Effect of Arterial Pressure and Inheritance on the Sodium Excretory Capacity of Normal Young Men

1978 ◽  
Vol 54 (6) ◽  
pp. 639-647 ◽  
Author(s):  
R. C. Wiggins ◽  
I. Basar ◽  
J. D. H. Slater
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sodium Excretion ◽  
Adult Sons ◽  
Isotonic Fluid ◽  
Renal Sodium Excretion ◽  
Fluid Load ◽  
Renal Sodium Handling ◽  
Highly Correlated ◽  
Sodium Handling

1. In normal young adult sons of normotensive parents the rate of renal sodium excretion is highly correlated with mean arterial pressure after a large intravenous isotonic fluid load. The correlation appeared to strengthen with time and was improved when the rate of sodium excretion was corrected for variations in the rate of glomerular filtration. 2. There was no such correlation in normal, age-matched sons of hypertensive parents. 3. In eight of the 20 normotensive sons of hypertensive parents studied, the rate of renal sodium excretion per unit of mean arterial pressure was significantly higher than in the sons of normotensive parents. 4. Because the sons of hypertensive parents are much more likely to become hypertensive than those of normotensive parents, we suggest that an abnormality of renal sodium handling precedes the development of demonstrable hypertension.

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.

Influence of the renal nerves on sodium excretion during progressive reductions in cardiac output

1995 ◽  
Vol 269 (3) ◽  
pp. R678-R690 ◽  
Author(s):  
T. E. Lohmeier ◽  
G. A. Reinhart ◽  
H. L. Mizelle ◽  
J. P. Montani ◽  
R. Hester ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Sodium Excretion ◽  
Pressure Control ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Renal Nerves ◽  
Sodium Retention

The purpose of this study was to elucidate the role of the renal nerves in promoting sodium retention during chronic reductions in cardiac output. In five dogs, the left kidney was denervated and the urinary bladder was surgically divided to allow separate 24-h urine collection from the innervated and denervated kidneys. Additionally, progressive reductions in cardiac output were achieved by employing an externally adjustable occluder around the pulmonary artery and by servo-controlling right atrial pressure (control = 0.9 +/- 0.2 mmHg) at 4.7 +/- 0.1, 7.5 +/- 0.1, and 9.8 +/- 0.2 mmHg for 3 days at each level. At the highest level of right atrial pressure, the 24-h values for mean arterial pressure (control = 97 +/- 3 mmHg) and cardiac output (control = 2,434 +/- 177 ml/min) were reduced approximately 25 and 55%, respectively; glomerular filtration rate fell by approximately 35% and renal plasma flow by approximately 65%. However, despite the sodium retention induced by these hemodynamic changes, there were no significant differences in renal hemodynamics or sodium excretion between the two kidneys during pulmonary artery constriction. In contrast, after release of the pulmonary artery occluder on day 9, sodium excretion increased more (approximately 28% during the initial 24 h) in innervated than in denervated kidneys. These results suggest that the renal nerves are relatively unimportant in promoting sodium retention in this model of low cardiac output but contribute significantly to the short-term elimination of sodium after partial restoration of cardiac output and mean arterial pressure.

[PP.30.05] BLOOD PRESSURE IN RELATION TO 24-HOUR URINARY SODIUM EXCRETION AND RENAL SODIUM HANDLING

2016 ◽  
Vol 34 ◽  
pp. e308
Author(s):  
K. Stolarz-Skrzypek ◽  
A. Bednarski ◽  
A. Franczyk ◽  
M. Folta ◽  
H. Barton ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Renal Sodium Handling ◽  
Sodium Handling

scholarly journals Effects of serelaxin on renal microcirculation in rats under control and high-angiotensin environments

2018 ◽  
Vol 314 (1) ◽  
pp. F70-F80 ◽  
Author(s):  
Weijian Shao ◽  
Carla B. Rosales ◽  
Camila Gonzalez ◽  
Minolfa C. Prieto ◽  
L. Gabriel Navar
Keyword(s):  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Excretion Rate ◽  
No Synthase ◽  
Urine Flow ◽  
Ang Ii ◽  
Afferent Arterioles

Serelaxin is a novel recombinant human relaxin-2 that has been investigated for the treatment of acute heart failure. However, its effects on renal function, especially on the renal microcirculation, remain incompletely characterized. Our immunoexpression studies localized RXFP1 receptors on vascular smooth muscle cells and endothelial cells of afferent arterioles and on principal cells of collecting ducts. Clearance experiments were performed in male and female normotensive rats and Ang II-infused male rats. Serelaxin increased mean arterial pressure slightly and significantly increased renal blood flow, urine flow, and sodium excretion rate. Group analysis of all serelaxin infusion experiments showed significant increases in GFR. During infusion with subthreshold levels of Ang II, serelaxin did not alter mean arterial pressure, renal blood flow, GFR, urine flow, or sodium excretion rate. Heart rates were elevated during serelaxin infusion alone (37 ± 5%) and in Ang II-infused rats (14 ± 2%). In studies using the in vitro isolated juxtamedullary nephron preparation, superfusion with serelaxin alone (40 ng/ml) significantly dilated afferent arterioles (10.8 ± 1.2 vs. 13.5 ± 1.1 µm) and efferent arterioles (9.9 ± 0.9 vs. 11.9 ± 1.0 µm). During Ang II superfusion, serelaxin did not alter afferent or efferent arteriolar diameters. During NO synthase inhibition (l-NNA), afferent arterioles also did not show any vasodilation during serelaxin infusion. In conclusion, serelaxin increased overall renal blood flow, urine flow, GFR, and sodium excretion and dilated the afferent and efferent arterioles in control conditions, but these effects were attenuated or prevented in the presence of exogenous Ang II and NO synthase inhibitors.

Neurohypophysial hormone influence on renal function in the New Zealand genetically hypertensive rat

1988 ◽  
Vol 118 (3) ◽  
pp. 422-428 ◽  
Author(s):  
N. Ashton ◽  
R. J. Balment
Keyword(s):  
Renal Function ◽  
New Zealand ◽  
Sodium Excretion ◽  
Urine Flow ◽  
Acute Effects ◽  
Hypertensive Rats ◽  
Renal Sodium Excretion ◽  
Hormone Influence ◽  
Sodium Handling ◽  
Genetically Hypertensive

Abstract. The acute effects of physiological levels of AVP and oxytocin administration on renal water and sodium handling have been investigated in New Zealand genetically hypertensive and normotensive rats. AVP infusion was associated with an antidiuresis in both normotensive and hypertensive rats and while normotensive rats also displayed a dose-related natriuresis, this was attenuated in hypertensive rats. Oxytocin administration had no effect on urine flow or sodium excretion in normotensive rats, but was associated with an antidiuresis in hypertensive rats. Combined hormone infusion produced a greater reduction in urine flow than following AVP alone in both normotensive and hypertensive groups and was associated with a potentiation of the natriuretic action of AVP in the hypertensive animals. The data suggest that the contribution of oxytocin to renal sodium excretion in hypertensive rats may be suppressed. A compensatory increase in basal AVP secretion in hypertensive rats may overcome their apparent renal insensitivity to AVP, to maintain appropriate sodium excretion. This intriguing disturbance in neurohypophysial function may reflect or possibly contribute to the hypertension of these animals.

Fibroblast growth factor 23 is associated with fractional excretion of sodium in patients with chronic kidney disease

2018 ◽  
Vol 34 (12) ◽  
pp. 2051-2057 ◽  
Author(s):  
Hong Xu ◽  
Ali Hashem ◽  
Anna Witasp ◽  
Rik Mencke ◽  
David Goldsmith ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Growth Factor ◽  
Sodium Excretion ◽  
Fibroblast Growth Factor 23 ◽  
Fractional Excretion ◽  
Urinary Sodium Excretion ◽  
Fibroblast Growth ◽  
Fractional Excretion Of Sodium ◽  
Renal Sodium Handling ◽  
Sodium Handling

Abstract Background Recent studies suggest that the phosphaturic hormone fibroblast growth factor 23 (FGF23) is involved in regulation of renal sodium excretion and blood pressure. There is evidence of both direct effects via regulation of the sodium-chloride symporter (NCC) in the distal tubule, and indirect effects through interactions with the renin–angiotensin–aldosterone system. However, clinical data on the association between FGF23 and renal sodium regulation is lacking. Herein, we investigated the associations of FGF23 with renal sodium handling and blood pressure in non-dialysis CKD patients. Methods This was a cross-sectional study encompassing 180 CKD patients Stage 1–5, undergoing renal biopsy. Plasma intact FGF23, 24-h urinary sodium excretion, fractional excretion of sodium (FENa) and blood pressure were measured at baseline. The association between FGF23 and renal sodium handling was explored by multivariate regression analysis. Results The median age was 52.8 years, 60.6% were men and the median estimated glomerular filtration rate (eGFR) was 50.6 mL/min/1.73 m2. In univariate analysis, FGF23 was positively associated with FENa (Spearman’s rho = 0.47; P < 0.001) and systolic blood pressure (rho = 0.17, P < 0.05), but not with plasma sodium, 24-h urinary sodium excretion or mean arterial blood pressure. The association between FGF23 and FENa remained significant after adjustment for potential confounders (multivariable adjusted β coefficient 0.60, P < 0.001). This association was stronger among the 107 individuals with eGFR <60 mL/min/1.73 m2 (β = 0.47, P = 0.04) and in the 73 individuals on any diuretics (β = 0.88, P < 0.001). Adjustment for measured GFR instead of eGFR did not alter the relationship. Conclusions FGF23 is independently associated with increased FENa in non-dialysis CKD patients. These data do not support the notion that FGF23 causes clinically significant sodium retention. Further studies are warranted to explore the mechanism underlying this association.

Verapamil prevents insulin antinatriuresis in euglycemic rats

1992 ◽  
Vol 262 (6) ◽  
pp. R1145-R1148 ◽  
Author(s):  
A. K. Gupta ◽  
R. Clark ◽  
K. A. Kirchner
Keyword(s):  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Calcium Entry ◽  
Urinary Sodium ◽  
Inulin Clearance ◽  
Insulin Administration ◽  
Lower Baseline

To determine whether calcium entry is necessary for insulin antinatriuresis, urinary sodium excretion was determined before and during euglycemic insulin administration in rats receiving verapamil (10 micrograms.kg-1.min-1) or vehicle. In vehicle rats, insulin reduced sodium excretion from 2.7 +/- 0.5 to 0.98 +/- 0.2 mu eq/min (P less than 0.05) without altering arterial pressure or inulin clearance. Insulin did not reduce sodium excretion in rats receiving verapamil. Baseline mean arterial pressure was lower in verapamil rats than in vehicle rats. To exclude the possibility that lower baseline arterial pressures prevented insulin antinatriuresis, insulin's effect on sodium excretion was determined in rats receiving captopril at a dose that reduced arterial pressure to the level observed in verapamil rats, and in verapamil rats with angiotensin II levels fixed to maintain arterial pressure equivalent to vehicle rats. In captopril rats, insulin reduced (P less than 0.05) sodium excretion from 1.07 +/- 0.3 to 0.3 +/- 0.01 mu eq/min, even though arterial pressure was not different from that in verapamil rats. Insulin failed to reduce sodium excretion in verapamil rats receiving angiotensin II. Thus verapamil prevents insulin antinatriuresis by renal mechanisms related to inhibition of calcium entry. Additionally, insulin antinatriuresis is independent of angiotensin II.

scholarly journals Renin Inhibition Improves Pressure Natriuresis in Essential Hypertension

2000 ◽  
Vol 11 (10) ◽  
pp. 1813-1818
Author(s):  
PIETER VAN PAASSEN ◽  
DICK DE ZEEUW ◽  
PAUL E. DE JONG ◽  
GERJAN NAVIS
Keyword(s):  
Essential Hypertension ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sodium Excretion ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Sodium Balance ◽  
Raas Blockade ◽  
Renin Inhibition ◽  
Pressure Natriuresis

Abstract. Pressure natriuresis (PN), i.e., a rise in renal sodium excretion in response to a higher BP, is involved in long-term BP regulation. PN is blunted in essential hypertension, but the mechanism is unknown. This study assessed the role of the renin-angiotensin-aldosterone system (RAAS) in PN in eight essential hypertensive men from the individual correlations between spontaneous fluctuations in BP and time corresponding changes in sodium excretion (collected at 2- and 4-h intervals for 48 h), during strict sodium balance, without treatment, and during renin inhibition (remikiren, 600 mg oral compound). Without treatment, daily values for mean arterial pressure were 109.5 ± 1.9 and 107 ± 1.9 mmHg, for urinary sodium excretion were 37.2 ± 2.8 and 42.0 ± 2.8 mmol/24 h, and for plasma renin activity were 2.34 ± 0.48 and 2.23 ± 0.44 nmol/L per h, respectively, for two consecutive days. During remikiren treatment, mean arterial pressure was 101.9 ± 1.7 and 100.8 ± 1.7 mmHg (P < 0.05, versus baseline). Urinary sodium excretion was 39.3 ± 3.7 and 45.2 ± 5.3 mmol/24 h (not significant versus baseline), and plasma renin activity was 0.79 ± 0.11 and 0.82 ± 0.13 nmol/L per h (P < 0.05 versus baseline). During remikiren treatment, BP correlated positively with sodium excretion in all patients but in only three of eight patients without treatment. The slope of the regression equation was steeper during remikiren treatment in seven of eight patients. Thus, the relationship between BP and natriuresis was more readily apparent during RAAS blockade, suggesting that RAAS activity blunts PN in hypertensive patients. Improved PN may contribute to the hypotensive effect of RAAS blockade and to maintenance of sodium balance at a lower BP level without volume expansion.

Effects of insulin and atrial natriuretic peptide on renal tubular sodium handling in sickle cell disease

2000 ◽  
Vol 278 (3) ◽  
pp. F499-F505 ◽  
Author(s):  
Jan C. ter Maaten ◽  
Erik H. Serné ◽  
Wim Statius van Eps ◽  
Pieter M. ter Wee ◽  
Ab J. M. Donker ◽  
...  
Keyword(s):  
Sickle Cell Disease ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Sodium Excretion ◽  
Low Dose ◽  
High Dose ◽  
Cell Disease ◽  
Control Subjects ◽  
Renal Sodium Handling ◽  
Sodium Handling

We assessed the effect of insulin and atrial natriuretic peptide (ANP) on renal sodium handling in eight patients with sickle cell disease (SCD), who are characterized by loss of vasa recta and long loops of Henle, and matched control subjects. During insulin infusion (50 mU ⋅ kg− 1 ⋅ h− 1), fractional sodium excretion decreased by 0.44 ± 0.72% ( P = 0.13) in patients with SCD and by 0.57 ± 0.34% ( P = 0.002) in control subjects, whereas fractional distal sodium reabsorption increased by 4.1 ± 1.5% ( P < 0.001) and 3.0 ± 1.5% ( P < 0.001), respectively. Low-dose (0.3 pmol ⋅ kg− 1 ⋅ h− 1) ANP infusion did not affect renal sodium handling in patients with SCD but increased fractional sodium excretion by 0.34 ± 0.22% ( P= 0.003) in control subjects. High-dose (2 μg/min) ANP increased natriuresis to a similar extent in both groups. Insulin's antinatriuretic effects predominated over the natriuretic effects of low-dose, but not high-dose, ANP. These data suggest that insulin's antinatriuretic effect is localized at a distal tubular site other than the long loops of Henle and that the long loops are involved in the natriuretic effect of low-dose ANP, possibly mediated by changes in medullary blood flow.

Arginine vasopressin potentiates natriuretic effect of atrial peptide

1989 ◽  
Vol 256 (3) ◽  
pp. H925-H927
Author(s):  
L. M. Graczak ◽  
L. K. Nicolodi ◽  
D. A. Hartupee ◽  
E. H. Blaine
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Glomerular Filtration ◽  
Arginine Vasopressin ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Dependent Manner ◽  
Functional Interaction ◽  
Natriuretic Effect ◽  
Dose Dependent

We investigated potentiation of atrial peptide (AP)-induced natriuresis by vasopressin in anesthetized rats. Increasing doses of vasopressin potentiated AP-induced natriuresis in a dose-dependent manner, e.g., sodium excretion during AP administration (290 ng/min) was 0.66 +/- 0.16, 2.02 +/- 0.68, 5.21 +/- 1.38 and 7.08 +/- 1.96 mu eq/min during infusion of 0.00, 0.78, 1.56, and 3.12 ng.kg-1.min-1 of vasopressin, respectively. Vasopressin alone had no effect on sodium excretion. In a second experiment, vasopressin (1.56 ng.kg-1.min-1) potentiated AP (128 ng/min)-induced natriuresis similar to that seen in the first experiment. In this experiment, glomerular filtration rate (GFR) and mean arterial pressure were monitored. Mean arterial pressure was no different between the groups treated with AP plus vasopressin and AP alone. Glomerular filtration was actually reduced in the group treated with vasopressin plus AP, suggesting that neither changes in GFR nor blood pressure were responsible for potentiation of the natriuresis. A third experiment compared the ability of 1-desamino-8-D-arginine vasopressin (dDAVP), a nonpressor analogue of vasopressin, to vasopressin in enhancing AP (145 ng/min)-induced natriuresis. The nonpressor analogue did not potentiate AP-induced natriuresis, whereas vasopressin had the same effect as in the first two experiments. These are the first studies to report a functional interaction between AP and vasopressin. They show that vasopressin potentiates AP-induced natriuresis without altering mean arterial pressure or GFR.

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