Effect of angiotensin II on renal water excretion

1975 ◽  
Vol 228 (1) ◽  
pp. 155-159 ◽  
Author(s):  
P Cadnapaphornchai ◽  
J Boykin ◽  
JA Harbottle ◽  
KM McDonald ◽  
RW Schrier
Keyword(s):  
Angiotensin Ii ◽  
Intravenous Infusion ◽  
Free Water ◽  
Competitive Inhibitor ◽  
Constant Infusion ◽  
Free Water Clearance ◽  
Water Excretion ◽  
Vasopressin Release ◽  
Urinary Osmolality ◽  
Renal Water Excretion

In the present study the effect of angiotensin II (AII) on renal water excretion was evaluated. In dogs undergoing a water diuresis, neither the intravenous (IV) (40ng/kg per min) nor intracarotid (5-10 ng/kg per min) infusion of AII significantly altered urinary osmolality (Uosm) or free-water clearance (CH2O). Intravenous infusion of a competitive inhibitor of AII (1-sarcosine,8-glycine AII) into hydropenic dogs also failed to alter Uosm and CH2O significantly. To examine whether AII might suppress, rather than stimulate, vasopressin release, AII was also infused into hydropenic animals. No effect on Uosm and CH2O was observed during the intracarotid infusion. A significant fall in Uosm and rise in CH2O occurred during the intravenous AII infusion, but reversal after cessation of the infusion was incomplete and statistically not significant. Some suppression of antidiuretic hormone (ADH) release during the intravenous infusion of AII, however, was suggested since no similar alteration in renal water excretion was observed during an intravenous AII infusion in hypophysectomized animals receiving a constant infusion of ADH. Taken together, the present results provide no evidence for a direct effect of AII to alter ADH release or to interfere with the peripheral action of ADH. Suppression of ADH release may sometimes occur with pressor doses of intravenous angiotensin, but this effect is clearly less consistent than previously observed with intravenous norepinephrine.

Effect of angiotensin II on urinary dilution in normal man

1964 ◽  
Vol 206 (4) ◽  
pp. 750-754 ◽  
Author(s):  
John R. Gill ◽  
Benjamin H. Barbour ◽  
J. D. H. Slater ◽  
Frederic C. Bartter
Keyword(s):  
Angiotensin Ii ◽  
Diabetes Insipidus ◽  
Renal Plasma Flow ◽  
Free Water ◽  
Normal Subjects ◽  
Diluting Segment ◽  
Free Water Clearance ◽  
Water Excretion ◽  
Urinary Osmolality ◽  
Disease States

Free water clearance (CHH2O) was studied in five normal subjects and in a patient with diabetes insipidus before and during the infusion of angiotensin II (Ciba), .2 µg/min. With angiotensin, CHH2O fell markedly, with only small changes in urinary osmolality both in the normal subjects and in the patient with diabetes insipidus. The fall in CHH2O was accompanied by a fall in UNaV, effective renal plasma flow (ERPF), and glomerular filtration rate (GFR). A physiological dose of Pitressin (25 mU/hr) given after the angiotensin, abolished CHH2O and markedly increased urinary osmolality while UNaV, ERPF, and GFR returned toward normal. The results may be best explained as a direct effect of angiotensin on renal hemodynamics, to decrease filtered sodium and water. Reabsorption of an increased fraction of filtered sodium and water by the proximal tubule would limit the amount reaching the diluting segment of the nephron and excreted in the urine. A possible role for angiotensin in the impaired water excretion of certain disease states, such as Addison's disease and congestive heart failure was suggested.

Vasopressin-independent alterations in renal water excretion in quadriplegia

1993 ◽  
Vol 265 (2) ◽  
pp. R460-R466 ◽  
Author(s):  
B. M. Wall ◽  
H. H. Williams ◽  
D. N. Presley ◽  
J. T. Crofton ◽  
L. Share ◽  
...  
Keyword(s):  
Cervical Spinal Cord ◽  
Free Water ◽  
Renal Tubules ◽  
Erect Posture ◽  
Free Water Clearance ◽  
Water Excretion ◽  
Vasopressin Release ◽  
Control Subjects ◽  
Cord Injury ◽  
Healthy Control

Postural effects on water excretion are known to be increased in patients with cervical spinal cord injury and may result in marked impairment of the ability to excrete a water load, especially in erect posture. Both vasopressin-dependent and vasopressin-independent mechanisms have been implicated. To assess the roles of these mechanisms and further identify the factors involved in the renal response to erect posture, sustained water loading studies were performed on 11 quadriplegic subjects and 9 healthy control subjects, supine and erect (sitting). Renal blood flow was assessed by p-aminohippurate clearance (CPAH) measurements in 7 quadriplegic and 5 control subjects. During maximal water diuresis, plasma vasopressin concentrations were reduced to unquantifiable levels in all subjects. Osmolar clearance, free water clearance (CH2O), and distal delivery of filtrate (DDF) were all lower in quadriplegic than in control subjects, supine and erect. The relationship between CH2O and DDF was the same in quadriplegic as in control subjects and was not altered by change in posture in either group. Creatinine clearance and CPAH were lower in erect than in supine posture in quadriplegic subjects but not in control subjects. We conclude that impairment of water excretion in stable normonatremic quadriplegic subjects can be attributed primarily to vasopressin-independent mechanisms involving reduced filtrate delivery to diluting segments of the renal tubules rather than to resistance to normal suppression of vasopressin release.

Natriuretic effect of atrial extract on isolated perfused rat kidney

1983 ◽  
Vol 61 (12) ◽  
pp. 1462-1466 ◽  
Author(s):  
A. D. Baines ◽  
A. J. DeBold ◽  
H. Sonnenberg
Keyword(s):  
Sodium Chloride ◽  
Angiotensin Ii ◽  
Rat Kidney ◽  
Free Water ◽  
Free Water Clearance ◽  
Variable Effect ◽  
Water Excretion ◽  
Perfused Rat Kidney ◽  
Natriuretic Effect ◽  
Renal Vascular

To examine the mechanisms underlying the natriuretic action of a partially purified extract of rat atria (AE) we injected the equivalent of one atrium into isolated perfused rat kidneys. Some kidneys received an infusion of angiotensin II at 0.5 ng/min throughout the experiment. In the absence of angiotensin AE had a variable effect on renal vascular resistance (RVR) but, in the presence of angiotensin II, AE consistently decreased RVR by 3% for 5 min followed by a slight increase. Inulin clearance and filtration fraction increased slightly but significantly. AE increased sodium, chloride, phosphate, and free water clearance but not potassium excretion. Ventricular extract had no effect on any of these variables. Furosemide (50–250 μg) increased sodium, chloride, and potassium but not phosphate or free water excretion. AE did not alter dopamine or norepinephrine excretion. We conclude that AE increases the glomerular filtration rate (GFR) and inhibits tubular reabsorption by mechanisms which differ, at least in part, from those affected by furosemide.

Nonosmotic release of vasopressin and renal aquaporins in impaired urinary dilution in hypothyroidism

2005 ◽  
Vol 289 (4) ◽  
pp. F672-F678 ◽  
Author(s):  
Yung-Chang Chen ◽  
Melissa A. Cadnapaphornchai ◽  
Jianhui Yang ◽  
Sandra N. Summer ◽  
Sandor Falk ◽  
...  
Keyword(s):  
Protein Expression ◽  
Renal Cortex ◽  
Free Water ◽  
Urine Osmolality ◽  
Protein Abundance ◽  
Oral Gavage ◽  
Water Excretion ◽  
Urinary Osmolality ◽  
Water Load ◽  
Fluid Delivery

The purpose of this study was to examine protein expression of renal aquaporins (AQP) and ion transporters in hypothyroid (HT) rats in response to an oral water load compared with controls (CTL) and HT rats replaced with l-thyroxine (HT+T). Hypothyroidism was induced by aminotriazole administration for 10 wk. Body weight, water intake, urine output, solute and urea excretion, and serum and urine osmolality were comparable among the three groups at the conclusion of the 10-wk treatment period. One hour after oral gavage of water (50 ml/kg body wt), HT rats demonstrated significantly less water excretion, higher minimal urinary osmolality, and decreased serum osmolality compared with CTL and HT+T rats. Despite the hyposmolality, plasma vasopressin concentration was elevated in HT rats. These findings in HT rats were associated with an increase in protein abundance of renal cortex AQP1 and inner medulla AQP2. AQP3, AQP4, and the Na-K-2Cl cotransporter were also increased. Moreover, 1 h following the oral water load, HT rats demonstrated a significant increase in the membrane-to-vesicle fraction of AQP2 by Western blot analysis. The defect in urinary dilution in HT rats was reversed by the V2 vasopressin antagonist OPC-31260. In conclusion, impaired urinary dilution in HT rats is primarily compatible with the nonosmotic release of vasopressin and increased protein expression of renal AQP2. The impairment of maximal solute-free water excretion in HT rats, however, appears also to involve diminished distal fluid delivery.

Osmoregulation of thirst and vasopressin during normal menstrual cycle

1988 ◽  
Vol 254 (4) ◽  
pp. R641-R647 ◽  
Author(s):  
T. J. Vokes ◽  
N. M. Weiss ◽  
J. Schreiber ◽  
M. B. Gaskill ◽  
G. L. Robertson
Keyword(s):  
Menstrual Cycle ◽  
Luteal Phase ◽  
Plasma Osmolality ◽  
Free Water ◽  
Urine Osmolality ◽  
Free Water Clearance ◽  
Vasopressin Release ◽  
Plasma Vasopressin ◽  
Normal Menstrual Cycle ◽  
Basal Plasma

Changes in osmoregulation during normal menstrual cycle were examined in 15 healthy women. In 10 women, studied repetitively during two consecutive menstrual cycles, basal plasma osmolality, sodium, and urea decreased by 4 mosmol/kg, 2 meq/l, and 0.5 mM, respectively (all P less than 0.02) from the follicular to luteal phase. Plasma vasopressin, protein, hematocrit, mean arterial pressure, and body weight did not change. In five other women, diluting capacity and osmotic control of thirst and vasopressin release were assessed in follicular, ovulatory, and luteal phases. Responses of thirst and/or plasma vasopressin, urine osmolality, osmolal and free water clearance to water loading, and infusion of hypertonic saline were normal and similar in the three phases. However, the plasma osmolality at which plasma vasopressin and urine osmolality were maximally suppressed as well as calculated osmotic thresholds for thirst and vasopressin release were lower by 5 mosmol/kg in the luteal than in the follicular phase. This lowering of osmotic thresholds for thirst and vasopressin release, which occurs in the luteal phase, is qualitatively similar to that observed in pregnancy and should be taken into account when studying water balance and regulation of vasopressin secretion in healthy cycling women.

Mechanism of Action of Indomethacin in Tubular Defects

PEDIATRICS ◽  
1985 ◽  
Vol 75 (3) ◽  
pp. 501-507
Author(s):  
Mario Usberti ◽  
Carmine Pecoraro ◽  
Stefano Federico ◽  
Bruno Cianciaruso ◽  
Bruna Guida ◽  
...  
Keyword(s):  
Prostaglandin E2 ◽  
Diabetes Insipidus ◽  
Mechanism Of Action ◽  
Nephrogenic Diabetes Insipidus ◽  
Fanconi Syndrome ◽  
Free Water ◽  
Synthesis Inhibitor ◽  
Free Water Clearance ◽  
Water Excretion ◽  
Water Load

Indomethacin, a potent prostaglandin synthesis inhibitor, has been proven to be effective in a number of tubular defects characterized by enhanced prostaglandin (namely, prostaglandin E2 (PGE2) production, but its mechanism of action is poorly understood. To elucidate further the mechanism(s) by which indomethacin reverses the abnormal tubular functions, five children with different tubular defects (nephrogenic diabetes insipidus, three cases; Fanconi syndrome, one case; and pseudohypoaldosteronism, one case) were treated with indomethacin. Indomethacin, 1 mg/kg every eight hours, was given for 1 week to all children and then was given chronically to four of the children who responded to the drug. Its use was suspended in a 10 year-old-boy with nephrogenic diabetes insipidus because it proved ineffective. To assess the site along the nephron where indomethacin affects the solute and water excretion, an acute water load study was performed in three responsive children before and during the treatment. Indomethacin did not significantly alter the glomerular filtration rate but was effective in reducing diuresis and levels of urinary sodium and potassium excretion. In the child with Fanconi syndrome, indomethacin was also effective in controlling the urinary loss of phosphate, urate, glucose, and bicarbonate. Results of the water load studies show that indomethacin decreases the delivery of solute from the proximal tubule, reduces the fractional free water clearance, and increases the urine-plasma osmolar ratio. The rate of urinary excretion of prostaglandin E2 was high in all five children; it decreased below normal values in four of them after 1 week of treatment. In the child with nephrogenic diabetes insipidus who did not respond to indomethacin therapy, prostaglandin E2 excretion decreased but the rate remained higher than normal. These results suggest that indomethacin induces retention of solute and water mainly through an enhanced proximal tubular reabsorption.

Effect of acute unilateral renal denervation on tubular sodium reabsorption in the dog

1977 ◽  
Vol 232 (1) ◽  
pp. F16-F19
Author(s):  
G. Nomura ◽  
T. Takabatake ◽  
S. Arai ◽  
D. Uno ◽  
M. Shimao ◽  
...  
Keyword(s):  
Renal Denervation ◽  
Renal Plasma Flow ◽  
Free Water ◽  
Sodium Reabsorption ◽  
Distal Nephron ◽  
Water Diuresis ◽  
Free Water Clearance ◽  
Water Excretion ◽  
Tubular Sodium Reabsorption ◽  
Renal Tubular

The effects of acute denervation of the kidney on renal tubular sodium and water excretion were studied in anesthetized, hypophysectomized, and cortisone-treated mongrel dogs during stable water diuresis produced by the infusion of 2.5% dextrose. In all experiments, denervation natriuresis, and diuresis were observed without significant change in glomerular filtration rate (GRF) and renal plasma flow (RPF). Fractional sodium delivery to the distal nephron (CNa + CH2O/100 ml GFR) and fractional free water clearance (CH23/100 ml GFR) was significantly greater in the denervated kidney compared with the innervated kidney (9.6+/-1.2 vs. 6.7+/-0.9% and 8.8+/-1.2 vs. 6.5+/-0.8%, respectively). Distal tubular sodium reabsorption (CH2O/(CNa + CH2O)) was not significantly different. We conclude that renal denervation primarily affects the proximal tubule as manifested by a decrease in the reabsorption of sodium and water. A small effect of denervation on the distal nephron is not completely ruled out.

Ovine fetal renal and hormonal responses to changes in plasma epinephrine

1991 ◽  
Vol 260 (1) ◽  
pp. R82-R89
Author(s):  
M. G. Ervin ◽  
R. Castro ◽  
D. J. Sherman ◽  
M. G. Ross ◽  
J. F. Padbury ◽  
...  
Keyword(s):  
Renal Function ◽  
Sodium Excretion ◽  
Free Water ◽  
Urine Osmolality ◽  
Plasma Epinephrine ◽  
Epinephrine Infusion ◽  
Free Water Clearance ◽  
Water Excretion ◽  
Fourfold Increase ◽  
Fetal Plasma

Circulating epinephrine alters atrial natriuretic factor (ANF) and arginine vasopressin (AVP) secretion, and all three hormones influence renal function. To quantify the relationships among fetal plasma epinephrine levels, fetal ANF and AVP secretion, and fetal renal function, six chronically catheterized fetal lambs (132 +/- 1 days gestation) received successive 40-min epinephrine infusions (0.1, 0.4, and 1.8 micrograms.min-1.kg-1). The second epinephrine infusion dose evoked significant increases in urine flow (V; 0.7 +/- 0.2 to 1.2 +/- 0.2 ml/min), free water clearance (CH2O; 0.3 +/- 0.1 to 0.7 +/- 0.1 ml/min), glomerular filtration rate (GFR; 3.9 +/- 0.7 to 5.4 +/- 0.8 ml/min), fractional water excretion (V/CH2O; 19 +/- 3 to 25 +/- 2%), mean arterial pressure (MAP; 45 +/- 3 to 51 +/- 4 mmHg), and a 94% increase in plasma ANF levels. A fourfold increase in the infusion dose significantly increased osmolar clearance (0.3 +/- 0.1 to 0.6 +/- 0.1 ml/min), sodium excretion (28 +/- 8 to 53 +/- 13 mueq/min), and plasma AVP levels (2.4 +/- 0.5 to 6.4 +/- 2.4 pg/ml) with no additional effect on V, CH2O, GFR, V/GFR, MAP, or plasma ANF levels. Urine osmolality and fractional sodium excretion did not change in response to epinephrine infusion. Our results demonstrate that epinephrine infusion stimulates fetal ANF secretion and to a lesser extent AVP secretion and significantly influences fetal renal function.

Renal water excretion before and after remission of nephrotic syndrome: Relationship between free water clearance and kidney function, arginine vasopressin, angiotensin II and aldosterone in plasma before and after oral water loading

1986 ◽  
Vol 71 (1) ◽  
pp. 97-104 ◽  
Author(s):  
E. B. Pedersen ◽  
H. Danielsen ◽  
S. S. Sørensen ◽  
B. Jespersen
Keyword(s):  
Nephrotic Syndrome ◽  
Angiotensin Ii ◽  
Arginine Vasopressin ◽  
Free Water ◽  
Control Group ◽  
Ang Ii ◽  
Free Water Clearance ◽  
Water Load ◽  
Control Subjects ◽  
Before And After

1. An oral water load of 20 ml/kg body wt. was given to eight patients with nephrotic syndrome before and after remission of the syndrome, and to 13 healthy control subjects. Urine volume (D), free water clearance (Cwater), plasma concentrations of arginine vasopressin (AVP), angiotensin II (ANG II) and aldosterone (Aldo), were determined before and three times during the first 4 h after loading. 2. D and Cwater increased to a significantly lower level (P < 0.01) after water loading in patients with nephrotic syndrome than in control subjects, but D and Cwater were normal after remission of the syndrome. The maximum increase in Cwater (ΔCwater max.) was 1.07 ml/min (median) before remission and 7.93 ml/min after, compared with 8.01 ml/min in the control group. 3. Creatinine clearance (Ccr) increased significantly after remission (63 ml/min to 88 ml/min, P < 0.01), and the fractional excretion of sodium was enhanced. AVP was higher in the nephrotic syndrome both before (2.9 pmol/l) and after remission (2.9 pmol/l) compared with the control group (1.8 pmol/l). ANG II and Aldo did not change after remission and remained at the same level as in the control group. 4. The elevation in ΔCwatermax after remission was accompanied by an increase in Ccr in all patients and ΔCwatermax. and Ccr were significantly correlated (ρ = 0.600, n = 16, P < 0.05). No relationship was found between the change in ΔCwater max. and ANG II and Aldo. 5. AVP was significantly suppressed in patients with nephrotic syndrome before remission, but not after remission nor in control subjects, so that although AVP did not differ in nephrotic patients before and after remission, AVP cannot be excluded as a contributory factor to the reduction in Cwater in the nephrotic syndrome. 6. It is concluded that patients with nephrotic syndrome excrete an oral water load slower than control subjects and that the excretion rate is normal after remission of the syndrome. It is suggested that the normalization of Cwater may be attributed to an increase in glomerular filtration rate or a decrease in proximal tubular sodium reabsorption, although a possible role for AVP has not been excluded.

Sildenafil reduces polyuria in rats with lithium-induced NDI

2012 ◽  
Vol 302 (1) ◽  
pp. F216-F225 ◽  
Author(s):  
Talita Rojas Sanches ◽  
Rildo Aparecido Volpini ◽  
Maria H. Massola Shimizu ◽  
Ana Carolina de Bragança ◽  
Fabíola Oshiro-Monreal ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Collecting Duct ◽  
Free Water ◽  
Free Water Clearance ◽  
Urinary Osmolality ◽  
Duct Cells ◽  
Collecting Duct Cells ◽  
Medullary Collecting Duct ◽  
Oxide Synthase

Lithium (Li)-treated patients often develop urinary concentrating defect and polyuria, a condition known as nephrogenic diabetes insipidus (NDI). In a rat model of Li-induced NDI, we studied the effect that sildenafil (Sil), a phosphodiesterase 5 (PDE5) inhibitor, has on renal expression of aquaporin-2 (AQP2), urea transporter UT-A1, Na+/H+ exchanger 3 (NHE3), Na+-K+-2Cl− cotransporter (NKCC2), epithelial Na channel (ENaC; α-, β-, and γ-subunits), endothelial nitric oxide synthase (eNOS), and inducible nitric oxide synthase. We also evaluated cGMP levels in medullary collecting duct cells in suspension. For 4 wk, Wistar rats received Li (40 mmol/kg food) or no treatment (control), some receiving, in weeks 2–4, Sil (200 mg/kg food) or Li and Sil (Li+Sil). In Li+Sil rats, urine output and free water clearance were markedly lower, whereas urinary osmolality was higher, than in Li rats. The cGMP levels in the suspensions of medullary collecting duct cells were markedly higher in the Li+Sil and Sil groups than in the control and Li groups. Semiquantitative immunoblotting revealed the following: in Li+Sil rats, AQP2 expression was partially normalized, whereas that of UT-A1, γ-ENaC, and eNOS was completely normalized; and expression of NKCC2 and NHE3 was significantly higher in Li rats than in controls. Inulin clearance was normal in all groups. Mean arterial pressure and plasma arginine vasopressin did not differ among the groups. Sil completely reversed the Li-induced increase in renal vascular resistance. We conclude that, in experimental Li-induced NDI, Sil reduces polyuria, increases urinary osmolality, and decreases free water clearance via upregulation of renal AQP2 and UT-A1.

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