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.

Renal responses to chronic cold exposure

2003 ◽  
Vol 81 (1) ◽  
pp. 22-27 ◽  
Author(s):  
Zhongjie Sun ◽  
Zhonge Zhang ◽  
Robert Cade
Keyword(s):  
Food Intake ◽  
Cold Exposure ◽  
Water Loss ◽  
Urine Output ◽  
Room Temperature ◽  
Urine Osmolality ◽  
Urine Flow ◽  
Receptor Mrna ◽  
The Difference ◽  
Renal Responses

The aim of this study was to assess our hypothesis that the release of antidiuretic hormone (ADH), the renal concentrating response to ADH, or both is decreased by prolonged cold exposure. Six groups (n = 6/group) of rats were used. Three groups were exposed to cold (5°C), while the remaining three groups were kept at room temperature (25°C). It was found that urine osmolality decreased significantly and serum osmolality increased significantly during cold exposure. The ratio of water/food intake was not affected by prolonged cold exposure. However, prolonged cold exposure increased the ratio of urine output/food intake in the cold-exposed rats, indicating that more urine flow is required by the cold-exposed rats to excrete the osmotic substance at a given food intake. The difference between water intake and urine output decreased significantly in the cold-exposed rats. Thus, prolonged cold exposure increases water loss from excretion. Renal concentrating responses to 24-h dehydration and Pitressin were decreased significantly in the cold-exposed rats. Plasma ADH levels remained unchanged, but renal ADH receptor (V2 receptor) mRNA was decreased significantly in the cold-exposed rats. The results strongly support the conclusion that cold exposure increases excretive water loss, and this may be due to suppression of renal V2 receptors rather than inhibition of ADH release.Key words: renal concentrating response, cold-induced dehydration, serum and urine osmolality, ADH, renal V2 receptor mRNA.

Alpha 2-adrenoceptor antagonism attenuates the diuretic response to acute cold exposure

1993 ◽  
Vol 265 (3) ◽  
pp. R689-R696 ◽  
Author(s):  
D. E. Allen ◽  
M. Gellai
Keyword(s):  
Cold Exposure ◽  
Room Temperature ◽  
Free Water ◽  
Endogenous Ligand ◽  
Water Diuresis ◽  
Free Water Clearance ◽  
Time Control ◽  
Acute Cold Exposure ◽  
Induced Hypertension ◽  
Diuretic Response

Renal alpha 2-adrenoreceptors modulate the hydrosmotic action of arginine vasopressin (AVP) through suppression of AVP-stimulated adenosine 3',5'-cyclic monophosphate (cAMP) accumulation. Circulating catecholamines, likely candidates for the endogenous ligand, are elevated during cold exposure (CE). These studies therefore tested the hypothesis that the diuresis observed with acute CE in rats is due in part to modulation of AVP's tubular action via alpha 2-adrenoceptor activation. Subjects were five male Brattleboro homozygous diabetes insipidus (DI) rats (358 +/- 8 g) receiving chronic AVP replacement (1 microgram.kg-1 x day-1) and seven Long-Evans (LE) normal rats (395 +/- 5 g). In a CE protocol, baseline measurements at room temperature (RT, 24 +/- 0.3 degrees C) were followed by 60-min exposure to 5 +/- 0.5 degrees C. Results were compared with those from a RT time control protocol. The selective alpha 2-antagonist yohimbine (YOH; 10 micrograms.kg-1 x min-1) or vehicle (VEH) was infused throughout the CE and RT protocols. In VEH-infused rats, CE increased urine flow by 63 +/- 12 (DI rats) and 31 +/- 4 microliters.min-1 x 100 g body wt-1 (LE rats), and mean arterial pressure by 36 +/- 1 (DI rats) and 32 +/- 2 mmHg (LE rats). The increased flow was largely a water diuresis, with changes in free water clearance averaging 45 +/- 11 (DI rats) and 28 +/- 3 microliters.min-1 x 100 g body wt-1 (LE rats). YOH treatment completely blunted the cold-induced diuresis in both strains but did not alter the CE-induced hypertension. Glomerular filtration rate was not affected by either CE or YOH infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Lithium-induced diuretic effect of antidiuretic hormone in rats

1976 ◽  
Vol 231 (6) ◽  
pp. 1754-1759 ◽  
Author(s):  
TP Dousa ◽  
LD Barnes
Keyword(s):  
Antidiuretic Hormone ◽  
Low Dose ◽  
Free Water ◽  
Renal Medulla ◽  
Urine Osmolality ◽  
Urinary Volume ◽  
Free Water Clearance ◽  
Sodium Potassium ◽  
Collecting Ducts

The effect of a low dose of lithium (1 meq/kg per day) on renal function and its response to antidiuretic hormone (ADH) was studied in unanesthetized rats. This dose of lithium itself had no influence on renal water and electrolyte excretion, but lithium-treated rats responded paradoxically to exogenous ADH by increases in urinary volume, excretion of total solutes, sodium, potassium, and phosphate. Administration of ADH in the presence of lithium led to a lowering of urine osmolality, but free water clearance was not significantly reduced. Adenylate cyclase from the renal medulla of animals treated with ADH and lithium had a lower response to synthetic vasopressin in vitro than in animals treated with lithium alone. The results suggest that exogenous ADHis diuretic in the presence of a low concentration of lithilm. The predominant mechanism for this diuresis is probably inhibition of electrolyte and isomotic water reabbsorption in various nephron segments, including those proximal to the collecting ducts. ADH also markedly increased urinary excretion of lithium and appears to promote accumulation of lithium in the renal medulla.

CHLORPROPAMIDE TREATMENT OF DIABETES INSIPIDUS IN CHILDREN

PEDIATRICS ◽  
1970 ◽  
Vol 45 (2) ◽  
pp. 246-253
Author(s):  
H. L. Vallet ◽  
M. Prasad ◽  
Richard B. Goldbloom
Keyword(s):  
Diabetes Insipidus ◽  
Urine Output ◽  
Free Water ◽  
Urine Osmolality ◽  
Current Evidence ◽  
Free Water Clearance ◽  
Concomitant Reduction ◽  
Treatment Of Diabetes ◽  
Early Phases ◽  
Antidiuretic Action

Oral chlorpropamide therapy was assessed in 10 children with pitressin-sensitive diabetes insipidus. A significant increase in urine osmolality occurred in eight of nine children studied pre- and post-treatment, with concomitant reduction in urine output and free water clearance. Mean 24-hour urine output during control periods was 5,410 ml (range, 3,000 to 12,000 ml). On chlorpropamide therapy, mean output fell to 2,790 ml (range, 1,200 to 5,500 ml). Complete withdrawal of intramuscular pitressin therapy was possible in 9 of the 10 patients, and these children have now been maintained on chlorpropamide alone for periods of up to 12 months. The principal complication of therapy was symptomatic hypoglycemia, which occurred in half the patients studied during the early phases of treatment. However, it was possible to eliminate this problem by reducing the dose of chlorpropamide while retaining sufficient antidiuretic effect to permit reasonable control of water balance. Current evidence suggests that the antidiuretic action of chlorpropamide may be due to enhancement of the sensitivity of the renal tubule to small amounts of vasopressin. For many, though not all, children with pitressin-sensitive diabetes insipidus, chlorpropamide is a fairly effective therapeutic agent. It is readily accepted by the patients in preference to frequent intramuscular injections of pitressin.

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.

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.

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.

scholarly journals Reduced AQP1, -2, and -3 levels in kidneys of rats with CRF induced by surgical reduction in renal mass

1998 ◽  
Vol 275 (5) ◽  
pp. F724-F741 ◽  
Author(s):  
Tae-Hwan Kwon ◽  
Jørgen Frøkiaer ◽  
Mark A. Knepper ◽  
Søren Nielsen
Keyword(s):  
Urine Output ◽  
Renal Mass ◽  
Collecting Duct ◽  
Free Water ◽  
Urine Osmolality ◽  
Urinary Concentration ◽  
Water Reabsorption ◽  
Similar Reduction ◽  
Urine Production ◽  
Quantitative Immunoblotting

Urinary concentration characteristically decreases in response to a reduction in renal mass in chronic renal failure (CRF). In the present study, we examined whether there are changes in the expression of aquaporins in rats where CRF was induced by 5/6 nephrectomy. Plasma creatinine levels were significantly elevated consistent with significant CRF: 135.7 ± 15.1 ( n = 17, CRF) vs. 33.9 ± 1.1 μmol/l ( n = 11, sham), P < 0.05. Two weeks after 5/6 nephrectomy, the remnant kidneys were hypertrophied, and total renal mass increased to 65 ± 3% of sham levels ( P < 0.05). Urine production increased markedly from 40 ± 2 to 111 ± 3 μl ⋅ min−1 ⋅ kg−1in CRF rats ( P < 0.05), whereas urine osmolality and solute-free water reabsorption decreased significantly. Quantitative immunoblotting of total kidney membrane fractions revealed a significant decrease in total kidney AQP2 expression in CRF rats to 43 ± 12% of sham levels ( P < 0.05). A similar reduction was observed for AQP1 and AQP3. Furthermore, the increased urine output and decreased urine osmolality persisted in CRF rats despite 7 days treatment with 1-desamino-[8-d-arginine]vasopressin (DDAVP, 0.1 μg/h sc) compared with untreated sham-operated controls. Also, there was no change in AQP2 expression (which remained at 38 ± 3% of sham levels, P < 0.05), urine output, or urine osmolality between CRF rats with or without DDAVP treatment. Immunocytochemistry confirmed the decreased AQP2 expression in collecting duct principal cells in CRF rats, with a predominant apical labeling. In conclusion, the results demonstrated that there was a significant vasopressin-resistant downregulation of AQP2 and AQP3 as well as downregulation of AQP1 associated with the polyuria in CRF rats.

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