Homeostatic efficiency of tubuloglomerular feedback in hydropenia, euvolemia, and acute volume expansion

1993 ◽  
Vol 264 (6) ◽  
pp. F930-F936 ◽  
Author(s):  
S. C. Thomson ◽  
R. C. Blantz
Keyword(s):  
Volume Expansion ◽  
Closed Loop ◽  
Polynomial Regression ◽  
Extracellular Volume ◽  
Tubuloglomerular Feedback ◽  
Maximum Value ◽  
Proximal Tubular ◽  
Extracellular Volume Expansion ◽  
Tubular Flow

We assessed the homeostatic efficiency of the tubuloglomerular feedback (TGF) system in Inactin-anesthetized Munich-Wistar rats by use of perturbation analysis in closed-loop micropuncture studies. Nephrons were studied in vivo under conditions of hydropenia (HYD, n = 17), euvolemia (EUV, n = 23), and acute isoncotic extracellular volume expansion (EXP, n = 15). Proximal tubular flow was perturbed in free-flowing nephrons with a microperfusion apparatus. Flow rate (VM) was measured upstream from the perturbation (VH) by a noninvasive optical technique. The dependence of VM on VH was estimated by polynomial regression. By using fractional compensation (C = -dVM/dVH), as an index of homeostatic efficiency, we constructed efficiency profiles (C vs. VH). At VH = 0, C tended toward higher values with decreasing volume status, although the effect did not achieve significance. The maximum value of C did not differ between groups. The efficiency profiles shifted leftward with each increment in volume (P < 0.03, HYD vs. EXP), suggesting that the TGF system adapts to acute increments in volume by shifting the efficiency profile in favor of a vasodilatory role.

A Role for Tubuloglomerular Feedback in Chronic Partial Ureteral Obstruction

Physiology ◽  
1993 ◽  
Vol 8 (2) ◽  
pp. 74-79
Author(s):  
P Morsing
Keyword(s):  
Renal Function ◽  
Arachidonic Acid ◽  
Ureteral Obstruction ◽  
Volume Expansion ◽  
Filtration Rate ◽  
Extracellular Volume ◽  
Tubuloglomerular Feedback ◽  
Arachidonic Acid Metabolites ◽  
Acid Metabolites ◽  
Extracellular Volume Expansion

Animals with partial ureteral obstruction have an inability to increase urinary output and glomerular filtration rate in response to an extracellular volume expansion. The mechanism may be a paradoxical resetting of tubuloglomerular feedback in the obstructed kidney, which impacts the roles of arachidonic acid metabolites and kinins in renal function.

Mechanism of natriuresis following intravascular and extracellular volume expansion

1969 ◽  
Vol 47 (2) ◽  
pp. 153-159 ◽  
Author(s):  
H. Sonnenberg ◽  
S. Solomon
Keyword(s):  
Blood Volume ◽  
Volume Expansion ◽  
Filtration Rate ◽  
Extracellular Volume ◽  
Extracellular Fluid ◽  
Sodium Reabsorption ◽  
Fluid Compartment ◽  
Proximal Tubular ◽  
Extracellular Volume Expansion ◽  
A Site

In clearance studies in rats, increases in filtration rate and electrolyte excretion were observed following both intravascular and extracellular fluid volume expansion. The inulin concentration ratio of proximal tubular fluid to plasma was decreased with extracellular expansion. Neither natriuresis nor fractional sodium reabsorption was related to the degree of intravascular expansion. Microperfusion studies demonstrated a decrease in proximal sodium reabsorption only when both intravascular and extravascular volumes were expanded; net sodium transport was not affected by a blood volume increase alone. From the data it is concluded that in the rat an increase in blood volume is followed by a rise of filtration rate and a fall of fractional reabsorption at a site distal to the proximal tubule, resulting in diuresis and natriuresis. If, in addition, the interstitial fluid compartment is expanded, a direct inhibition of the active transport component of proximal Na+ reabsorption occurs.

Restoration of tubuloglomerular feedback in volume-expanded rats by angiotensin II

1990 ◽  
Vol 259 (4) ◽  
pp. F565-F572 ◽  
Author(s):  
J. Schnermann ◽  
J. P. Briggs
Keyword(s):  
Angiotensin Ii ◽  
Volume Expansion ◽  
Extracellular Volume ◽  
Isotonic Saline ◽  
Tubuloglomerular Feedback ◽  
Plasma Angiotensin ◽  
Single Nephron ◽  
Saline Administration ◽  
Flow Pressure ◽  
Extracellular Volume Expansion

Experiments were performed in anesthetized rats to examine whether angiotensin II corrects the attenuation of tubuloglomerular feedback (TGF) responses produced by acute extracellular volume expansion. Volume expansion was achieved by an infusion of isotonic saline at a rate of 9 ml/h. When urine flow had stabilized, an increase in loop of Henle flow from 0 to 45 nl/min caused a fall in stop-flow pressure (PSF) by 3.7 +/- 0.3 mmHg and in single-nephron glomerular filtration rate (SNGFR) by 5.1 +/- 1.7 nl/min. During continued saline administration angiotensin II was infused at 16, 48, or 96 ng.kg-1.min-1 while renal arterial pressure was held constant by suprarenal aortic clamping. The mean responses of PSF increased to 5.9 +/- 0.6, 9.8 +/- 0.7, and 14.9 +/- 1.7 mmHg. Angiotensin II infused at 54 ng.kg-1.min-1 increased the SNGFR response to 15.1 +/- 2.1 nl/min, whereas kidney GFR and distal SNGFR fell. Subcapsular pressure was not significantly altered by angiotensin II infusion (16 ng.kg-1.min-1). Plasma angiotensin (y, pg/ml) as a function of angiotensin II infusion rate (x, ng.kg-1.min-1 for approximately 20 min) was found to fit the function y = 2.89 + 3.53x. An infusion of approximately 15 ng.kg-1.min-1 restored plasma angiotensin levels in the volume-expanded rats to hydropenic values. These data confirm that angiotensin II may play a role as a physiological regulator of TGF sensitivity.

Kinin and tubuloglomerular feedback in normal and hydronephrotic rats

1991 ◽  
Vol 260 (6) ◽  
pp. F868-F873 ◽  
Author(s):  
P. Morsing ◽  
A. E. Persson
Keyword(s):  
Volume Expansion ◽  
Turning Point ◽  
Extracellular Volume ◽  
Tubuloglomerular Feedback ◽  
Glomerular Function ◽  
Flow Pressure ◽  
Extracellular Volume Expansion ◽  
And Control ◽  
Stop Flow

The role of bradykinin in resetting the tubuloglomerular feedback (TGF) mechanism was studied with the stop-flow technique in control and hydronephrotic Inactin-anesthetized rats. Glomerular function was assessed by measuring stop-flow pressure (Psf); the maximal decrease in stop-flow pressure (delta Psf) with increased loop of Henle perfusion and the perfusion that elicited half-maximal delta Psf, the turning point (TP), were determined. Bradykinin infusion resulted in resetting of TGF in both control and hydronephrotic rats but in different directions. A decreased sensitivity was found in control rats (TP increased from 18.6 to 26.4 and 16.8 to 22.1 nl/min on systemic and intratubular administration, respectively). In hydronephrotic rats the sensitivity of TGF increased. TP decreased from 19.9 to 15.2 nl/min with bradykinin administered systemically and from 18.4 to 15.0 nl/min on intratubular administration. These results show that exogenous kinin administration mimics the effects of extracellular volume expansion on TGF resetting and demonstrate a difference in resetting in hydronephrotic and control kidneys.

Role of Oxytocin in the Natriuresis of Extracellular Volume Expansion

1969 ◽  
Vol 130 (4) ◽  
pp. 1276-1279 ◽  
Author(s):  
S. G. Massry ◽  
H. Vorherr ◽  
C. R. Kleeman
Keyword(s):  
Volume Expansion ◽  
Extracellular Volume ◽  
Extracellular Volume Expansion

Extracellular Volume Expansion Caused by Protein Malnutrition in Peritoneal Dialysis Patients with Appropriate Salt and Water Removal

2008 ◽  
Vol 28 (4) ◽  
pp. 407-412 ◽  
Author(s):  
M.-José Fernández-Reyes ◽  
M.-Auxiliadora Bajo ◽  
Gloria del Peso ◽  
Dabaiba Regidor ◽  
Covadonga Hevia ◽  
...  
Keyword(s):  
Peritoneal Dialysis ◽  
Volume Expansion ◽  
Extracellular Volume ◽  
Protein Malnutrition ◽  
Water Removal ◽  
Dialysis Patients ◽  
Extracellular Volume Expansion

Atriopeptin stimulation of rectal gland function in Squalus acanthias

1985 ◽  
Vol 249 (3) ◽  
pp. R348-R354 ◽  
Author(s):  
R. Solomon ◽  
M. Taylor ◽  
D. Dorsey ◽  
P. Silva ◽  
F. H. Epstein
Keyword(s):  
Volume Expansion ◽  
Epithelial Transport ◽  
Extracellular Volume ◽  
Chloride Secretion ◽  
Hormonal Control ◽  
Rectal Gland ◽  
Gland Function ◽  
Stimulation Of

The rectal gland of the shark plays a significant role in the homeostasis of extracellular volume. Regulation of rectal gland function is under hormonal control, but the precise identity of the humoral mediator is unknown. Atriopeptin stimulates rectal gland chloride secretion in vivo. This stimulation of epithelial transport is accompanied by systemic and local hemodynamic effects. Atriopeptin also stimulates chloride secretion by the in vitro perfused rectal gland, an effect that is not accompanied by hemodynamic changes. Extracts of shark heart, but not muscle, brain, kidney, or intestine, contain a heat-stable trypsin-sensitive substance capable of in vitro stimulation of rectal gland chloride secretion. Electron micrographic analysis reveals multiple neurosecretory-like granules in atrial cardiocytes that are only rarely seen in ventricular cardiocytes. By using the in vitro perfused gland as a biologic assay, serum obtained after extracellular volume expansion reveals the presence of a rectal gland stimulatory factor that is not present in serum before expansion. These results are consistent with the hypothesis that atriopeptin is present in shark cardiocytes and is released during volume expansion. The atriopeptin stimulates rectal gland chloride secretion, providing a negative feedback mechanism for the regulation of extracellular volume.

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