Mechanism for inhibition of renin release by acute plasma volume expansion in the dog

1985 ◽  
Vol 248 (2) ◽  
pp. F206-F211 ◽  
Author(s):  
M. W. Roy ◽  
C. E. Ott ◽  
W. J. Welch ◽  
J. H. Downs ◽  
T. A. Kotchen
Keyword(s):  
Plasma Volume ◽  
Volume Expansion ◽  
Chloride Transport ◽  
Renin Secretion ◽  
Renin Release ◽  
Renal Nerves ◽  
Plasma Volume Expansion ◽  
Renal Nerve ◽  
Albumin Infusion ◽  
Renal Tubular

Plasma volume expansion alters renal tubular sodium chloride transport and renal nerve activity. The purpose of this study was to determine the mechanism(s) for inhibition of renin secretion by acute volume expansion with albumin in the anesthetized dog. In dogs with a single intact kidney, albumin infusion decreased renin release by 86% and significantly increased renal blood flow, glomerular filtration rate, and sodium excretion. Albumin volume expansion inhibited renin secretion to a lesser extent in dogs with denervated filtering kidneys and in dogs with innervated nonfiltering kidneys. In dogs with denervated nonfiltering kidneys, albumin infusion did not change renin secretion. Comparable volume expansion was produced in all groups. Thus, inhibition of renin release by acute plasma volume expansion is dependent on both a renal tubular mechanism and the integrity of the renal nerves. Partial inhibition of renin release was observed with interruption of either one of the mechanisms, whereas interruption of both mechanisms totally abolished the effect of acute plasma volume expansion on renin secretion.

THE EFFECT OF VAGOTOMY AND DENERVATION OF THE CAROTID SINUS ON DIURESIS FOLLOWING PLASMA VOLUME EXPANSION

1959 ◽  
Vol 37 (1) ◽  
pp. 81-90 ◽  
Author(s):  
J. W. Pearce
Keyword(s):  
Plasma Volume ◽  
Volume Expansion ◽  
Carotid Sinus ◽  
Urine Flow ◽  
Flow Section ◽  
Plasma Volume Expansion ◽  
Reflex Mechanism ◽  
Albumin Infusion ◽  
Stretch Receptors ◽  
Afferent Vagal

The hypothesis exists that afferent vagal fibers, arising in cardiac atrial stretch receptors, serve as the sensory limb of a reflex mechanism sensitive to variations in blood volume and producing corresponding changes in urine flow. Section of the vagi did not, however, prevent the diuretic and chloruretic response to expansion of the plasma volume with isotonic infusions. Carotid sinus denervation alone or combined with vagotomy also failed to prevent the diuresis and chloruresis following infusion in most experiments, although in a few cases the response was absent or diminished after the combined procedure. Reasons are given for believing that the bovine albumin infusion used did not act directly on the kidney to increase urine output, but rather through a reflex mechanism which could not have depended on the integrity of the vagi. It is concluded that receptors additional to those in the cardiac atria and the carotid sinus must contribute to the sensory component of a reflex mechanism regulating plasma volume.

scholarly journals Albumin infusion rate and plasma volume expansion: a randomized clinical trial in postoperative patients after major surgery

Critical Care ◽  
2019 ◽  
Vol 23 (1) ◽  
Author(s):  
Svajunas Statkevicius ◽  
Johan Bonnevier ◽  
Jane Fisher ◽  
Björn P. Bark ◽  
Erik Larsson ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Randomized Clinical Trial ◽  
Plasma Volume ◽  
Infusion Rate ◽  
Volume Expansion ◽  
Major Surgery ◽  
Plasma Volume Expansion ◽  
Albumin Infusion

THE EFFECT OF VAGOTOMY AND DENERVATION OF THE CAROTID SINUS ON DIURESIS FOLLOWING PLASMA VOLUME EXPANSION

1959 ◽  
Vol 37 (1) ◽  
pp. 81-90 ◽  
Author(s):  
J. W. Pearce
Keyword(s):  
Plasma Volume ◽  
Volume Expansion ◽  
Carotid Sinus ◽  
Urine Flow ◽  
Flow Section ◽  
Plasma Volume Expansion ◽  
Reflex Mechanism ◽  
Albumin Infusion ◽  
Stretch Receptors ◽  
Afferent Vagal

The hypothesis exists that afferent vagal fibers, arising in cardiac atrial stretch receptors, serve as the sensory limb of a reflex mechanism sensitive to variations in blood volume and producing corresponding changes in urine flow. Section of the vagi did not, however, prevent the diuretic and chloruretic response to expansion of the plasma volume with isotonic infusions. Carotid sinus denervation alone or combined with vagotomy also failed to prevent the diuresis and chloruresis following infusion in most experiments, although in a few cases the response was absent or diminished after the combined procedure. Reasons are given for believing that the bovine albumin infusion used did not act directly on the kidney to increase urine output, but rather through a reflex mechanism which could not have depended on the integrity of the vagi. It is concluded that receptors additional to those in the cardiac atria and the carotid sinus must contribute to the sensory component of a reflex mechanism regulating plasma volume.

Increased renal tubular sodium reabsorption during exercise-induced hypervolemia in humans

2001 ◽  
Vol 91 (3) ◽  
pp. 1229-1236 ◽  
Author(s):  
Kei Nagashima ◽  
Jauchia Wu ◽  
Stavros A. Kavouras ◽  
Gary W. Mack
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Plasma Volume ◽  
Volume Expansion ◽  
Tubular Reabsorption ◽  
Proximal Tubules ◽  
Plasma Volume Expansion ◽  
Saline Loading ◽  
Exercise Induced ◽  
Renal Tubular

We tested the hypothesis that renal tubular Na+ reabsorption increased during the first 24 h of exercise-induced plasma volume expansion. Renal function was assessed 1 day after no-exercise control (C) or intermittent cycle ergometer exercise (Ex, 85% of peak O2 uptake) for 2 h before and 3 h after saline loading (12.5 ml/kg over 30 min) in seven subjects. Ex reduced renal blood flow ( p-aminohippurate clearance) compared with C (0.83 ± 0.12 vs. 1.49 ± 0.24 l/min, P < 0.05) but did not influence glomerular filtration rates (97 ± 10 ml/min, inulin clearance). Fractional tubular reabsorption of Na+ in the proximal tubules was higher in Ex than in C ( P < 0.05). Saline loading decreased fractional tubular reabsorption of Na+ from 99.1 ± 0.1 to 98.7 ± 0.1% ( P < 0.05) in C but not in Ex (99.3 ± 0.1 to 99.4 ± 0.1%). Saline loading reduced plasma renin activity and plasma arginine vasopressin levels in C and Ex, although the magnitude of decrease was greater in C ( P < 0.05). These results indicate that, during the acute phase of exercise-induced plasma volume expansion, increased tubular Na+ reabsorption is directed primarily to the proximal tubules and is associated with a decrease in renal blood flow. In addition, saline infusion caused a smaller reduction in fluid-regulating hormones in Ex. The attenuated volume-regulatory response acts to preserve distal tubular Na+ reabsorption during saline infusion 24 h after exercise.

Effects of Long-term Nitric Oxide Synthesis Inhibition on Plasma Volume Expansion and Fetal Growth in the Pregnant Rat

Hypertension ◽  
1995 ◽  
Vol 26 (6) ◽  
pp. 1019-1023 ◽  
Author(s):  
Sofía P. Salas ◽  
Fernando Altermatt ◽  
Mauricio Campos ◽  
Andrea Giacaman ◽  
Pedro Rosso
Keyword(s):  
Nitric Oxide ◽  
Fetal Growth ◽  
Plasma Volume ◽  
Volume Expansion ◽  
Nitric Oxide Synthesis ◽  
Plasma Volume Expansion ◽  
Pregnant Rat ◽  
Synthesis Inhibition

scholarly journals Increased susceptibility of db/db mice to rosiglitazone-induced plasma volume expansion: role of dysregulation of renal water transporters

2013 ◽  
Vol 305 (10) ◽  
pp. F1491-F1497 ◽  
Author(s):  
Li Zhou ◽  
Gang Liu ◽  
Zhanjun Jia ◽  
Kevin T. Yang ◽  
Ying Sun ◽  
...  
Keyword(s):  
Plasma Volume ◽  
Volume Expansion ◽  
Urine Volume ◽  
Plasma Osmolality ◽  
Underlying Mechanism ◽  
Fluid Retention ◽  
Receptor Subtype ◽  
Fluorescent Nanoparticles ◽  
Peroxisome Proliferator ◽  
Plasma Volume Expansion

Thiazolidinediones (TZDs), which are synthetic peroxisome proliferator-activated receptor subtype-γ (PPARγ), agonists are highly effective for treatment of type 2 diabetes. However, the side effect of fluid retention has significantly limited their application. Most of the previous studies addressing TZD-induced fluid retention employed healthy animals. The underlying mechanism of this phenomenon is still incompletely understood, particularly in the setting of disease state. The present study was undertaken to examine rosiglitazone (RGZ)-induced fluid retention in db/db mice and to further investigate the underlying mechanism. In response to RGZ treatment, db/db mice exhibited an accelerated plasma volume expansion as assessed by hematocrit (Hct) and fluorescent nanoparticles, in parallel with a greater increase in body weight, compared with lean controls. In response to RGZ-induced fluid retention, urinary Na+ excretion and urine volume were significantly increased in lean mice. In contrast, the natriuretic and diuretic responses were significantly blunted in db/db mice. RGZ db/db mice exhibited a parallel decrease in plasma Na+ concentration and plasma osmolality, contrasting to unchanged levels in lean controls. Imunoblotting analysis showed downregulation of renal aquaporin (AQP) 2 expression in response to RGZ treatment in lean mice but not in db/db mice. Renal AQP3 protein expression was unaffected by RGZ treatment in lean mice but was elevated in db/db mice. In contrast, the expression of Na+/H+ exchanger-3 (NHE3) and NKCC2 was unchanged in either mouse strain. Together these results suggest that compared with the lean controls, db/db mice exhibited accelerated plasma volume expansion that was in part due to the inappropriate response of renal water transporters.

Exercise stroke volume relative to plasma-volume expansion

1988 ◽  
Vol 64 (1) ◽  
pp. 404-408 ◽  
Author(s):  
M. K. Hopper ◽  
A. R. Coggan ◽  
E. F. Coyle
Keyword(s):  
Stroke Volume ◽  
Plasma Volume ◽  
Volume Expansion ◽  
Peripheral Resistance ◽  
Submaximal Exercise ◽  
Upright Position ◽  
Plasma Volume Expansion ◽  
Trained Subjects ◽  
The Difference ◽  
Dextran Solution

The effects of plasma-volume (PV) expansion on stroke volume (SV) (CO2 rebreathing) during submaximal exercise were determined. Intravenous infusion of 403 +/- 21 ml of a 6% dextran solution before exercise in the upright position increased SV 11% (i.e., 130 +/- 6 to 144 +/- 5 ml; P less than 0.05) in untrained males (n = 7). Further PV expansion (i.e., 706 +/- 43 ml) did not result in a further increase in SV (i.e., 145 +/- 4 ml). SV was somewhat higher during supine compared with upright exercise when blood volume (BV) was normal (i.e., 138 +/- 8 vs. 130 +/- 6 ml; P = 0.08). PV expansion also increased SV during exercise in the supine position (i.e., 138 +/- 8 to 150 +/- 8 ml; P less than 0.05). In contrast to these observations in untrained men, PV expansion of endurance-trained men (n = 10), who were naturally PV expanded, did not increase SV during exercise in the upright or supine positions. When BV in the untrained men was increased to match that of the endurance-trained subjects, SV was observed to be 15% higher (165 +/- 7 vs. 144 +/- 5 ml; P less than 0.05), whereas mean blood pressure and total peripheral resistance were significantly lower (P less than 0.05) in the trained compared with untrained subjects during upright exercise at a similar heart rate. The present findings indicate that exercise SV in untrained men is preload dependent and that increases in exercise SV occur in response to the first 400 ml of PV expansion. It appears that approximately one-half of the difference in SV normally observed between untrained and highly endurance-trained men during upright exercise is due to a suboptimal BV in the untrained men.

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