F91-F98
Author(s):  
R. D. Manning
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Renal Plasma Flow ◽  
Urinary Sodium Excretion ◽  
Renal Hemodynamics ◽  
Fluid Volume ◽  
Urinary Sodium ◽  
Plasma Aldosterone Concentration

The effects of long-term hypoproteinemia on renal hemodynamics, arterial pressure, and fluid volume were studied in eight conscious dogs over a 34-day period. Plasma protein concentration (PPC) was decreased by daily plasmapheresis, and the effects of decreasing and increasing sodium intake were measured. By the 12th day of plasmapheresis, during which sodium intake was 30 meq/day, PPC had decreased to 2.5 g/dl from a control value of 7.2 g/dl, mean arterial pressure had decreased to 78% of control, glomerular filtration rate (GFR) was 75.2% of control, and urinary sodium excretion was decreased. By day 18 of plasmapheresis, estimated renal plasma flow (ERPF) was decreased to 60% of control due to the decreased arterial pressure and an increase in renal vascular resistance. Also, plasma renin activity and plasma aldosterone concentration were both increased, and the relationship between mean arterial pressure and urinary sodium excretion was distinctly shifted to the left along the arterial pressure axis. In contradistinction to acute experiments, chronic hypoproteinemia results in decreases in GFR, ERPF, and urinary sodium excretion and has marked effects on both fluid volume and arterial pressure regulation.

Cardiovascular and renal actions of C-type natriuretic peptide

1992 ◽  
Vol 262 (1) ◽  
pp. H308-H312 ◽  
Author(s):  
A. J. Stingo ◽  
A. L. Clavell ◽  
L. L. Aarhus ◽  
J. C. Burnett
Keyword(s):  
Arterial Pressure ◽  
Natriuretic Peptide ◽  
Sodium Excretion ◽  
Sodium Reabsorption ◽  
Bolus Administration ◽  
Systemic Hemodynamic ◽  
Biological Responses ◽  
Anesthetized Dogs ◽  
Group 2 ◽  
Group 1

Studies were performed in two groups of anesthetized dogs (n = 5 per group) to determine the cardiovascular and renal actions of synthetic C-type natriuretic peptide (CNP). Systemic infusion of CNP (group 1; 10 and 50 ng.kg-1.min-1 iv) resulted in marked cardiovascular hemodynamic effects characterized by a decrease in mean arterial pressure, cardiac output, and atrial pressures in association with a decrease in sodium excretion. Bolus administration of CNP (group 2; 5 micrograms/kg iv) to minimize cardiovascular hemodynamic changes resulted in only a transient decrease in arterial pressure. Sodium excretion decreased despite a return of arterial pressure to baseline. These biological responses were associated with increases in plasma guanosine 3',5'-cyclic monophosphate (cGMP) in both groups but with no change in urinary cGMP. With both systemic infusion or bolus administration of CNP, significant increases in plasma aldosterone were observed in association with increases in distal nephron sodium reabsorption. This study demonstrates that CNP exhibits profound systemic hemodynamic actions and is indirectly, or perhaps directly, antinatriuretic.

Plasma arginine vasopressin during neck suction in upright sitting man

1987 ◽  
Vol 114 (2) ◽  
pp. 243-248 ◽  
Author(s):  
P. Norsk ◽  
F. Bonde-Petersen ◽  
J. Warberg
Keyword(s):  
Arterial Pressure ◽  
Arginine Vasopressin ◽  
Venous Pressure ◽  
Haemoglobin Concentration ◽  
Plasma Osmolality ◽  
Systolic Arterial Pressure ◽  
Plasma Sodium ◽  
Fluid Restriction ◽  
Vasopressin Secretion ◽  
Plasma Arginine

Abstract. In order to examine the influence of carotid baroreceptor stimulation on arginine vasopressin secretion, 8 normal healthy males were subjected to static neck suction of −3.3 kPa for 20 min in the upright sitting position after overnight food and fluid restriction. The plasma concentration of arginine vasopressin did not change significantly during neck suction. However, in 3 subjects the termination of neck suction induced large increases in plasma arginine vasopressin from 1.8 to 63.7 ng/l, from 0.7 to 34.3 ng/l and from 2.1 to 19.0 ng/l, respectively. Two subjects experienced symptoms such as nausea and paleness during neck suction. Systolic arterial pressure increased slightly but significantly during neck suction from 15.3 ± 0.3 to 15.7 ± 0.4 kPa (N = 7, P < 0.05), whereas mean arterial pressure, diastolic arterial pressure, central venous pressure, heart rate, plasma osmolality, plasma sodium and potassium were unchanged. Haemoglobin concentration in blood and haematocrit increased significantly during and after neck suction, whereas plasma volume decreased. We conclude that neck suction with a negative pressure of 3.3 kPa in upright sitting man does not significantly affect plasma arginine vasopressin. However, termination of the stimulation induces large increases in some subjects. This may be explained by a direct effect on the vagus nerve or by a selective deloading of carotid baroreceptors.

Renal Function in Saline-Loaded Dogs with Minimal Sodium Excretion

1973 ◽  
Vol 51 (2) ◽  
pp. 148-152 ◽  
Author(s):  
Mortimer Levy ◽  
Earle A. Lockhart
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Sodium Excretion ◽  
Perfusion Pressure ◽  
Sodium Reabsorption ◽  
Sodium Retention ◽  
Arterial Blood ◽  
Saline Loading ◽  
Blood Pressure Fall ◽  
Pressure Fall

In this laboratory, dogs acutely saline-loaded to 7–8% body weight and treated with large doses of antidiuretic hormone and deoxycorticosterone acetate will excrete on the average 400–700 μequiv/min of sodium. We have been able to study five dogs, similarly treated, which for no apparent cause showed a trivial natriuretic response following comparable volume expansion. Postexpansion sodium excretion varied from 30 to 150 μequiv/min. Glomerular filtration rate and arterial blood pressure remained constant, but in each case p-aminohippurate clearance rate (CPAH) fell in response to acute saline loading. Renal vasodilatation with acetylcholine and elevation of perfusion pressure with noradrenaline reversed the sodium retention. Fractional reabsorption in the proximal tubule was normal, and the loop of Henle appeared to be the major nephron site responsible for the augmented sodium reabsorption. Constancy of arterial blood pressure, fall in CPAH, and response to altered intrarenal hemodynamics seem to characterize these saline-loaded dogs with minimal sodium excretion as a unique population.

Sodium Excretion in Man, and Adaptation to a Low-Sodium Diet: Effect of Intravenous Sodium Chloride

1979 ◽  
Vol 57 (3) ◽  
pp. 225-231 ◽  
Author(s):  
D. Gordon ◽  
W. S. Peart
Keyword(s):  
Sodium Chloride ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Plasma Sodium ◽  
Normal Male ◽  
Renal Sodium Excretion ◽  
Portal Monitor ◽  
Intravenous Sodium ◽  
Oral Sodium

1. The aim of this study was to test whether a postulated gastrointestinal or portal monitor of sodium intake plays any part in adjusting renal sodium excretion when dietary sodium is reduced. 2. Normal male subjects were given 50 mmol of sodium chloride intravenously three times daily for 3 days to replace or to supplement a constant oral intake of sodium chloride. 3. When oral sodium chloride was replaced with intravenous sodium chloride, renal sodium excretion remained constant. 4. When oral sodium chloride was kept constant, sodium administered as intravenous sodium chloride was promptly excreted in three out of four subjects. There was a delay in the increase in sodium excretion in the fourth subject. 5. Infusions containing 50 mmol of sodium chloride in 50 ml given intravenously over 22 min produced a rise in plasma sodium concentration and a fall in concentration of total plasma solids. 6. These results provide no evidence for a gastrointestinal or portal monitor of sodium intake, but do not disprove the existence of such a monitor.

Effects of a Body Cast on Aldosterone and Sodium Excretion in Dogs With Experimental Ascites

1958 ◽  
Vol 192 (3) ◽  
pp. 538-542 ◽  
Author(s):  
James O. Davis ◽  
Wilmot C. Ball
Keyword(s):  
Arterial Pressure ◽  
Sodium Excretion ◽  
Plasma Sodium ◽  
Abdominal Pressure ◽  
Aldosterone Secretion ◽  
Electrolyte Excretion ◽  
Sodium Potassium ◽  
Low Sodium ◽  
Sodium Loss ◽  
Body Cast

The effects of application of a plaster body cast upon aldosterone and sodium excretion were studied in eight dogs with experimental ascites. In association with an increase in intra-abdominal pressure, aldosterone output declined and sodium excretion increased. In three dogs net sodium loss occurred and in three animals the low sodium-potassium ratio of fecal electrolyte excretion characteristic of increased circulating aldosterone returned to normal. The increased sodium excretion was not attributable to elevated GFR as GFR was frequently unchanged or reduced. Furthermore, no consistent alterations in plasma sodium or potassium, T-1824 dye space in plasma or arterial pressure were detected. It is suggested that aldosterone secretion was decreased as a result of an increase in intra-abdominal pressure which inhibited filtration of fluid into the peritoneal cavity to form ascites.

Effects of α-adrenergic blockade on sodium excretion in normal and chronic salt retaining dogs

1976 ◽  
Vol 54 (3) ◽  
pp. 209-218 ◽  
Author(s):  
Shyan-Yih Chou ◽  
Paul H. Liebman ◽  
Leon F. Ferder ◽  
Daniel L. Levin ◽  
Roy J. Cacciaguida ◽  
...  
Keyword(s):  
Sodium Excretion ◽  
Urine Volume ◽  
Vena Cava ◽  
Free Water ◽  
Urinary Sodium Excretion ◽  
Blocking Agent ◽  
Major Effect ◽  
Sodium Reabsorption ◽  
Adrenergic Blockade ◽  
Free Water Clearance

The α-adrenergic blocking agent phenoxybenzamine (PBA) was administered intravenously (10 μg kg−1 min−1) during a steady state water diuresis under pentothal anesthesia to six normal dogs, six dogs with chronic thoracic inferior vena cava constriction and ascites (caval dogs) and seven dogs chronically salt depleted by sodium restriction and furosemide administration. In normal dogs urinary sodium excretion increased significantly from 265 ± 56 (SEM) to 370 ± 65 μequiv./min, whereas no increase in sodium excretion was noted in either caval dogs or salt depleted animals after PBA. In all three groups urine volume, fractional free water clearance and distal sodium load did not change significantly. In normal dogs, distal tubular sodium reabsorption decreased significantly from 73.4 ± 2.8% to 63.1 ± 4.0%, whereas no change was noted in caval or salt depleted dogs. Blood pressure and renal hemodynamics were not significantly altered by PBA administration in any group. These data demonstrate a natriuretic effect of α-adrenergic blockade in normal dogs with the major effect in the water clearing segment of the nephron. The absence of any effect in chronic caval or salt depleted dogs suggests that increased α-adrenergic activity does not play a significant role in the sodium retention of these animals.

Gastrointestinal osmoreceptors and renal sodium excretion in humans

2000 ◽  
Vol 278 (2) ◽  
pp. R287-R294 ◽  
Author(s):  
Lars Juel Andersen ◽  
Thomas Ulrik Skram Jensen ◽  
Morten Heiberg Bestle ◽  
Peter Bie
Keyword(s):  
Hypertonic Saline ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Extracellular Volume ◽  
Isotonic Saline ◽  
Plasma Sodium ◽  
Salt Loading ◽  
Water Loading ◽  
Renal Sodium Excretion ◽  
Stimulation Of

The hypothesis that natriuresis can be induced by stimulation of gastrointestinal osmoreceptors was tested in eight supine subjects on constant sodium intake (150 mmol NaCl/day). A sodium load equivalent to the amount contained in 10% of measured extracellular volume was administered by a nasogastric tube as isotonic or hypertonic saline (850 mM). In additional experiments, salt loading was replaced by oral water loading (3.5% of total body water). Plasma sodium concentration increased after hypertonic saline (+3.1 ± 0.7 mM), decreased after water loading (−3.8 ± 0.8 mM), and remained unchanged after isotonic saline. Oncotic pressure decreased by 9.4 ± 1.2, 3.7 ± 1.2, and 10.7 ± 1.3%, respectively. Isotonic saline induced an increase in renal sodium excretion (104 ± 15 to 406 ± 39 μmol/min) that was larger than seen with hypertonic saline (85 ± 15 to 325 ± 39 μmol/min) and water loading (88 ± 11 to 304 ± 28 μmol/min). Plasma ANG II decreased to 22 ± 6, 35 ± 6, and 47 ± 5% of baseline after isotonic saline, hypertonic saline, and water loading, respectively. Plasma atrial natriuretic peptide (ANP) concentrations and urinary excretion rates of endothelin-1 were unchanged. In conclusion, stimulation of osmoreceptors by intragastric infusion of hypertonic saline is not an important natriuretic stimulus in sodium-replete subjects. The natriuresis after intragastric salt loading was independent of ANP but can be explained by inhibition of the renin-angiotensin system.

Influence of the plasma protein concentration on renal function

1991 ◽  
Vol 80 (5) ◽  
pp. 427-433 ◽  
Author(s):  
Allan D. Cumming ◽  
Adam Linton
Keyword(s):  
Renal Function ◽  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Plasma Protein ◽  
Sodium Excretion ◽  
Protein Concentration ◽  
Experimental Studies ◽  
Plasma Osmolality ◽  
Sodium Reabsorption ◽  
Plasma Protein Concentration

1. The effect of the plasma protein concentration on renal function remains controversial. Most, but not all, experimental studies suggest that a reduced plasma protein concentration perfusing the kidney may reduce tubular sodium reabsorption. Hypoproteinaemic disease states are usually associated with sodium retention, which is not always volume-dependent. 2. We induced a 21% and 24% reduction in plasma total protein and plasma albumin, respectively, in unanaesthetized sheep by acute extracorporeal plasmapheresis. Arterial pressure did not change, and changes in circulatory volume were minimised by infusion of crystalloid to maintain pulmonary artery occlusion pressure, measured using a Swann-Ganz pulmonary artery catheter. 3. After plasmapheresis, there was no significant change in creatinine clearance, sodium excretion, plasma renin activity or urinary kallikrein excretion. 4. After plasmapheresis, there was a significant reduction in plasma osmolality, increase in urine osmolality and fall in free water clearance. 5. The results suggest that in the absence of detectable changes in circulating volume or arterial pressure, acute hypoproteinaemia is associated with significant changes in renal water handling, but has no direct effect on sodium excretion or on renal release of renin and kallikrein.

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