Role of arginine vasopressin on fluid and electrolyte balance in rats exposed to high altitude

1981 ◽  
Vol 240 (3) ◽  
pp. R182-R186
Author(s):  
R. M. Jones ◽  
F. T. LaRochelle ◽  
S. M. Tenney
Keyword(s):  
Water Intake ◽  
Arginine Vasopressin ◽  
Urine Output ◽  
Urine Volume ◽  
Urine Concentration ◽  
Hypoxic Exposure ◽  
Electrolyte Balance ◽  
Paired Samples ◽  
Reduced Water

Normal rats (N) and rats with hereditary hypothalamic diabetes insipidus (DI) were employed to examine the role of arginine vasopressin (AVP) in the reduction of water intake and urine output during hypoxic exposure. The pattern of reduced water intake followed by recovery was similar in both N and DI rats during 7 days of hypobaric hypoxia (inspired O2 pressure of 75 Torr). Water intake was markedly reduced during the first 6 h of hypoxic exposure in both groups, whereas urine output did not decrease significantly until after 6 h in DI rats and after 18 h in N rats. Total urinary excretion of AVP in N rats decreased and remained depressed during 7 days of hypoxia. (AVP excretion corrected for osmolar clearance was unchanged.) Plasma AVP of conscious N rats was 2.7 +/- 0.40 pg/ml plasma during normoxia and 2.4 +/- 0.74 pg/ml plasma after 2 h of exposure to inspired O2 fractional concentrations of 0.105 (paired samples). We conclude that AVP is not a major factor in the decreased water intake and urine output observed during hypoxia, and that the initial disturbance is a reduced water intake that leads to negative water balance, reduced urine volume, increased urine concentration, and hyperosmotic volume contraction. The reduced or unchanged AVP release in normal rats during hypoxia appears to be inappropriate.

Impairment of osmotically stimulated AVP release in patients with primary polydipsia

1993 ◽  
Vol 265 (6) ◽  
pp. R1247-R1252 ◽  
Author(s):  
A. M. Moses ◽  
B. Clayton
Keyword(s):  
Diabetes Insipidus ◽  
Arginine Vasopressin ◽  
Plasma Osmolality ◽  
Normal Subjects ◽  
Urine Concentration ◽  
Published Data ◽  
Posterior Pituitary ◽  
Primary Polydipsia ◽  
Number Of Factors

The secretion of arginine vasopressin (AVP) from the posterior pituitary is primarily and finely regulated by the osmolality of plasma. Even though a number of factors alter osmolality-induced release of AVP, there are no published data in humans that have addressed the role of chronic overhydration on this phenomenon. To address this problem we have identified eight patients with primary polydipsia using criteria not involving measurement of AVP, and have subjected them to standardized infusions of hypertonic saline. These patients had less AVP in both plasma and urine in relation to plasma osmolality than was found in normal subjects. In addition, their rate of rise of plasma and urine AVP was less than in normal subjects. Their osmotic threshold for AVP release may have been higher than normal. These data demonstrate that chronic overhydration in humans downregulates the release of AVP in response to hypertonicity. This phenomenon may explain the impairment of urine concentration in patients with primary polydipsia and emphasizes the basis of the difficulty that may occur clinically in differentiating between patients with primary polydipsia and partial central diabetes insipidus.

The effects of water deprivation and water loading during treatment with 1-deamino-8-D-arginine vasopressin in central diabetes insipidus in childhood

1981 ◽  
Vol 97 (3) ◽  
pp. 358-360 ◽  
Author(s):  
Dorothy J. Becker ◽  
Thomas P. Foley
Keyword(s):  
Diabetes Insipidus ◽  
Water Intake ◽  
Arginine Vasopressin ◽  
Urine Output ◽  
Water Deprivation ◽  
Fluid Intake ◽  
Marked Decrease ◽  
Central Diabetes Insipidus ◽  
Water Loading ◽  
Serum Osmolarity

Abstract. Nine children aged 72/12 to 179/12 years with central diabetes insipidus were subjected to water deprivation and water loading during treatment with 1-deamino-8-D-arginine vasopressin (DDVAP). Urine output remained unchanged despite the large differences in water intake. Serum osmolarity was not significantly affected by water deprivation. However, there was a marked decrease in serum osmolarity during water loading. This was not accompanied by any symptoms of haemodilution. Thus patients apparently tolerate large variations in fluid intake during therapy with DDVAP.

scholarly journals Endoplasmic reticulum chaperone BiP/GRP78 knockdown leads to autophagy and cell death of arginine vasopressin neurons in mice

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Yohei Kawaguchi ◽  
Daisuke Hagiwara ◽  
Takashi Miyata ◽  
Yuichi Hodai ◽  
Junki Kurimoto ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Arginine Vasopressin ◽  
Urine Volume ◽  
Neuronal Loss ◽  
Protective Role ◽  
Unfolded Protein ◽  
The Unfolded Protein Response ◽  
Vasopressin Neurons

AbstractThe immunoglobulin heavy chain binding protein (BiP), also referred to as 78-kDa glucose-regulated protein (GRP78), is a pivotal endoplasmic reticulum (ER) chaperone which modulates the unfolded protein response under ER stress. Our previous studies showed that BiP is expressed in arginine vasopressin (AVP) neurons under non-stress conditions and that BiP expression is upregulated in proportion to the increased AVP expression under dehydration. To clarify the role of BiP in AVP neurons, we used a viral approach in combination with shRNA interference for BiP knockdown in mouse AVP neurons. Injection of a recombinant adeno-associated virus equipped with a mouse AVP promoter and BiP shRNA cassette provided specific BiP knockdown in AVP neurons of the supraoptic (SON) and paraventricular nuclei (PVN) in mice. AVP neuron-specific BiP knockdown led to ER stress and AVP neuronal loss in the SON and PVN, resulting in increased urine volume due to lack of AVP secretion. Immunoelectron microscopy of AVP neurons revealed that autophagy was activated through the process of AVP neuronal loss, whereas no obvious features characteristic of apoptosis were observed. Pharmacological inhibition of autophagy by chloroquine exacerbated the AVP neuronal loss due to BiP knockdown, indicating a protective role of autophagy in AVP neurons under ER stress. In summary, our results demonstrate that BiP is essential for the AVP neuron system.

Renal and hormonal responses to prolonged atrial stretch

1990 ◽  
Vol 258 (5) ◽  
pp. R1286-R1290 ◽  
Author(s):  
S. Kaufman
Keyword(s):  
Urine Output ◽  
Urine Volume ◽  
Right Atrial ◽  
Electrolyte Balance ◽  
Hormonal Responses ◽  
Renal Response ◽  
Physiological Importance ◽  
Reflex Pathways ◽  
The Relationship ◽  
Atrial Receptors

The relationship between prolonged (6 h) atrial stretch, urine output, and plasma atrial natriuretic factor (ANF) was investigated in conscious rats. On inflation of a balloon at the superior venal caval-right atrial junction, urine volume and sodium output increased. However, this renal response was no longer apparent after the first hour, and there were no further changes in urine output when the balloon was deflated. This transient renal response was most marked during the first 30 min of balloon inflation, at which time plasma ANF was also elevated. At 6 h, plasma ANF was still elevated, although urine output had, by then, returned to normal. On deflation of the balloon, plasma ANF levels returned to normal. It is clear that the renal and hormonal responses to atrial stretch may be temporally uncoupled. This probably reflects adaptation of the atrial volume receptors in the absence of such an effect on ANF release. Although this might be interpreted to mean that ANF is not of physiological importance in fluid and electrolyte balance, a more plausible explanation is that ANF needs the backing of the reflex pathways arising from stimulation of the atrial receptors to express its natriuretic activity.

scholarly journals Collecting duct-specific knockout of adenylyl cyclase type VI causes a urinary concentration defect in mice

2012 ◽  
Vol 302 (1) ◽  
pp. F78-F84 ◽  
Author(s):  
Karl P. Roos ◽  
Kevin A. Strait ◽  
Kalani L. Raphael ◽  
Mitsi A. Blount ◽  
Donald E. Kohan
Keyword(s):  
Adenylyl Cyclase ◽  
Water Intake ◽  
Arginine Vasopressin ◽  
Water Deprivation ◽  
Collecting Duct ◽  
Urine Volume ◽  
Urine Osmolality ◽  
Camp Accumulation ◽  
Water Excretion ◽  
Normal Water

Collecting duct (CD) adenylyl cyclase VI (AC6) has been implicated in arginine vasopressin (AVP)-stimulated renal water reabsorption. To evaluate the role of CD-derived AC6 in regulating water homeostasis, mice were generated with CD-specific knockout (KO) of AC6 using the Cre/loxP system. CD AC6 KO and controls were studied under normal water intake, chronically water loaded, or water deprived; all of these conditions were repeated in the presence of continuous administration of 1-desamino-8-d-arginine vasopressin (DDAVP). During normal water intake or after water deprivation, urine osmolality (Uosm) was reduced in CD AC6 KO animals vs. controls. Similarly, Uosm was decreased in CD AC6 KO mice vs. controls after water deprivation+DDAVP administration. Pair-fed (with controls) CD AC6 KO mice also had lower urine osmolality vs. controls. There were no detectable differences between KO and control animals in fluid intake or urine volume under any conditions. CD AC6 KO mice did not have altered plasma AVP levels vs. controls. AVP-stimulated cAMP accumulation was reduced in acutely isolated inner medullary CD (IMCD) from CD A6 KO vs. controls. Medullary aquaporin-2 (AQP2) protein expression was lower in CD AC6 KO mice vs. controls. There were no differences in urinary urea excretion or IMCD UT-A1 expression; however, IMCD UT-A3 expression was reduced in CD AC6 KO mice vs. controls. In summary, AC6 in the CD regulates renal water excretion, most likely through control of AVP-stimulated cAMP accumulation and AQP2.

scholarly journals Role of Renal Nerves in the Treatment of Renovascular Hypertensive Rats withL-Arginine

2014 ◽  
Vol 2014 ◽  
pp. 1-7
Author(s):  
Sonia Alves Gouvea ◽  
Renata V. Tiradentes ◽  
Cintia H. Santuzzi ◽  
Vinícius Mengal ◽  
Henrique de A. Futuro Neto ◽  
...  
Keyword(s):  
Water Intake ◽  
Control Level ◽  
Urine Volume ◽  
Renal Nerves ◽  
Hypertensive Rats ◽  
Renal Nerve ◽  
Arterial Blood ◽  
Pressure Water ◽  
Natriuretic Effect

The purpose was to determine the role of renal nerves in mediating the effects of antihypertensive treatment withL-arginine in a renovascular hypertension model. The 2K1C (two-kidney one-clip model) hypertensive rats were submitted to bilateral surgical-pharmacological renal denervation. The animals were subdivided into six experimental groups: normotensive control rats (SHAM), 2K1C rats, 2K1C rats treated withL-arginine (2K1C + L-arg), denervated normotensive (DN) rats, denervated 2K1C (2K1C + DN) rats, and denervated 2K1C + L-arg (2K1C + DN + L-arg) rats. Arterial blood pressure, water intake, urine volume, and sodium excretion were measured. The 2K1C rats exhibited an increase in the mean arterial pressure (MAP) (from 106 ± 3 to 183 ± 5.8 mmHg,P<0.01), whereasL-arg treatment induced a reduction in the MAP (143 ± 3.4 mmHg) without lowering it to the control level. Renal nerve denervation reduced the MAP to normotensive levels in 2K1C rats with or without chronicL-arg treatment.L-arg and denervation induced increases in water intake and urine volume, andL-arg caused a significant natriuretic effect. Our results suggest that renal sympathetic activity participates in the genesis and the maintenance of the hypertension and also demonstrate that treatment withL-arg alone is incapable of normalizing the MAP and that the effect of such treatment is not additive with the effect of kidney denervation.

The role of renal nerves in the response to dipsogenic stimuli in the rat

1978 ◽  
Vol 56 (5) ◽  
pp. 731-734 ◽  
Author(s):  
Michael D. Sharpe ◽  
Gordon J. Mogenson ◽  
Franco R. Calaresu
Keyword(s):  
Water Intake ◽  
Water Deprivation ◽  
Neural Control ◽  
Renal Denervation ◽  
Urine Volume ◽  
Renal Nerves ◽  
Total Water ◽  
Physiological Processes ◽  
Drinking Response

The effect of bilateral renal denervation on water intake and urine volume during specific thirst challenges was studied in rats. Renal denervation attenuated significantly the drinking response elicited by the administration of 30% polyethylene glycol (PG, extracellular challenge) but had no effect on the drinking response after an intracellular challenge (2.5 M NaCl) or after a 24-h water deprivation period. Furthermore, during a PG challenge total water intake was the same in two groups of rats, one with denervated kidneys and the other with β-adrenergic neural activity in efferent renal nerves eliminated by blocking agents. Urine volumes were not affected by PG administration or water deprivation in denervated rats but were increased significantly after administration of 2.5 M NaCl. These results indicate that renal nerves play an important role in the physiological processes controlling extracellular thirst, and suggest that this role may be related to the neural control of release of renin.

scholarly journals Early Coaching to Increase Water Intake in CKD

2021 ◽  
Author(s):  
Mariia D. Ivanova ◽  
Anatoliy I. Gozhenko ◽  
Tommy Crestanello ◽  
Dmytro D. Ivanov
Keyword(s):  
Renal Function ◽  
Randomized Trial ◽  
Kidney Function ◽  
Water Intake ◽  
Urine Volume ◽  
Oral Solution ◽  
Increase Water Intake ◽  
Group Randomized Trial ◽  
Ckd Stage ◽  
Patient Reported

<b><i>Introduction:</i></b> In observational studies, increased water intake improves kidney function but not in adults with CKD stage 3 and more. CKD WIT trial has shown a nonsignificant gradual decline in kidney function after 1 year of coaching to increase water intake (CIWI) [<xref ref-type="bibr" rid="ref1">1</xref>]. We propose that CIWI may benefit in CKD stage 1–2 (G1 and G2) and depends on functional renal functional reserve (RFR) [<xref ref-type="bibr" rid="ref2">2</xref>, <xref ref-type="bibr" rid="ref3">3</xref>]. <b><i>Objective:</i></b> Parallel-group randomized trial was aimed to determinate the effectiveness of CIWI dependence of estimated glomerular filtration rate (eGFR) stage and RFR in adults with CKD 1–2 stages. <b><i>Methods:</i></b> CKD WIT trial was taken as the basis for prospective multicenter randomized trial named “Early Coaching to Increase Water Intake in CKD (ECIWIC).” The primary outcome was the change in kidney function by eGFR from baseline to 12 months. Secondary outcomes included 1-year change in urine albumin/Cr ratio, and patient-reported overall quality of health (QH) ranged from 0 (worst possible) to 10 (best possible). CIWI aimed to have the diuresis being 1.7–2 L. There were 4 groups with nondiet sodium restriction which consisted of 31 patients each: 2 groups with CKD G1 and CKD G2, undergoing CIWI and 2 others with CKD G1 and CKD G2 without CIWI (Fig. 1a). Overall checks were made at 0, 6, and 12 months. RFR evaluation was performed using 0.45% sodium chloride oral solution. <b><i>Results:</i></b> Of our randomized 124 patients (mean age 53.2 years; men 83 [67%], 0 died), mean change in 24-h urine volume was 0.6 L per day in G1 with CIWI group and 0.5 L in G2. No statistically significant data on eGFR depending CIWI were obtained (Fig. <xref ref-type="fig" rid="f01">1</xref>b). However, the trend suggests that CIWI improves eGFR in CKD G1 (from 95 to 96 mL/min/1.73 m<sup>2</sup>) and preserves eGFR decline in CKD G2 (78–78). The QH values were also preserved (from 7 to 7 in G1 and G2 groups). Although coaching to maintain the same water intake did not preserve physiological and pathological eGFR decreasing in CKD G1-2 (G1 from 96 to 93, G2 from 76 to 73; <i>t</i> = 0.6, <i>p</i> = 0.29, and <i>p</i> ≤ 0.05 in all groups) and the QH was declined (from 7 to 6 in both groups). An individual analysis of the RFR has shown that patients with RFR more than 50% (G1 19 patients, 61%, and G2 13 patients, 42%) had reliable preservation of eGFR with its increase of 1.5 mL/min on CIWI, while patients with low functional renal reserve had a drop of eGFR at 1.1 mL/min/m<sup>2</sup> within 12 months. Patients with low normal serum sodium levels have shown worse results on CIWI. <b><i>Conclusions:</i></b> With CKD G1, the CIWI leads to the preservation of the renal function with its increase of GFR per 1 mL/min/m<sup>2</sup>/per year in comparison with the same water intake. In CKD G2, the CIWI prevents physiological and pathological loss of renal function, and RFR above 50% aids restoration of eGFR both in CKD G1-2. ECIWIC trial demonstrates benefit of CIWI in patients with CKD 1–2 and preserved RFR.

Chronic intravenous administration of V1 arginine vasopressin agonist results in sustained hypertension

1994 ◽  
Vol 267 (2) ◽  
pp. H751-H756 ◽  
Author(s):  
A. W. Cowley ◽  
E. Szczepanska-Sadowska ◽  
K. Stepniakowski ◽  
D. Mattson
Keyword(s):  
Body Weight ◽  
Arginine Vasopressin ◽  
Plasma Catecholamines ◽  
Plasma Osmolality ◽  
Sprague Dawley ◽  
Prolonged Administration ◽  
Chronic Stimulation ◽  
Sustained Hypertension ◽  
Sprague Dawley Rats

Despite the well-recognized vasoconstrictor and fluid-retaining actions of vasopressin, prolonged administration of arginine vasopressin (AVP) to normal animals or humans fails to produce sustained hypertension. The present study was performed to elucidate the role of the V1 receptor in determining the ability of AVP to produce sustained hypertension. Conscious Sprague-Dawley rats with implanted catheters were infused with the selective V1 agonist, [Phe2,Ile3,Orn8]vasopressin (2 ng.kg-1.min-1), for 14 days in amounts that were acutely nonpressor. Blood pressure (MAP), heart rate (HR), body weight, and water intake (WI) were determined daily. Plasma AVP, plasma catecholamines norepinephrine and epinephrine, plasma osmolality, and electrolyte concentration were determined before and on days 1 and 7 of infusion. MAP increased significantly by 10.4 +/- 4.5 mmHg on day 1 and rose to 22 +/- 5 mmHg above control by day 14 (transient decrease on days 6-9) and then fell to control levels after the infusion was stopped. HR did not change significantly. Plasma AVP immunoreactivity increased from 2.5 +/- 0.3 to 10.9 +/- 2.1 pg/ml, whereas norepinephrine tended to fall only on day 1, with epinephrine only slightly elevated on day 7. No evidence of fluid retention was found, and rats lost sodium only on the first day of V1 agonist infusion. Body weight increased throughout the study but was unrelated to the changes of MAP. We conclude that chronic stimulation of V1 receptors results in sustained hypertension in rats.

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