Effects of gonadectomy on sexually dimorphic antidiuretic action of vasopressin in conscious rats

1994 ◽  
Vol 267 (2) ◽  
pp. R536-R541 ◽  
Author(s):  
Y. X. Wang ◽  
J. T. Crofton ◽  
H. Liu ◽  
D. P. Brooks ◽  
L. Share
Keyword(s):  
Estrous Cycle ◽  
Urine Volume ◽  
Free Water ◽  
Female Rats ◽  
Intact Male ◽  
Free Water Clearance ◽  
Urinary Osmolality ◽  
Arterial Blood ◽  
Antidiuretic Action ◽  
Water Clearance

The present study examined whether the antidiuretic response to vasopressin is affected by the estrous cycle and by gonadectomy in conscious, chronically instrumented hydrated rats. Infusion of vasopressin (10-100 pg.min-1.kg body wt-1) resulted in a dose-dependent antidiuresis. Urine volume and free water clearance decreased and urinary osmolality increased with no significant changes in mean arterial blood pressure, heart rate, osmolar clearance, and urinary sodium and potassium excretion. The antidiuretic response to vasopressin was significantly greater in intact male and estrous female rats than in intact female rats in the other phases of the estrous cycle. Thus the calculated doses of vasopressin to reduce urine flow and free water clearance, as well as to increase urinary osmolality 50% from their control values, were significantly higher in nonestrous females than in males and estrous females. Gonadectomy was without effect on the antidiuretic potency of vasopressin in males, but in gonadectomized females the antidiuretic response to vasopressin was enhanced to a level similar to that observed in intact males. These data indicate that the antidiuretic activity of vasopressin is affected not only by gender but also by phase of the estrous cycle and that the ovarian hormone(s) may modulate the antidiuretic action of vasopressin.

Cooperative mechanisms of acute antidiuretic response to bendroflumethiazide in rats with lithium-induced nephrogenic diabetes insipidus

2010 ◽  
Vol 88 (12) ◽  
pp. 1191-1201 ◽  
Author(s):  
S. Mostafa Shid Moosavi ◽  
Masoud Haghani
Keyword(s):  
Diabetes Insipidus ◽  
Nephrogenic Diabetes Insipidus ◽  
Urine Volume ◽  
Free Water ◽  
Urine Flow ◽  
Water Reabsorption ◽  
Free Water Clearance ◽  
Urinary Osmolality ◽  
Antidiuretic Effect ◽  
Water Clearance

The exact mechanism underlying thiazides-induced paradoxical antidiuresis in diabetes insipidus is still elusive, but it has been hypothesized that it is exerted either via Na+-depletion activating volume-homeostatic reflexes to decrease distal delivery, or direct stimulation of distal water reabsorption. This study examined how these two proposed mechanisms actually cooperate to induce an acute bendroflumethiazide (BFTZ)-antidiuretic effect in nephrogenic diabetes insipidus (NDI). Anaesthetized rats with lithium (Li)-induced NDI were prepared in order to measure their renal functional parameters, and in some of them, bilateral renal denervation (DNX) was induced. After a 30 min control clearance period, we infused either BFTZ into 2 groups, NDI+BFTZ and NDI/DNX+BFTZ, or its vehicle into a NDI+V group, and six 30 min experimental clearance periods were taken. During BFTZ infusion in the NDI+BFTZ group, transiently elevated Na+ excretion was associated with rapidly increased urinary osmolality and decreased free water clearance, but Li clearance and urine flow declined in the later periods. However, in the NDI/DNX+BFTZ group, there was persistently elevated Na+ excretion with unchanged Li clearance and urine flow during the experimental period, while alterations in free water clearance and urinary osmolality resembled those in the NDI+BFTZ group. In conclusion, BFTZ initially exerted two direct effects of natriuresis–diuresis and stimulating free water reabsorption at the distal nephron in NDI, which together elevated Na+ excretion and urinary osmolality but kept the urine volume unchanged in the first hour. Thereafter, the resultant sodium depletion led to the activation of neural reflexes that reduced distal fluid delivery to compensate for BFTZ-induced natriuresis–diuresis which, in cooperation with the direct distal BFTZ-antidiuretic effect, resulted in excretion of urine with a low volume, high osmolality, and normal sodium.

Potentiation of the natriuretic effect of clonidine following indomethacin in the rat

1991 ◽  
Vol 69 (8) ◽  
pp. 1196-1203 ◽  
Author(s):  
Dorothea E. Blandford ◽  
Donald D. Smyth
Keyword(s):  
Sodium Excretion ◽  
Infusion Rate ◽  
Urine Volume ◽  
Free Water ◽  
Vehicle Group ◽  
Prostaglandin E ◽  
Free Water Clearance ◽  
Prostaglandin Production ◽  
Natriuretic Effect ◽  
Water Clearance

Previous studies have demonstrated a diuretic effect of clonidine at low intrarenal infusion rates with a natriuretic effect being observed at high infusion rates (≥3 μg∙kg−1∙min−1). The natriuresis at high infusion rates may have been secondary to increased renal prostaglandin production. We therefore evaluated the effects of indomethacin (a cyclooxygenase inhibitor) on the response to cionidine in the anesthetized rat. Intrarenal infusions of saline (vehicle) or clonidine (0.1, 0.3, 1, and 3 μg∙kg−1∙min−1) were examined both in the presence and absence of pretreatment with indomethacin (5 mg/kg, i.p.). Clonidine produced a dose-related increase in urine volume and free water clearance at 0.3, 1, and 3 μg∙kg−1∙min−1 as compared with the vehicle group. Sodium excretion and osmolar excretion were increased only at the highest infusion rate investigated. Following indomethacin pretreatment, clonidine produced a greater increase in urine volume at each infusion rate investigated. The indomethacin pretreatment also resulted in a potentiation of the natriuretic effect of clonidine at all infusion rates. Interestingly, this was associated with an increase in osmolar clearance but not free water clearance. These effects of indomethacin were reversed by infusion of prostaglandin E2. An infusion of prostaglandin E2 attenuated the indomethacin-induced increase in both urine flow rate and sodium excretion, indicating that the effects of indomethacin were mediated by prostaglandin inhibition. These results suggest that endogenous prostaglandin production attenuates the renal effects of clonidine, and as well, that in the presence of α2-adrenoceptor stimulation, prostaglandin E2 mediates an antidiuretic and antinatriuretic effect.Key words: clonidine, indomethacin, prostaglandin E2, diuresis, natriuresis.

RENAL DIURESIS AFTER INJECTIONS OF THE FRESHWATER EEL AND ANTIDIURESIS ARGININE VASOTOCIN IN (ANGUILLA ANGUILLA L.)

1974 ◽  
Vol 61 (3) ◽  
pp. 487-500 ◽  
Author(s):  
I. W. HENDERSON ◽  
N. A. M. WALES
Keyword(s):  
Body Weight ◽  
Glomerular Filtration ◽  
Free Water ◽  
Anguilla Anguilla ◽  
Arginine Vasotocin ◽  
Free Water Clearance ◽  
Response Characteristics ◽  
Arterial Blood ◽  
Urine Production ◽  
Water Clearance

SUMMARY The renal responses of the freshwater-adapted eel, Anguilla anguilla L. to arginine vasotocin ([8-arginine]-oxytocin) have been examined. The quality of the responses to the intravenously administered peptide was found to vary with the dose. Less than 0·1 ng/kg body weight reduced glomerular filtration rate, free water clearance and rate of urine production for up to 60 min. Doses greater than 1·0 ng/kg body weight induced a 'glomerular diuresis', i.e. increased rates of urine production, glomerular filtration and free water clearance for 40–60 min. Neither the diuretic nor the antidiuretic doses produce changes in urinary composition, and no obvious direct tubular actions of the peptide were found. Arterial blood pressure, measured in the dorsal aorta, increased with some of the diuretic doses, whilst the lower doses (less than 10 ng/kg body weight) had little or no cardiovascular actions. The mechanisms involved in these dose—response characteristics are discussed with particular regard to the renal function of lower vertebrates. It is suggested that arginine vasotocin plays a primary or secondary role in the modulation of 'glomerular intermittency'.

A Role for Sodium-Retaining Steroids in the Regulation of Proximal Tubular Sodium Reabsorption in Man

1972 ◽  
Vol 42 (4) ◽  
pp. 423-432 ◽  
Author(s):  
John R. Gill ◽  
Catherine S. Delea ◽  
F. C. Bartter
Keyword(s):  
Flow Rate ◽  
Sodium Excretion ◽  
Free Water ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Diluting Segment ◽  
Free Water Clearance ◽  
Urinary Osmolality ◽  
Glomerular Filtrate ◽  
Water Clearance

1. The response to an infusion of 4% (w/v) fructose in water was determined in fifteen women on a daily sodium intake of 100 mEq/day. The results were compared with those obtained during a similar infusion on another day after treatment with deoxycorticosterone (20 mg/day; seven subjects), or spironolactone (200 mg/day; eight subjects), for 1 day before the day of study. 2. Treatment with deoxycorticosterone significantly (P < 0·01) decreased sodium excretion (from a mean value of 391 to 192 μEq/min) and urine flow rate (from 14·3 to 12·4 ml min−1 100 ml−1 of glomerular filtrate) without a change in urinary osmolality or the clearance of inulin. The steroid also increased the fractional reabsorption of sodium at the diluting segment of the nephron, but this increase in reabsorption was not sufficient to compensate for the decrease in delivery of sodium to the site, so that absolute free-water clearance decreased. 3. Treatment with spironolactone significantly (P < 0·01) increased sodium excretion (from 349 to 437 μEq/min) and urine flow rate (from 12·5 to 14·4 ml min−1 100 ml−1 of glomerular filtrate) with essentially no change in urinary osmolality or in inulin clearance. Spironolactone also decreased the fractional reabsorption of sodium at the diluting segment of the nephron, but the degree of inhibition of reabsorption was not sufficient to prevent an increase in free-water clearance as a result of increased delivery of sodium to the site. 4. The findings support the concept that changes in circulating aldosterone can alter the renal excretion of sodium in man by affecting its reabsorption in the proximal tubule as well as in the distal tubule.

scholarly journals Evaluation of 24h Urine Volume as an Indicator of Uosm:Posm Ratio and Free Water Clearance in Pregnant Women

2015 ◽  
Vol 29 (S1) ◽  
Author(s):  
Amy McKenzie ◽  
Colleen Muñoz ◽  
Erica Perrier ◽  
Liliana Jimenez ◽  
Lawrence Armstrong
Keyword(s):  
Pregnant Women ◽  
Urine Volume ◽  
Free Water ◽  
Free Water Clearance ◽  
Water Clearance

Sex differences in the cardiovascular and renal actions of vasopressin in conscious rats

1997 ◽  
Vol 272 (1) ◽  
pp. R370-R376 ◽  
Author(s):  
Y. X. Wang ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Sex Difference ◽  
Free Water ◽  
Urine Osmolality ◽  
Urine Flow ◽  
Female Rats ◽  
Male Rats ◽  
Separate Experiment ◽  
Free Water Clearance ◽  
Dose Dependent ◽  
Antidiuretic Action

The present study was carried out to investigate whether prostaglandins (PG) are involved in the mechanism that contributes to the sex difference in the antidiuretic and pressor actions of vasopressin. The experiments were performed in conscious male and nonestrous female rats. In hydrated rats, the graded infusion of vasopressin (10-1,000 pg.min 1.kg body wt-1) resulted in a dose-dependent antidiuresis: decreases in urine flow and free water clearance and an increase in urine osmolality. These responses were significantly greater in male than in nonestrous female rats. Pretreatment with a cyclooxygenase inhibitor, indomethacin (10 mg/kg body wt iv), significantly enhanced the antidiuretic response to vasopressin in both sexes. However, the magnitude of this enhancement was greater in female than in male rats. Thus indomethacin abolished the sex difference in the antidiuretic response to vasopressin. In a separate experiment in rats without water hydration and urine collection, infusion of pressor doses of vasopressin (1,000-6,000 pg.min-1.kg body wt-1) resulted in a greater increase in blood pressure in male than in nonestrous female rats. Treatment with indomethacin enhanced this response equivalently in both sexes and thus did not affect the sex difference in the pressor action of vasopressin. These data indicate that renal PG may mediate, at least in part, the sex difference in the antidiuretic action of vasopressin, whereas vascular PG seem not to play an important role in the sex difference in the pressor action of vasopressin.

Renal and humoral responses to sustained cardiopulmonary baroreceptor deactivation in humans

1991 ◽  
Vol 260 (3) ◽  
pp. R642-R648 ◽  
Author(s):  
J. A. Miller ◽  
J. S. Floras ◽  
K. L. Skorecki ◽  
L. M. Blendis ◽  
A. G. Logan
Keyword(s):  
Lower Body Negative Pressure ◽  
Renal Plasma Flow ◽  
Venous Pressure ◽  
Plasma Concentrations ◽  
Free Water ◽  
Plasma Norepinephrine ◽  
Free Water Clearance ◽  
Arterial Blood ◽  
Cardiopulmonary Baroreflex ◽  
Water Clearance

The renal and neurohumoral effects of prolonged cardiopulmonary baroreflex unloading and the relationship of these changes to urinary sodium excretion have not been well documented in humans. In this study, 12 normal males underwent lower body negative pressure at -15 mmHg for 90 min, a maneuver that deactivates cardiopulmonary baroreceptors. Glomerular filtration rate (GFR), effective renal plasma flow (ERPF), and filtration fraction (FF) were measured in eight of these subjects using inulin and p-aminohippuric acid clearance techniques. During reduction of central venous pressure, arterial blood pressure and heart rate did not change. Plasma concentrations of atrial natriuretic factor (ANF) decreased markedly (22 +/- 2 to 12 +/- 1 pg/ml, P = 0.0001) as did the second messenger of ANF's biological action, guanosine 3',5'-cyclic monophosphate, whereas renin and vasopressin were not significantly altered. There was a significant rise in plasma norepinephrine (1.6 +/- 0.2 to 2.4 +/- 0.4 nmol/l, P = 0.03). GFR (104 +/- 9 to 68 +/- 6 ml/min, P = 0.007) and FF (0.18 +/- 0.01 to 0.14 +/- 0.01, P = 0.007) decreased significantly, with maintenance of ERPF. There was a significant antinatriuresis without an antikaliuresis and a significant reduction in free water clearance. These changes in renal hemodynamics are unlike the known effects of renal vasoconstrictors, and the alterations in solute and free water clearance are consistent with the removal of the known actions of ANF from tubular target sites. Taken together, our findings suggest that a mechanism other than activation of vasoconstrictors, possibly the diminution of the influence of ANF on the kidney, may be operative in the renal adjustments to cardiopulmonary baroreflex deactivation in humans.

THE ACUTE EFFECTS OF INFUSED ADRENAL STEROIDS ON RENAL FUNCTION IN ADRENALECTOMIZED DOGS

1961 ◽  
Vol 37 (2) ◽  
pp. 263-278 ◽  
Author(s):  
J. D. H. Slater ◽  
Paul Mestitz ◽  
Geoffrey Walker ◽  
J. D. N. Nabarro
Keyword(s):  
Urine Volume ◽  
Free Water ◽  
Potassium Excretion ◽  
Adrenal Steroids ◽  
Acute Effects ◽  
Filtration Fraction ◽  
Free Water Clearance ◽  
Sodium And Potassium ◽  
Slow Absorption ◽  
Water Clearance

ABSTRACT Infusions of cortisol (11β,17,21-trihydroxy-pregn-4-ene-3,20-dione), prednisolone (11β,17,21-trihydroxy-pregna-1,4-diene-3,20-dione), aldosterone (11β,21-dihydroxy-3,20-dione-pregn-4-en-18-al), and adrenal cortical extract have been given to four adrenalectomized dogs. The changes of inulin, creatinine, para-aminohippuric acid clearances, urine volume, and sodium and potassium excretion have been measured. Between experiments oral replacement therapy was given to obviate the effect of slow absorption of previously injected steroids. The effects of steroid-free control infusions have been studied. Varying the rate of infusion from 1.0–2.6 ml/min, and sodium from 0–170 μeq/min has little effect on glomerular filtration rates (G. F. R.). Infusions of cortisol (1.5 and 10 mg/h), prednisolone (2 mg/h) and adrenal cortical extract (10 ml/h) raised the G. F. R. and lowered the filtration fraction. As the G. F. R. increased the ratio creatinine: inulin clearance fell. The different dogs varied in their responses. Infusions of prednisolone and cortisol (1.5 mg/h) usually increased sodium output as G. F. R. rose. With aldosterone, adrenal cortical extract and cortisol (10 mg/h) there was sodium retention in three of the four dogs, the fourth was resistant to the sodium retaining action of these steroids while the plasma level was high. All steroid infusions increased potassium excretion. Cortisol increased free water clearance independent of G. F. R. provided the infusion rate exceeded 2 ml/min, prednisolone increased both osmolar and free water clearance, aldosterone increased osmolar clearance and reduced free water clearance.

scholarly journals Selective V2-Receptor Vasopressin Antagonism Decreases Urinary Aquaporin-2 Excretion in Patients with Chronic Heart Failure

1999 ◽  
Vol 10 (10) ◽  
pp. 2165-2170
Author(s):  
PIERRE-YVES MARTIN ◽  
WILLIAM T. ABRAHAM ◽  
XU LIEMING ◽  
BEATRIZ R. OLSON ◽  
RON M. OREN ◽  
...  
Keyword(s):  
Heart Failure ◽  
Steady State ◽  
Chronic Heart Failure ◽  
Collecting Duct ◽  
Free Water ◽  
Free Water Clearance ◽  
Urinary Osmolality ◽  
Aquaporin 2 ◽  
V2 Receptor ◽  
Water Clearance

Abstract. Aquaporin-2 (AQP-2), a water channel located on the apical membrane of collecting duct cells, regulates water reabsorption under the control of vasopressin (AVP). Using an antibody directed to human AQP-2, a quantitative Western blot analysis was performed to determine the collecting duct responsiveness to an oral, nonpeptide, V2 receptor antagonist (VPA-985) in patients with chronic NYHA II and III heart failure. Standards were derived by conjugating the immunizing peptide to maleimide-activated bovine serum albumin and a standard curve was generated for each blot. Quantification of baseline steady-state AQP-2 excretion was done by collecting urine on the day before study drug administration. The next day patients received either placebo or VPA-985 at one of four different doses and urine was collected every 2 h. Thereafter, urinary AQP-2 excretion was calculated as a ratio of the urine flow and was expressed in pmol/h. During baseline, steady-state excretion did not change significantly (T0-T2, 458 ± 44; T2-T4, 443 ± 35; T4-T6, 422 ± 35; T6-T8, 401 ± 30). Compared to placebo, urinary AQP-2 excretion decreased significantly and in all groups in a dose-dependent manner during VPA-985 administration. The most impressive decrease was observed in the 250-mg group (T0-T2, 89 ± 5; T2-T4, 50 ± 18; T4-T6, 43 ± 22; T6-T8, 42 ± 23; P < 0.001 during each period compared with baseline and placebo results). VPA-985 significantly increased solute-free water clearance and urine output and significantly decreased urinary osmolality. Urinary AQP-2 excretion correlated best with solute-free water clearance during T0-T2 and T2-T4 collection, but a correlation with urinary osmolality and urinary output was also found during these periods. In conclusion, AQP-2 urinary excretion, as measured by quantitative Western analysis, is a sensitive biologic marker to assess the short-term responsiveness of the collecting duct to a V2 receptor AVP antagonist in chronic heart failure.

Effect of forward acceleration on renal function

1962 ◽  
Vol 17 (3) ◽  
pp. 413-416 ◽  
Author(s):  
John F. Watson ◽  
Rita M. Rapp
Keyword(s):  
Negative Pressure ◽  
Human Subjects ◽  
Renal Plasma Flow ◽  
Urine Volume ◽  
Free Water ◽  
Free Water Clearance ◽  
Water Excretion ◽  
Normal Human ◽  
Negative Pressure Breathing ◽  
Water Clearance

The effect of forward acceleration on renal hemodynamics, electrolyte excretion, and water clearance has been studied in six normal human subjects. Forward acceleration produced a slight increase in glomerular filtration rate and effective renal plasma flow during and after stress. After centrifugation there was a 20–35-min lag before the appearance of an increase in urine volume and free water clearance. These changes in water excretion were transient and were not accompanied by a natriuresis nor associated with changes in serum osmolality. Physiologic responses to forward acceleration and negative pressure breathing were compared. It was suggested that forward acceleration, like negative pressure breathing, may induce an increase in intrathoracic blood volume which inhibits the release of antidiuretic hormone via a nonosmotic volume-sensitive receptor mechanism located within the intrathoracic vascular space. Submitted on September 14, 1961

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