EFFECTS OF ARGININE-, LYSINE- AND LEUCINE-VASOPRESSIN ON URINARY OSMOLALITY AND RATE OF URINE FLOW IN HYDRATED RATS AND DOGS

1959 ◽  
Vol XXXII (I) ◽  
pp. 134-141 ◽  
Author(s):  
Niels A. Thorn
Keyword(s):  
Arginine Vasopressin ◽  
Urine Osmolality ◽  
Urine Flow ◽  
The Other ◽  
Maximum Increase ◽  
Urinary Osmolality ◽  
Lysine Vasopressin

ABSTRACT Arginine-, lysine- and leucine-vasopressin, injected i. v. into hydrated rats or dogs caused different patterns of response in that urine osmolality fell much more slowly after the maximum increase following arginine-vasopressin, than after the other two preparations. Using 3 different parameters for antidiuretic response, arginine-vasopressin was somewhat more potent than leucine-vasopressin in both rats and dogs, considerably more potent than lysine-vasopressin in rats, and much more so in dogs.

Sex difference in urinary concentrating ability of rats with water deprivation

1996 ◽  
Vol 270 (3) ◽  
pp. R550-R555 ◽  
Author(s):  
Y. X. Wang ◽  
J. T. Crofton ◽  
J. Miller ◽  
C. J. Sigman ◽  
H. Liu ◽  
...  
Keyword(s):  
Water Deprivation ◽  
Plasma Concentrations ◽  
Plasma Osmolality ◽  
Urine Osmolality ◽  
Ovarian Hormones ◽  
Urine Flow ◽  
The Other ◽  
Consumptive Behavior ◽  
Urinary Concentrating Ability ◽  
Previous Demonstration

Our previous demonstration of sexual dimorphism in the antidiuretic response to exogenous vasopressin prompted us to investigate the response to moderately high levels of endogenous vasopressin stimulated by water deprivation in conscious rats. After 24 h water deprivation, urine flow was significantly higher and urine osmolality lower in females than in males. Plasma concentrations of vasopressin were higher in females than in males after water deprivation, but plasma osmolality did not differ. Gonadectomy, which had no effect in dehydrated males, decreased urine flow and increased urine osmolality in females to levels observed in intact and gonadectomized males. Spontaneous water intake was also measured and found to be lower in males and estrous females than in females in the other phases of the estrous cycle. These observations support the concept that there is a gender difference in the antidiuretic responsiveness to endogenous vasopressin, that this difference is dependent upon the ovarian hormones, and that it may lead to differences in consumptive behavior.

Mechanism of cold diuresis in the rat

1983 ◽  
Vol 244 (2) ◽  
pp. F210-F216 ◽  
Author(s):  
M. L. Morgan ◽  
R. J. Anderson ◽  
M. A. Ellis ◽  
T. Berl
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Osmolality ◽  
Urine Osmolality ◽  
Urine Flow ◽  
Hemodynamic Parameters ◽  
Water Excretion ◽  
Urinary Osmolality ◽  
6 Hydroxydopamine ◽  
Renal Water Excretion

The effect of cold exposure (CE) on renal water excretion has not been clearly delineated. Conscious rats were exposed to decreased ambient temperature (15 degrees C). Forty-five minutes of CE resulted in reversible increases in urine flow and decreases in urine osmolality. The diuresis was not due to a diminished response to vasopressin (VP), as the antidiuresis associated with 500 microU of Pitressin given to water-diuresing rats was comparable at 15 and 30 degrees C. To determine whether the diuresis was due to intrarenal factors, glomerular filtration rate, renal blood flow, sodium excretion, and osmolar clearances were measured and found to be equivalent during control and cold conditions. To determine whether the observed diuresis was due to suppression of endogenous VP, VP-free Brattleboro rats undergoing a constant VP infusion were cold exposed. In these rats, CE was not associated with a change in either urine flow or urinary osmolality. This antidiuretic hormone-mediated mechanism was corroborated by a decrease in immunoassayable VP levels. To determine the mechanism whereby CE suppresses endogenous VP, plasma osmolality and hemodynamic parameters were measured. Although CE was not associated with a change in plasma osmolality, it did result in a significant increase in both mean arterial pressure and cardiac index. Pretreatment of rats with 6-hydroxydopamine prevented both the increase in mean arterial pressure and cold diuresis. We conclude that the diuresis observed upon exposure to 15 degrees C results from nonosmotic suppression of endogenous VP, as a consequence of the increase in mean arterial pressure.

Role of arginine vasopressin in fetal renal response to hypertonicity

1986 ◽  
Vol 251 (1) ◽  
pp. F156-F163
Author(s):  
L. L. Woods ◽  
C. Y. Cheung ◽  
G. G. Power ◽  
R. A. Brace
Keyword(s):  
Renal Function ◽  
Arginine Vasopressin ◽  
Urine Osmolality ◽  
Maternal Blood ◽  
Urine Flow ◽  
Fetal Blood ◽  
Fetal Plasma ◽  
Fetal Urine ◽  
Sustained Increase

We studied the effects of hyperosmolality on fetal renal function and the role of arginine vasopressin (AVP) in these responses. NaCl (9%) was injected intravenously into chronically catheterized ewes and their fetuses, followed by a continuous infusion of 9% NaCl into the ewes. The fetuses were either normal, infused with AVP, or infused with an AVP antagonist. In normal fetuses NaCl injection caused fetal and maternal blood osmolalities to be elevated by 10-15 mosmol/kg for 4 h with no change in fetal blood volume; fetal plasma AVP rose 42%. Fetal arterial pressures rose transiently by 2-10 mmHg. Fetal urine flow rose transiently by 73% after NaCl injection and then averaged 27% below control after 1 h, whereas fetal urine osmolality increased from 188 +/- 31 to 282 +/- 33 mosmol/kg. In a second group of fetuses AVP infusion alone caused fetal urine osmolality to increase by 123 +/- 39 mosmol/kg and urine flow to fall 31%, whereas in a third group the antagonist alone had no effect on urine flow or osmolality. After hypertonic injection into fetuses infused with AVP or the antagonist, the transient changes were similar to those in normal fetuses. However, the sustained increase in urine osmolality and decrease in flow after hypertonic injection were abolished in AVP-infused and antagonist-infused fetuses. Thus it appears that the transient changes in fetal renal function after hypertonic injection are not AVP-induced and may be due to transient increases in arterial pressure, whereas the prolonged changes in urine flow and osmolality appear to be mediated by increases in fetal plasma AVP levels.

The Responses to Water Deprivation in Lithium-Treated Patients with and without Polyuria

1982 ◽  
Vol 63 (6) ◽  
pp. 549-554 ◽  
Author(s):  
D. B. Morgan ◽  
M. D. Penney ◽  
R. P. Hullin ◽  
T. H. Thomas ◽  
D. P. Srinivasan
Keyword(s):  
Water Intake ◽  
Water Deprivation ◽  
Urine Osmolality ◽  
Drug Group ◽  
Urine Flow ◽  
The Other ◽  
Control Group ◽  
Manic Depressive ◽  
Renal Concentrating Mechanism ◽  
Depressive Patients

1. Urine osmolality and plasma and urine arginine vasopressin (AVP) were measured before, during and at the end of 23 h of water deprivation in four groups of subjects. There were eight non-polyuric manic-depressive patients taking lithium (the lithium group), seven manic-depressive patients taking other psychotropic drugs but not lithium (the other drug group), seven healthy subjects (the control group) and three lithium-treated patients with polyuria (the polyuric lithium group). 2. The lithium group had a resistance to the effect of AVP on the renal tubule with a fivefold increase in AVP excretion at a given urine osmolality. However, their water homoeostasis was intact as they lost no more weight during water deprivation than did the control group. 3. The relationship beween urine osmolality and AVP excretion has been defined from these results and the effect of lithium treatment on it has been characterized. The results suggest that lithium competitively inhibits the effect of AVP on the renal concentrating mechanism but does not decrease the ‘theoretical’ maximum urine osmolality. 4. The other drug group had a high basal urine flow which was due to a primary increase in water intake. The responsiveness of the renal concentrating mechanism to AVP was the same in this group as in the control group. 5. The polyuric lithium group had the highest basal urine flow and lost the greatest amount of weight during water deprivation. Neither urine osmolality nor AVP excretion was at a maximum in the basal state, as both increased during water deprivation. These relationships between urine osmolality and AVP excretion indicated a much greater resistance to AVP than in the other lithium-treated patients. 6. We suggest that these patients are polyuric as they become thirsty and drink before their AVP secretion increases to levels high enough to overcome the resistance to AVP. The results suggest, however, that in the basal state their water intake may be more than the minimum determined by the resistance to AVP.

Fetal renal contribution to amniotic fluid osmolality during maternal hypertonicity

1986 ◽  
Vol 250 (2) ◽  
pp. R235-R239
Author(s):  
L. L. Woods
Keyword(s):  
Amniotic Fluid ◽  
Continuous Infusion ◽  
Arginine Vasopressin ◽  
Urine Osmolality ◽  
Uterine Wall ◽  
Urine Flow ◽  
Bulk Flow ◽  
Vasopressin Antagonist ◽  
Fetal Plasma ◽  
Fetal Urine

The contribution of fetal urine to the increase in amniotic fluid osmolality during maternal hypertonicity was studied in chronically catheterized sheep of 130-135 days gestation. Nine percent NaCl was injected simultaneously into fetal and maternal veins, followed by a continuous infusion into the maternal vein. Maternal and fetal plasma osmolalities rose by 15 +/- 1 (SE) and 13 +/- 1 mosmol/kg, respectively, and remained constant for 4 h. Fetal urine osmolality rose significantly from 188 +/- 31 to 277 +/- 32 mosmol/kg within 1 h and remained constant thereafter. Fetal urine flow rose transiently, fell to normal within 10 min, and averaged 70% of normal beyond 1 h. Amniotic fluid osmolality rose by 10.8 +/- 2.8 mosmol/kg over 4 h. Following hypertonic injection into three fetuses blocked by the arginine vasopressin antagonist d(CH2)5D-tyr(Et)VAVP, urine osmolality did not change, and amniotic fluid osmolality rose by 2.7 +/- 0.3 mosmol/kg. Thus it appears that the increase in amniotic fluid osmolality during maternal hypertonicity may be due largely to an increased fetal urine osmolality coupled with a decreased flow of fetal urine into the amniotic space, rather than to bulk flow of fluid across the membranes and uterine wall.

Urinary osmolality as a function of flow rates in several diuretic states

1963 ◽  
Vol 204 (4) ◽  
pp. 548-554 ◽  
Author(s):  
Wolfgang Herms ◽  
Peter H. Abbrecht ◽  
Fernando Alzamora ◽  
Richard L. Malvin
Keyword(s):  
Arterial Occlusion ◽  
Urine Osmolality ◽  
Urine Flow ◽  
Osmotic Diuresis ◽  
Flow Rates ◽  
Urinary Osmolality ◽  
Ringer’S Solution ◽  
Renal Concentrating Mechanism ◽  
Urinary Concentrating Ability ◽  
And Control

The effect of different solute loads on the renal concentrating mechanism was evaluated at different glomerular filtration rates (GFR). GFR was varied by partial ureteral or arterial occlusion in dogs undergoing osmotic diuresis. A Ringer's solution was infused to which the following solutes were added so that the final concentrations of the solutes were as follows: a) 383 mm/liter mannitol + 255–285 mm/liter NaCl; b) 500 mm/liter urea; c) 193 mm/liter mannitol; d) 300 mm/liter urea + 385 mm/ liter mannitol. Steady-state values for GFR, urine flow, and urine osmolalities were obtained for the occluded and control kidneys and expressed as the ratio occluded-to-control. Changing the sodium chloride load did not alter the correlation between flow rate and urine osmolality as found in previous experiments with dogs which were not infused with additional sodium. However, variations in the urea and mannitol load did alter this relationship. The greater the mannitol load the lower was the osmolality ratio at any given GFR. The results indicate that both urea trapping and urine flow rates are important determinants of urinary concentrating ability.

Effects of vasopressin-glycine and vasopressin-glycine-lysine-arginine on renal function in the rat

1986 ◽  
Vol 108 (2) ◽  
pp. 255-260 ◽  
Author(s):  
C. J. Lote ◽  
A. J. McVicar ◽  
D. G. Smyth
Keyword(s):  
Body Weight ◽  
Filtration Rate ◽  
Urine Osmolality ◽  
Urine Flow ◽  
Control Group ◽  
Precursor Molecule ◽  
Antidiuretic Activity ◽  
Molar Basis ◽  
Lysine Vasopressin ◽  
Vasopressin Receptors

ABSTRACT The peptides vasopressin-Gly and vasopressin-Gly-Lys-Arg occur as part of the sequence of the vasopressin-neurophysin precursor molecule and may be released from the hypothalamus and/or pituitary. [8-Lysine]-vasopressin-Gly (LVP-Gly) and [8-lysine]-vasopressin-Gly-Lys-Arg were administered i.v. to conscious, water-diuretic rats. The renal effects of the peptides were assessed by comparison with the actions of [8-lysine]-vasopressin (LVP) which was administered to separate groups of rats. LVP-Gly and LVP-Gly-Lys-Arg were weakly antidiuretic. LVP-Gly-Lys-Arg was the more potent of the two peptides, but on a molar basis it only had about 10% of the antidiuretic activity of LVP. LVP-Gly and LVP-Gly-Lys-Arg at 10 pmol/h per 100 g body weight (equivalent to the maximal antidiuretic dose of LVP) slightly decreased (P < 0·001) urine flow without causing significant changes in urine osmolality. LVP (10 pmol/h per 100 g body weight) promoted a marked natriuresis (P < 0·001 ) but LVP-Gly and LVP-Gly-Lys-Arg were not natriuretic, even at the dose which was markedly antidiuretic (100 pmol/h per 100 g body weight). Osmolal output decreased at all doses during administration of the extended peptides, but was not significantly changed in the control group or by LVP. Inulin clearance was decreased by about 30% during administration of both LVP and LVP-Gly-Lys-Arg at 100 pmol/h per 100 g body weight. It is concluded that LVP-Gly and LVP-Gly-Lys-Arg show weak antidiuretic activities and that the effect on urine flow may be partly due to a decrease in glomerular filtration rate (GFR). The decrease in osmolal output produced by the peptides is also a likely consequence of an effect on GFR. It is suggested that LVP-Gly and LVP-Gly-Lys-Arg have a low potential for activation of tubular vasopressin receptors, as shown by the weak antidiuretic activity and lack of a natriuretic action, but that they have a relatively stronger action on glomerular vasopressin receptors. J. Endocr. (1986) 108, 255–260

Interactions between ADH and prostaglandins in isolated erythrocyte-perfused rat kidney

1987 ◽  
Vol 252 (2) ◽  
pp. F331-F337 ◽  
Author(s):  
W. Lieberthal ◽  
M. L. Vasilevsky ◽  
C. R. Valeri ◽  
N. G. Levinsky
Keyword(s):  
Sodium Excretion ◽  
Rat Kidney ◽  
Urine Osmolality ◽  
Sodium Reabsorption ◽  
Urinary Osmolality ◽  
Hemodynamic Characteristics ◽  
Urinary Concentrating Ability ◽  
Tubular Morphology ◽  
Isolated Kidneys

Interactions between antidiuretic hormone (ADH) and renal prostaglandins in the regulation of sodium reabsorption and urinary concentrating ability were studied in isolated erythrocyte-perfused rat kidneys (IEPK). In this model, hemodynamic characteristics are comparable to those found in vivo, and tubular morphology is preserved throughout the period of perfusion. [Deamino]-D-arginine vasopressin (dDAVP) markedly reduced fractional sodium excretion (FE Na) in the IEPK from 3.5 +/- 0.6 to 0.45 +/- 0.14%. After indomethacin, FE Na fell still further to 0.08 +/- 0.02%. In the absence of dDAVP indomethacin had no effect on sodium excretion; FE Na was 2.4 +/- 0.6% in control and 2.0 +/- 0.4% in indomethacin-treated groups. dDAVP increased urine osmolality in the IEPK to 741 +/- 26 mosmol/kg. When prostaglandin synthesis was blocked with indomethacin, urinary osmolality increased further to 1,180 +/- 94 mosmol/kg. In isolated kidneys perfused without erythrocytes (IPK), dDAVP decreased FENa from 14.5 +/- 1.8% to 9.6 +/- 1.2%; addition of indomethacin had no further effect. dDAVP increased urine osmolality only modestly to 350 +/- 12 mosmol/kg in the IPK and indomethacin did not increase concentrating ability further (342 +/- 7 mosmol/kg). Thus the IEPK (unlike the IPK) can excrete a markedly hypertonic urine in response to ADH. ADH also enhances tubular reabsorption of sodium in the IEPK. Prostaglandins inhibit both these actions of ADH but do not directly affect sodium excretion in the absence of the hormone.

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.

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