Effect of short-term administration of vasopressin on arterial pressure and norepinephrine turnover in Long–Evans rats

1987 ◽  
Vol 65 (10) ◽  
pp. 2142-2146 ◽  
Author(s):  
R. L. Kline ◽  
K.-Y. Chow ◽  
P. F. Mercer
Keyword(s):  
Arterial Pressure ◽  
Water Intake ◽  
Urine Output ◽  
Plasma Osmolality ◽  
Chronic Administration ◽  
Urine Osmolality ◽  
Cardiovascular Reflexes ◽  
High Dose ◽  
Normal Fluid ◽  
Long Evans

Vasopressin (AVP) in acute experiments has been shown to influence cardiovascular reflexes, but the effect of a more prolonged administration of AVP on the sympathetic nervous system has not been investigated. Long–Evans rats were treated for 7 days with AVP (Pitressin tannate in oil, with single daily doses of 100 or 500 mU∙100 g−1, s.c.) to determine whether AVP alters norepinephrine (NE) turnover in kidney, intestine, or skeletal muscle. Control rats were given equal doses of peanut oil daily. NE turnover was determined by measuring the decline in tissue levels of NE for 8 h after inhibition of tyrosine hydroxylase with α-methyl-p-tyrosine (300 mg∙kg−1, i.p. every 4 h). Measurements of water intake, urine output, and urine osmolality showed that chronic administration of the high dose, but not the low dose, of AVP produced maintained increases in urine osmolality and decreases in water intake and urine output. Body weight, plasma osmolality, plasma electrolytes, and hematocrit were not significantly altered by AVP treatment, but mean arterial pressure was elevated significantly (control, 105 ± 3 mmHg versus AVP, 119 ± 4 mmHg, p < 0.05) (1 mmHg = 133.3 Pa) in the high dose group. Plasma renin activity was decreased slightly, but significantly in rats treated with the high dose of AVP. Compared with results in control animals, there were no statistically significant changes in NE turnover after chronic administration of either the low or the high dose of AVP. The results indicate that administration of AVP for 7 days to rats in normal fluid balance does not result in a decrease in NE turnover in peripheral organs.

Water and electrolyte exchange in rats exposed to cold

1968 ◽  
Vol 46 (6) ◽  
pp. 873-881 ◽  
Author(s):  
Melvin J. Fregly
Keyword(s):  
Food Intake ◽  
Water Intake ◽  
Cold Exposure ◽  
Urine Output ◽  
Plasma Osmolality ◽  
Urine Osmolality ◽  
Total Output ◽  
Electrolyte Loss ◽  
Sodium And Potassium ◽  
Electrolyte Exchange

Exposure of rats to air at 6 °C for 10 days increased food intake and urine output but failed to affect water intake. A comparison of water with food intake revealed a smaller water intake for a given food intake for cold-exposed than for control rats. The urine output at a given water intake was also greater for cold-exposed rats. In addition, cold exposure failed to affect urine osmolality significantly. Thus, the greater solute output accompanying cold exposure was accomplished by increasing urine flow rather than by concentrating urine. These results suggest possible mechanisms for both the relative dehydration and increased plasma osmolality observed after removal of rats from cold air. Both fecal and urinary routes of sodium and potassium excretion were increased by cold exposure; however, fecal excretions of both potassium and sodium were greater fractions of the total output during cold exposure than prior to it. Although cold exposure tends to induce a relative dehydration in rats, an important factor limiting the extent of the dehydration may be increased fecal electrolyte loss.

scholarly journals Urine and Plasma Osmolality in Patients with Autosomal Dominant Polycystic Kidney Disease: Reliable Indicators of Vasopressin Activity and Disease Prognosis?

2015 ◽  
Vol 41 (3) ◽  
pp. 248-256 ◽  
Author(s):  
Niek F. Casteleijn ◽  
Debbie Zittema ◽  
Stephan J.L. Bakker ◽  
Wendy E. Boertien ◽  
Carlo A. Gaillard ◽  
...  
Keyword(s):  
Water Intake ◽  
Plasma Osmolality ◽  
Urine Osmolality ◽  
Kidney Volume ◽  
Polycystic Kidney ◽  
Estimated Gfr ◽  
Total Kidney Volume ◽  
Autosomal Dominant Polycystic Kidney ◽  
Crude Analysis

Background: Vasopressin plays an essential role in osmoregulation, but has deleterious effects in patients with ADPKD. Increased water intake to suppress vasopressin activity has been suggested as a potential renoprotective strategy. This study investigated whether urine and plasma osmolality can be used as reflection of vasopressin activity in ADPKD patients. Methods: We measured urine and plasma osmolality, plasma copeptin concentration, total kidney volume (TKV, by MRI) and GFR (125I-iothalamate). In addition, change in estimated GFR (eGFR) during follow-up was assessed. Results: Ninety-four patients with ADPKD were included (56 males, age 40 ± 10, mGFR 77 ± 32 ml/min/1.73 m2, TKV 1.55 (0.99-2.40) l. Urine osmolality, plasma osmolality and copeptin concentration were 420 ± 195, 289 ± 7 mOsmol/l and 7.3 (3.2-14.6) pmol/l, respectively. Plasma osmolality was associated with copeptin concentration (R = 0.54, p < 0.001), whereas urine osmolality was not (p = 0.4). In addition, urine osmolality was not associated with TKV (p = 0.3), in contrast to plasma osmolality (R = 0.52, p < 0.001) and copeptin concentration (R = 0.61, p < 0.001). Fifty-five patients were followed for 2.8 ± 0.8 years. Baseline plasma and urine osmolality were not associated with change in eGFR (p = 0.6 and p = 0.3, respectively), whereas baseline copeptin concentration did show an association with change in eGFR, in a crude analysis (St. β = -0.41, p = 0.003) and also after adjustment for age, sex and TKV (St. β = -0.23, p = 0.05). Conclusions: These data suggest that neither urine nor plasma osmolality are valid measures to identify ADPKD patients that may benefit from increasing water intake. Copeptin appears a better alternative for this purpose.

scholarly journals The Vasopressin System in the Risk of Diabetes and Cardiorenal Disease, and Hydration as a Potential Lifestyle Intervention

2018 ◽  
Vol 72 (Suppl. 2) ◽  
pp. 21-27 ◽  
Author(s):  
Sofia Enhörning ◽  
Olle Melander
Keyword(s):  
Type 2 Diabetes ◽  
Water Intake ◽  
Kidney Diseases ◽  
Urine Volume ◽  
Plasma Osmolality ◽  
Premature Mortality ◽  
Urine Osmolality ◽  
High Plasma ◽  
Effective Prevention

Background: Type 2 diabetes, chronic kidney disease (CKD) and its cardiovascular complications are increasing as health problems worldwide. These diseases are interrelated with overlapping occurrence and once diabetes is established, the risk of cardiorenal disease is dramatically elevated. Thus, a search for unifying modifiable risk factors is key for effective prevention. Summary: Elevated fasting plasma concentration of vasopressin, measured with the marker copeptin, predicts new onset type 2 diabetes as well as renal function decline. Furthermore, we recently showed that increased plasma copeptin concentration independently predicts the development of both CKD and other specified kidney diseases. In consequence, high copeptin is an independent risk factor for cardiovascular disease and premature mortality in both diabetes patients and in the general population. Vasopressin is released when plasma osmolality is high, and the easiest way to lower plasma vasopressin and copeptin concentration is to increase water intake. In a human water intervention experiment with 1 week of 3 L/day increased water intake, the one third of the participants with the greatest copeptin reduction (water responders) were those with a phenotype of low water intake (high habitual plasma copeptin and urine osmolality, and low urine volume). The water-responders had a copeptin reduction of 41% after 1 week of increased water intake compared to a control week; in contrast, a 3% reduction occurred in the other two thirds of the study participants. Among water responders, increased water intake also induced a reduction in fasting glucagon concentration. Key Messages: Elevated copeptin, a measure of vasopressin, is a risk marker of metabolic and cardiorenal diseases and may assist in the detection of individuals at higher risk for these diseases. Furthermore, individuals with high copeptin and other signs of low water intake may experience beneficial glucometabolic effects of increased water intake. Future randomized control trials investigating effects of hydration on glucometabolic and renal outcomes should focus on individuals with signs of low water intake including high plasma copeptin concentration.

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.

Effect of insulin on regional vascular resistances in conscious rats

1996 ◽  
Vol 270 (2) ◽  
pp. R450-R455
Author(s):  
E. Qadir ◽  
J. P. Porter
Keyword(s):  
Skeletal Muscle ◽  
Arterial Pressure ◽  
Low Dose ◽  
Chronic Administration ◽  
High Dose ◽  
Ganglionic Blockade ◽  
Conscious Rats ◽  
Before And After ◽  
Vascular Beds ◽  
Renal Vascular

In the rat, but not in humans and other mammals, chronic administration of insulin produces hypertension. The present aim was to determine the effect of acute insulin infusion on regional vascular resistances and to determine the neurogenic contribution to the response. Conscious rats were infused with insulin (2 or 6 mU/min) before and after ganglionic blockade with chlorisondamine (5 mg/kg). The low dose of insulin produced an increase in arterial pressure and hindquarter vascular resistance; the high dose produced a gradual decrease in arterial pressure and renal resistance. After ganglionic blockade, the hindquarter vasoconstriction produced by the low dose was abolished. The high dose of insulin produced both hindquarter and renal vasodilation. Thus the low dose of insulin had a selective neurogenic vasoconstrictor effect in rat skeletal muscle vascular beds. With higher doses, direct vasodilatory effects in both skeletal muscle and renal vascular beds appeared. This greater sensitivity of the sympathoexcitatory effects of insulin in rats may explain the ability of chronic insulin infusions to increase blood pressure in this species.

scholarly journals Catecholaminergic neurons in the comissural region of the nucleus of the solitary tract modulate hyperosmolality-induced responses

2015 ◽  
Vol 309 (9) ◽  
pp. R1082-R1091 ◽  
Author(s):  
Andre H. Freiria-Oliveira ◽  
Graziela T. Blanch ◽  
Gustavo R. Pedrino ◽  
Sergio L. Cravo ◽  
David Murphy ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Water Intake ◽  
Pressor Response ◽  
Plasma Osmolality ◽  
Solitary Tract ◽  
Inhibitory Mechanisms ◽  
Body Fluid Homeostasis ◽  
Pressure Water ◽  
Acute Increase ◽  
Renal Responses

Noradrenergic A2 neurons of the nucleus of the solitary tract (NTS) have been suggested to contribute to body fluid homeostasis and cardiovascular regulation. In the present study, we investigated the effects of lesions of A2 neurons of the commissural NTS (cNTS) on the c-Fos expression in neurons of the hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei, arterial pressure, water intake, and urinary excretion in rats with plasma hyperosmolality produced by intragastric 2 M NaCl (2 ml/rat). Male Holtzman rats (280–320 g) received an injection of anti-dopamine-β-hydroxylase-saporin (12.6 ng/60 nl; cNTS/A2-lesion, n = 28) or immunoglobulin G (IgG)-saporin (12.6 ng/60 nl; sham, n = 24) into the cNTS. The cNTS/A2 lesions increased the number of neurons expressing c-Fos in the magnocellular PVN in rats treated with hypertonic NaCl (90 ± 13, vs. sham: 47 ± 20; n = 4), without changing the number of neurons expressing c-Fos in the parvocellular PVN or in the SON. Contrary to sham rats, intragastric 2 M NaCl also increased arterial pressure in cNTS/A2-lesioned rats (16 ± 3, vs. sham: 2 ± 2 mmHg 60 min after the intragastric load; n = 9), an effect blocked by the pretreatment with the vasopressin antagonist Manning compound (0 ± 3 mmHg; n = 10). In addition, cNTS/A2 lesions enhanced hyperosmolality-induced water intake (10.5 ± 1.4, vs. sham: 7.7 ± 0.8 ml/60 min; n = 8–10), without changing renal responses to hyperosmolality. The results suggest that inhibitory mechanisms dependent on cNTS/A2 neurons reduce water intake and vasopressin-dependent pressor response to an acute increase in plasma osmolality.

scholarly journals Acute Increases in Water Consumption Supress Copeptin in Low Drinkers

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1389-1389
Author(s):  
Abigail Colburn ◽  
Adam Seal ◽  
HyunGyu Suh ◽  
Stavros Kavouras
Keyword(s):  
Water Intake ◽  
Water Consumption ◽  
Plasma Osmolality ◽  
Urine Osmolality ◽  
Acute Effect ◽  
State University ◽  
Effect Of Water ◽  
Funding Sources ◽  
Bottom Quartile ◽  
Main Effect

Abstract Objectives To assess the acute effect of adequate water consumption on copeptin, a marker of arginine vasopressin, in low drinkers. Methods Six healthy (5 males, 1 female) low drinkers (age 43 ± 7 y, BMI 30.5 ± 3) were recruited based on self-reported daily water consumption ≤1.5 L·day−1 in males or 1.0 L·day−1 in females (854 ± 432 mL·d−1) and 24-h urine osmolality ≥800 mmol·kg−1 (968 ± 114 mmol·kg−1). Participants completed two counterbalanced crossover 11-h protocols. They were provided either the Institute of Medicine's recommended amount of water excluding food (males: 3 L, females: 2 L, HWI) or an amount representing the bottom quartile of water consumption observed in the National Health and Nutrition Examination Survey (males: 0.5 L, females: 0.4 L, LWI). Food was provided to participants and standardized to body weight (100 kJ·Kg−1) using a consistent ratio of macronutrients. Blood samples were collected at hours 700, 800, 900, 1200, 1300, 1400, 1600, 1700, and 1800. Results There was a significant main effect of water intake on plasma osmolality (F = 11.838, P = 0.018) with greater values in LWI at 1200 (HWI: 287 ± 3, LWI: 291 ± 3; P = 0.013), 1400 (HWI: 287 ± 4, LWI: 291 ± 5; P = 0.049), and 1700 (HWI: 287 ± 2, LWI: 292 ± 4; P = 0.004). There was also a significant main effect of water intake on copeptin (F = 9.848, P = 0.026) with higher values in LWI at 0800 (HWI: 6.1 ± 2.3, LWI: 8.7 ± 3.7; P = 0.016), 0900 (HWI: 5.3 ± 2.4, LWI: 9.2 ± 4.5; P = 0.013), 1200 (HWI: 4.2 ± 1.9, LWI: 7.8 ± 4.6; P = 0.021), 1400 (HWI: 4.3 ± 1.8, LWI: 8.3 ± 4.7; P = 0.033), 1600 (HWI: 4.7 ± 2.5, LWI: 7.6 ± 4.5; P = 0.049), and 1800 (HWI: 4.4 ± 2.5, LWI: 7.8 ± 5.2; P = 0.048). Water intake did not influence change in plasma volume (P = 0.214). Conclusions Copeptin was suppressed in response to acute increases in water consumption via suppression of plasma osmolality. Copeptin may serve as a sensitive marker for changes in total water intake. Funding Sources This study was supported by Arizona State University College of Health Solutions.

Role of vasopressin in fetal homeostasis

1982 ◽  
Vol 242 (6) ◽  
pp. F740-F744
Author(s):  
S. S. Daniel ◽  
R. I. Stark ◽  
M. K. Husain ◽  
L. V. Baxi ◽  
L. S. James
Keyword(s):  
Urine Output ◽  
Plasma Osmolality ◽  
Urine Osmolality ◽  
Maternal Plasma ◽  
Third Trimester ◽  
The Third ◽  
Plasma Vasopressin ◽  
The Relationship ◽  
Linear Correlations

The role of vasopressin (VP) and the kidney in the maintenance of solute and volume homeostasis was studied in chronically instrumented fetal lambs during the third trimester. Plasma VP, urine and plasma osmolality, and urine output were measured in 74 simultaneous samples. The results show a strong positive nonlinear correlation between plasma VP and osmolality when a latter is higher than 290 mosmol/kg (r = 0.803, P = 0.03) and between plasma VP and urine osmolality (r = 0.806, P = 0.05). No correlation was found between fetal and maternal plasma VP. However, linear correlations were found in plasma osmolality and sodium concentrations between mother and fetus; mean maternal-fetal gradients were 4 mosmol/kg and 3.1 meq/liter, respectively. The highest values for plasma VP and osmolality found in our study were 7.0 pg/ml and 317 mosmol/kg, respectively. There values corresponded to urine output of 0.02 ml.kg-1.min-1 and osmolality of 517 mosmol/kg. In conclusion, there studies demonstrate that the relationship among plasma osmolality, plasma vasopressin concentration, and urine osmolality in the lamb fetus are qualitatively similar to those of the adult. The results suggest that the fetal neurohypophysis and kidney may participate in the maintenance of fetal osmolar and volume homeostasis.

Effect of arterial pressure on drinking and urinary responses to angiotensin II

1988 ◽  
Vol 254 (1) ◽  
pp. R69-R74 ◽  
Author(s):  
M. D. Evered ◽  
M. M. Robinson ◽  
P. A. Rose
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Water Intake ◽  
Fluid Loss ◽  
High Dose ◽  
Ang Ii ◽  
Intravenous Injections ◽  
Drinking Response ◽  
High Doses ◽  
The Relationship

To investigate the relationship between angiotensin II (ANG II) and mean arterial pressure (MAP) in the control of drinking in rats, we infused ANG II intravenously at constant rates (either 50 or 100 ng.kg-1.min-1 for 90 min) and varied MAP by intravenous injections of diazoxide (5-20 mg/kg). Rats were pretreated with captopril to block the endogenous synthesis of ANG II. When given alone, low and high doses of ANG II increased MAP approximately 30 and 50 mmHg, respectively. The low but not the high dose significantly increased water intake above control levels. Both doses caused such a large diuresis and natriuresis that the net effect was fluid loss. Reducing MAP toward normal greatly increased the drinking response to the high but not the low dose of ANG II and reduced the urinary solute and water loss to both doses. These results support the hypothesis that water intake and net fluid gain are inhibited when MAP is above normal. When MAP was reduced below normal in rats given constant infusions of ANG II the amount of water drunk and net fluid gain was proportional to the dose of ANG II but not the dose of diazoxide, the degree of hypotension, or urinary losses. This is consistent with previous reports that ANG II is essential for the drinking response to hypotension. Furthermore, it demonstrates that ANG II is not merely permissive but probably the signal controlling water intake when arterial pressure is reduced below normal.

Long-term blood pressure and metabolic effects of vasopressin with servo-controlled fluid volume

1984 ◽  
Vol 247 (3) ◽  
pp. R537-R545 ◽  
Author(s):  
A. W. Cowley ◽  
D. C. Merrill ◽  
E. W. Quillen ◽  
M. M. Skelton
Keyword(s):  
Arterial Pressure ◽  
Infusion Pump ◽  
Chronic Administration ◽  
Urine Osmolality ◽  
Total Body Weight ◽  
Sodium Concentration ◽  
Fluid Volume ◽  
Metabolic Effects ◽  
Plasma Sodium ◽  
Pressure Plasma

Studies were performed in normal mongrel dogs (n = 8) to assess whether changes observed with chronic administration of vasopressin (AVP) were a result of direct actions of AVP or the consequence of changes in body fluid volume. AVP was infused continuously for 2 wk (0.36 ng X kg-1 X min-1 iv), while total body weight and body water (TBW) were maintained constant (+/- 50 g) using a servo-controlled system. A metabolic cage was mounted on sensitive force transducers for continuous monitoring of TBW. The summed voltage output of these transducers was used to servo control an intravenous infusion pump that adjusted the rate of water intake required for maintenance of a constant TBW. AVP infused under these conditions chronically increased plasma AVP levels from 2 to 22 pg/ml but resulted in no change of average 24-h mean arterial pressure, plasma sodium, or osmolality. Urine excretion decreased from 800 to 200 ml/day, whereas urine osmolality increased from 430 to 1,200 mosmol/kg and remained at these levels throughout the 2-wk AVP infusion. A net loss of 20 meq sodium occurred during the 1st day of AVP infusion but thereafter was unchanged. Plasma sodium and osmolality were unchanged from control during AVP infusions. We conclude that AVP-induced changes of arterial pressure, plasma sodium concentration and osmolality, renal escape, suppression of renin activity, and most of the observed natriuresis are events normally dependent on volume expansion.

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