Antidiuresis and vasopressin release with hypoxemia and hypercapnia in conscious dogs

1984 ◽  
Vol 247 (1) ◽  
pp. R127-R134 ◽  
Author(s):  
C. E. Rose ◽  
R. J. Anderson ◽  
R. M. Carey
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Partial Pressure ◽  
Free Water ◽  
Urine Osmolality ◽  
Hypercapnic Acidosis ◽  
Free Water Clearance ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Hemodynamic Function

determine the effects of acute blood gas derangements on renal water and solute excretion and vasopressin secretion, six unanesthetized mongrel dogs were studied during 1) combined acute hypoxemia and hypercapnic acidosis [arterial O2 partial pressure (PaO2) 36 +/- 1 Torr, arterial CO2 partial pressure (PaCO2) 54 +/- 2 Torr, pH 7.18 +/- 0.01], 2) acute hypoxemia (PaO2 33 +/- 2 Torr, PaCO2 33 +/- 1 Torr, pH 7.34 +/- 0.01), and 3) acute hypercapnic acidosis (PaO2 83 +/- 3 Torr, PaCO2 53 +/- 1 Torr, pH 7.19 +/- 0.02). Combined acute hypoxemia and hypercapnic acidosis increased (P less than 0.05) mean arterial pressure, but renal hemodynamic function deteriorated with decreased (P less than 0.05) glomerular filtration rate and increased (P less than 0.05) renal vascular resistance. Moreover free water clearance became more negative (P less than 0.05) and urine osmolality increased (P less than 0.05). During acute hypoxemia or acute hypercapnic acidosis alone, mean arterial pressure and renal hemodynamic function were unchanged but free water clearance became more negative (P less than 0.05). During acute hypoxemia, urine osmolality increased (P less than 0.05) comparably with values observed during combined acute hypoxemia and hypercapnic acidosis. Plasma vasopressin concentrations increased profoundly (P less than 0.05) during combined hypoxemia and hypercapnic acidosis and during acute hypoxemia alone and were significantly elevated (P less than 0.05) above the increased plasma vasopressin concentrations observed during acute hypercapnic acidosis. We conclude that acute hypoxemia and hypercapnic acidosis result in impairment of renal water excretion, probably mediated through vasopressin secretion.

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.

Effect of ethanol ingestion on plasma vasopressin and water balance in humans

1982 ◽  
Vol 242 (5) ◽  
pp. R522-R527 ◽  
Author(s):  
G. Eisenhofer ◽  
R. H. Johnson
Keyword(s):  
Hypertonic Saline ◽  
Free Water ◽  
Urine Osmolality ◽  
Saline Infusion ◽  
Ethanol Ingestion ◽  
Free Water Clearance ◽  
Vasopressin Release ◽  
Plasma Vasopressin ◽  
Hypertonic Saline Infusion ◽  
Water Clearance

The effects of 75 ml ethanol ingested over 60 min on plasma osmolality (Posmol) and plasma vasopressin (PAVP) in four normal subjects were studied. In the 1st h of the investigation PAVP fell, then rose, even though plasma ethanol levels were still rising. The rise in PAVP was preceded by a rise in Posmol corrected for the influence of ethanol. The fall in PAVP was followed by an increase in free water clearance and a decrease in urine osmolality, while the later rise in PAVP was followed by a decrease in free water clearance (CH2O) and a rise in urine osmolality. The relationship between PAVP and Posmol was then studied during intravenous (iv) hypertonic saline infusion in five subjects. The results were compared with those from a second infusion in the same subjects after ingestion of ethanol (0.5 ml/kg). Ethanol reduced vasopressin release in response to iv hypertonic saline infusion, and this correlated with a reduced decrease in CH2O. We conclude that ethanol inhibits PAVP release by decreasing the response of the osmosodium receptors to changes in plasma tonicity.

Time course of changes in plasma vasopressin during atrial distension

1982 ◽  
Vol 60 (9) ◽  
pp. 1210-1218 ◽  
Author(s):  
J. R. Ledsome ◽  
N. Wilson ◽  
J. Ngsee
Keyword(s):  
Left Atrial ◽  
Time Course ◽  
Free Water ◽  
Urine Osmolality ◽  
Free Water Clearance ◽  
Mean Values ◽  
Plasma Vasopressin ◽  
The Mean ◽  
Plasma Arginine ◽  
Left Atrial Distension

Distension of the left atrium in chloralose anaesthetized dogs causes a diuresis and dilution of the urine. It has been reported previously that if distension of the atrium is maintained then urine flow reaches a peak after 50 min and then declines. A radioimmunoassay was used to measure plasma arginine vasopressin (AVP) at 10-min intervals before, during, and after atrial distension for 90 min. Plasma AVP decreased during atrial distension and did not increase until after the atrial distension was removed.Urine volume and free-water clearance increased and urine osmolality decreased, to reach maximum changes after 50 min. Although there was then a decline in some experiments, after reaching the peak changes, the mean values of the group did not show any statistically significant decline. Thus the urinary changes were also present for the 90 min of left atrial distension. The results are consistent with the hypothesis that the.diuretic response to left atrial distension is dependent upon decreased release of AVP from the neurohypophysis.

Effect of sodium fluoride on concentrating and diluting ability in the rat

1977 ◽  
Vol 232 (4) ◽  
pp. F335-F340 ◽  
Author(s):  
J. D. Wallin ◽  
R. A. Kaplan
Keyword(s):  
Cyclic Amp ◽  
Urine Volume ◽  
Free Water ◽  
Urine Osmolality ◽  
Inhibitory Effect ◽  
Sprague Dawley ◽  
Free Water Clearance ◽  
Sprague Dawley Rats ◽  
Direct Inhibitory Effect ◽  
Hereditary Hypothalamic Diabetes Insipidus

Mechanisms for the concentrating defect produced by fluoride were examined in the rat. Free-water clearance at all levels of delivery was normal after 5 days of chronic fluoride administration in the hereditary hypothalamic diabetes insipidus rat. In the Sprague-Dawley rats, during moderate fluoride administration (120 micronmol/kg per day), urine osmolality and cyclic AMP excretion decreased and urine volume increased, but after exogenous vasopressin, volume decreased and osmolality and cyclic AMP increased appropriately. During larger daily doses of fluoride (240 micronmol/kg per day) urinary osmolality and cyclic AMP decreased and volume increased, which was similar to the changes seen during lower fluoride dosages, but these parameters did not change after exogenous vasopressin. These data suggest that ascending limb chloride reabsorption is unaltered by fluoride administration; in the presence of sufficient fluoride, collecting tubular cells apparently do not generate cyclic AMP or increase permeability appropriately in response to vasopressin. The postulated defect is felt to be due to either a decrease in ATP availability or to a direct inhibitory effect of fluoride on the vasopressin-dependent cyclic AMP generating system.

Cardiovascular, renal, and endocrine responses to intravenous endothelin in conscious dogs

1988 ◽  
Vol 255 (6) ◽  
pp. R1064-R1068 ◽  
Author(s):  
K. L. Goetz ◽  
B. C. Wang ◽  
J. B. Madwed ◽  
J. L. Zhu ◽  
R. J. Leadley
Keyword(s):  
Vascular Endothelial Cells ◽  
Peripheral Resistance ◽  
Free Water ◽  
Urine Osmolality ◽  
Urinary Sodium Excretion ◽  
Conscious Dogs ◽  
Plasma Norepinephrine ◽  
Vascular Endothelial ◽  
Free Water Clearance ◽  
Physiological Processes

Endothelin is a recently discovered vasoconstrictor peptide that is synthesized in certain vascular endothelial cells. We have identified the cardiovascular, renal, and hormonal responses that can be elicited in conscious dogs by intravenous administration of endothelin at rates of 10 and 30 ng.kg-1.min-1 for 60 min (0.24 and 0.72 nmol.kg-1/1-h infusion). Each dose of endothelin increased total peripheral resistance, arterial pressure, and left atrial pressure and decreased heart rate and cardiac output. Hematocrit increased by 4.8% (NS) and 22.9% (P less than 0.01) in response to the lower and higher infusion rates, respectively. Urinary sodium excretion, urine osmolality, and osmolar clearance decreased and free water clearance increased. The lower dose of endothelin decreased plasma norepinephrine and increased plasma atriopeptin. The higher dose increased plasma levels of vasopressin, renin, aldosterone, norepinephrine, epinephrine, and atriopeptin. The higher infusion rate of the peptide caused one or more brief vomiting episodes in four of five dogs. Although it is not yet known whether endothelin is a circulating hormone, it is clear that this peptide is capable of causing profound cardiovascular, renal, and endocrine alterations in conscious dogs. The possible relevance of these observations to physiological processes and to pathological conditions such as hypertension remains to be established.

Contralateral renal function after unilateral renal vein ligation

1959 ◽  
Vol 197 (5) ◽  
pp. 1093-1096
Author(s):  
Joseph H. Perlmutt
Keyword(s):  
Renal Function ◽  
Renal Vein ◽  
Left Renal Vein ◽  
Free Water ◽  
Urine Osmolality ◽  
Tubular Reabsorption ◽  
Experimental Conditions ◽  
Free Water Clearance ◽  
Excretion Rates ◽  
The Right

The effect of increased pressure in one kidney, produced by ligation of its vein, on contralateral renal function was investigated in eight anesthetized dogs. Kidney function was determined under the same experimental conditions in five dogs, but without renal vein ligation. For the latter group, renal function, on the average, remained reasonably stable. After left renal vein ligation, findings for the right kidney were as follows: a) decreased urine flow, amounting maximally to 9.5–41.4% of control flows; b) slight increase of questionable significance in creatinine clearance; c) inconstant changes in PAH clearance; d) increase in urine osmolality to hypertonic values; e) decrease in solute-free water clearance; f) slight rise of questionable significance in total solute clearance; and g) either no change or inconstant changes in excretion rates Na+ and K+. The data indicate that the oliguria resulted solely from increased renal tubular reabsorption of water, suggesting liberation of antidiuretic hormone as the possible mechanism. Direct nervous influences on tubular reabsorption of water cannot, however, be presently 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.

Morphological and functional comparisons of normal and hypertrophied kidneys of adult domestic fowl (Gallus gallus)

1990 ◽  
Vol 258 (2) ◽  
pp. F403-F413
Author(s):  
C. M. Gregg ◽  
R. F. Wideman
Keyword(s):  
Domestic Fowl ◽  
Renal Mass ◽  
Plasma Osmolality ◽  
Free Water ◽  
Urine Osmolality ◽  
Osmotic Diuresis ◽  
Free Water Clearance ◽  
Permanent Loss ◽  
The Right ◽  
Water Clearance

Similar to mammals, kidneys of domestic fowl undergo compensatory hypertrophy after loss of functional renal mass. Because this species continues to develop new nephrons for up to 12-wk posthatch, renal hyperplasia might play a significant role in compensatory growth. Either transient or permanent loss of approximately 60% of the right kidney was produced in 2- to 3-wk-old roosters by simple ureteral transection or by removing a 1-mm segment of ureter at the level of the ischiadic artery, respectively. In the latter (experimental) group, right anterior and medial divisions atrophied leaving only the posterior division intact. Spontaneous reanastomosis occurred in the former (reconnected) group, and all three divisions were present at death. Control birds were untouched as were the left kidneys of experimental and reconnected birds. At 40-50 wk, renal function was measured separately in right and left kidneys of all groups during five different infusion protocols. Compared with control kidneys, experimental kidneys had a 50-60% weight gain, and their glomerular size distribution profile was shifted to the right (larger glomeruli). Reconnected kidneys were not hypertrophied, and their profile was shifted to the left (smaller glomeruli). Neither group had significant formation of new nephrons. Once variations in kidney weight were taken into account, there were no differences between hypertrophied (experimental) and control kidneys in urine flow rate (UFR), glomerular filtration rate (GFR), paraaminohippuric acid (PAH) clearance, UFR/GFR, urine osmolality, urine/plasma osmolality, osmolal clearance, free water clearance, Na and K load, absolute Na and K excretion, and fractional Na and K excretion except as follows: 1) during infusion of isotonic mannitol-dextrose at 0.1 ml.min-1.kg body wt-1 experimental kidneys had a lower fractional excretion of K than control kidneys, and 2) during brisk osmotic diuresis (isotonic mannitol-dextrose at 0.4 ml.min-1.kg body wt-1) experimental kidneys had higher UFR and free water clearance and lower urine osmolality and urine/plasma osmolality than control kidneys. Reconnected kidneys differed from control kidneys in only 1 of 210 comparisons. Permanent loss of functional renal mass in young birds produces significant compensatory renal hypertrophy that is due to enlargement of existing nephrons rather than formation of new nephrons. Hypertrophied kidneys function like normal kidneys except under conditions of brisk osmotic diuresis.

Effect of cortisol on vasopressin response to hypertonic saline in fetal sheep

1989 ◽  
Vol 257 (4) ◽  
pp. R861-R865
Author(s):  
T. L. Bennett ◽  
J. C. Rose
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Partial Pressure ◽  
Hypertonic Saline ◽  
Arginine Vasopressin ◽  
Positive Influence ◽  
Serum Osmolality ◽  
Base Line ◽  
Fetal Sheep ◽  
Cortisol Levels

To determine the effect of cortisol on vasopressin responses to hyperosmolality, we infused hypertonic saline (HS) (12 meq/kg NaCl) into nine chronically cannulated fetal sheep ranging from 110 to 132 days of gestation. The experiment was performed twice on each fetus, once during a continuous cortisol infusion and once during a vehicle infusion. Administration of HS resulted in a prompt increase in serum osmolality from 292.1 +/- 1.8 to 310.4 +/- 2.5 mosmol/kg. Decreases were seen in pH, partial pressure of O2, and hematocrit from 7.37 +/- 0.01 to 7.31 +/- 0.01, from 22.5 +/- 1.6 to 20.0 +/- 2.0 mmHg, and from 35.6 +/- 1.7 to 32.6 +/- 1.6, respectively. Mean arterial pressure increased from 41.3 +/- 1.4 to 48.9 +/- 2.0 mmHg (P less than 0.01). Arginine vasopressin (AVP) rose from base line after HS (P = 0.11 vehicle experiments, P = 0.04 cortisol experiments), and AVP responses were greater in the cortisol experiments than in the vehicle experiments (delta AVP = 21.9 +/- 10.9 vs. 3.1 +/- 0.9 pg/ml, P = 0.05). Also there was a correlation noted between differences in AVP response and cortisol levels (P less than 0.04). We conclude that cortisol exerts a positive influence on the AVP response to HS in fetal sheep.

Genetic AVP deficiency abolishes cold-induced diuresis but does not attenuate cold-induced hypertension

2006 ◽  
Vol 290 (6) ◽  
pp. F1472-F1477 ◽  
Author(s):  
Zhongjie Sun
Keyword(s):  
Cold Exposure ◽  
Urine Output ◽  
Room Temperature ◽  
Control Period ◽  
Free Water ◽  
Renal Medulla ◽  
Urine Osmolality ◽  
Free Water Clearance ◽  
Receptor Mrna ◽  
Induced Hypertension

Chronic cold exposure causes hypertension and diuresis. The aim of this study was to determine whether vasopressin (AVP) plays a role in cold-induced hypertension and diuresis. Two groups of Long-Evans (LE) and two groups of homozygous AVP-deficient Brattleboro (VD) rats were used. Blood pressure (BP) was not different among the four groups during a 2-wk control period at room temperature (25°C, warm). After the control period, one LE group and one VD group were exposed to cold (5°C); the remaining groups were kept at room temperature. BP and body weight were measured weekly during exposure to cold. Food intake, water intake, urine output, and urine osmolality were measured during weeks 1, 3, and 5 of cold exposure. At the end of week 5, all animals were killed and blood was collected for measurement of plasma AVP. Kidneys were removed for measurement of renal medulla V2 receptor mRNA and aquaporin-2 (AQP-2) protein expression. BP of LE and VD rats increased significantly by week 2 of cold exposure and reached a high level by week 5. BP elevations developed at approximately the same rate and to the same degree in LE and VD rats. AVP deficiency significantly increased urine output and solute-free water clearance and decreased urine osmolality. Chronic cold exposure increased urine output and solute-free water clearance and decreased urine osmolality in LE rats, indicating that cold exposure caused diuresis in LE rats. Cold exposure failed to affect these parameters in VD rats, suggesting that the AVP system is responsible for cold-induced diuresis. Cold exposure did not alter plasma AVP in LE rats. Renal medulla V2 receptor mRNA and AQP-2 protein expression levels were decreased significantly in the cold-exposed LE rats, suggesting that cold exposure inhibited renal V2 receptors and AVP-inducible AQP-2 water channels. We conclude that 1) AVP may not be involved in the pathogenesis of cold-induced hypertension, 2) the AVP system plays a critical role in cold-induced diuresis, and 3) cold-induced diuresis is due to suppression of renal V2 receptors and the associated AQP-2 water channels, rather than inhibition of AVP release.

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