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.

Comparative Effect of Diuretics on Renal Water Excretion in Hyponatraemic Oedematous Disorders

1982 ◽  
Vol 62 (2) ◽  
pp. 235-238 ◽  
Author(s):  
V. L. Szatalowicz ◽  
P. D. Miller ◽  
J. W. Lacher ◽  
J. A. Gordon ◽  
R. W. Schrier
Keyword(s):  
Plasma Osmolality ◽  
Comparative Effect ◽  
Water Excretion ◽  
Urinary Osmolality ◽  
Renal Water Excretion

1. The effects of intravenous chlorthiazide and frusemide on urinary osmolality were compared in 19 hyponatraemic oedamatous patients. 2. Frusemide (1 mg/kg) caused production of a dilute urine (urine/plasma osmolality ratio, Uosm./Posm., 1.64–0.84, P < 0.01) whereas chlorthiazide (10 mg/kg) did not (Uosm./Posm. 1.54–1.34, not significant). 3. The osmolar clearance (Cosm.) was higher after frusemide than after chlorthiazide (11.45 vs 4.99 ml/min, P < 0.01). When the doses of frusemide (0.25–0.5 mg/kg) and chlorthiazide (20 mg/kg) were chosen to give a similar Cosm. (7.25 vs 7.48 ml/min, not significant), the Uosm./Posm. was still lower after frusemide (2.20–1.00, P < 0.001) than after chlorthiazide (1.75–1.26, P < 0.01). 4. Exogenous vasopressin did not increase the low Uosm./Posm. after frusemide (1.00–1.00, not significant) but increased the ratio after chlorthiazide (1.34–1.68, P < 0.001). 5. These results indicate that frusemide, but not chlorthiazide, leads to the excretion of a dilute urine in hyponatraemic oedematous patients. This dilution is not due to a greater solution excretion but is associated with a resistance to the action of vasopressin.

Vagally mediated regulation of renal function in conscious primates

1986 ◽  
Vol 250 (4) ◽  
pp. H546-H549
Author(s):  
S. F. Vatner ◽  
W. T. Manders ◽  
D. R. Knight
Keyword(s):  
Renal Function ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Rhesus Monkeys ◽  
Volume Expansion ◽  
Urine Flow ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Water Excretion

The effects of vagal denervation (VD) were examined on responses of Na+ and water excretion to acute volume expansion (18 ml/kg of 6% dextran in saline) in six conscious rhesus monkeys with chronic sinoaortic denervation (SAD). After SAD, volume expansion increased mean arterial pressure (from 95 +/- 6.6 to 119 +/- 7.5 mmHg), right atrial pressure (from 1.3 +/- 0.7 to 5.9 +/- 1.8 mmHg), urine flow (from 0.08 +/- 0.01 to 0.68 +/- 0.20 ml/min), and Na+ excretion (from 1.30 +/- 0.45 to 29.51 +/- 10.40 mueq/min). After VD, volume expansion increased mean arterial and right atrial pressures similarly, but induced significantly lower (P less than 0.05) increases in urine flow (from 0.05 +/- 0.01 to 0.19 +/- 0.03 ml/min) and Na+ excretion (from 0.87 +/- 0.27 to 11.50 +/- 6.13 mueq/min). Thus vagal mechanisms appear to play an important role in mediating excretion of Na+ and water in response to acute volume expansion in the conscious primate.

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.

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.

Influence of kinins and angiotensin II on the regulation of papillary blood flow

1988 ◽  
Vol 255 (4) ◽  
pp. F690-F698 ◽  
Author(s):  
R. J. Roman ◽  
M. L. Kaldunski ◽  
A. G. Scicli ◽  
O. A. Carretero
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Sodium Bicarbonate ◽  
Sodium Excretion ◽  
Sodium Bicarbonate Solution ◽  
Urine Osmolality ◽  
Urine Flow ◽  
Water Excretion ◽  
Cortical Blood Flow ◽  
Blood Flows

The influence of kinins and angiotensin II on the regulation of renal cortical and papillary blood flow and sodium and water excretion was examined in rats. Superficial cortical and papillary blood flows were measured using a laser-Doppler flowmeter. Papillary blood flow increased 50% after enalaprilat (60 micrograms/kg) and phosphoramidon (5.5 micrograms.kg-1.min-1) were given along with 0.3 M sodium bicarbonate solution to inhibit degradation of kinins and enhance urinary kallikrein activity. Infusion of a kinin antagonist, D-Arg-Hyp-Thi-D-Phe-bradykinin (5 micrograms/min), returned papillary blood flow to control levels. Urine flow and sodium excretion increased after the administration of the kininase inhibitors and sodium bicarbonate, while glomerular filtration rate (GFR) and outer cortical blood flow were unaltered. The kinin antagonist did not alter sodium and water excretion in rats receiving the kininase inhibitors and bicarbonate. Administration of the kinin antagonist alone lowered papillary blood flow by 20%, without affecting outer cortical blood flow or GFR. Urine flow decreased and urine osmolality increased after the rats received the kinin antagonist, but sodium excretion remained unaltered. To assess the role of angiotensin II in the control of papillary blood flow, kinin receptors were blocked by infusion of an antagonist, and the effects of enalaprilat and saralasin were studied. Papillary blood flow increased after blockade of the angiotensin II system in rats receiving the kinin antagonist. These results indicate that the kallikrein-kinin and renin-angiotensin systems participate in the regulation of papillary blood flow.

Effect of baroreceptor denervation on stimulation of drinking by angiotensin II in conscious dogs

1991 ◽  
Vol 260 (3) ◽  
pp. E333-E337 ◽  
Author(s):  
C. K. Klingbeil ◽  
V. L. Brooks ◽  
E. W. Quillen ◽  
I. A. Reid
Keyword(s):  
Blood Pressure ◽  
Drinking Water ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Plasma Osmolality ◽  
Plasma Angiotensin ◽  
High Doses ◽  
Stimulation Of

Angiotensin II causes marked stimulation of drinking when it is injected centrally but is a relatively weak dipsogen when administered intravenously. However, it has been proposed that the dipsogenic action of systemically administered angiotensin II may be counteracted by the pressor action of the peptide. To test this hypothesis, the dipsogenic action of angiotensin II was investigated in dogs, in which low and high baroreceptor influences had been eliminated by denervation of the carotid sinus, aortic arch, and heart. In five sham-operated dogs, infusion of angiotensin II at 10 and 20 ng.kg-1.min-1 increased plasma angiotensin II concentration to 109.2 +/- 6.9 and 219.2 +/- 38.5 pg/ml and mean arterial pressure by 20 and 29 mmHg, respectively, but did not induce drinking. In four baroreceptor-denervated dogs, the angiotensin II infusions produced similar increases in plasma angiotensin II concentration and mean arterial pressure but, in contrast to the results in the sham-operated dogs, produced a dose-related stimulation of drinking. Water intake with the low and high doses of angiotensin II was 111 +/- 44 and 255 +/- 36 ml, respectively. The drinking responses to an increase in plasma osmolality produced by infusion of hypertonic sodium chloride were not different in the sham-operated and baroreceptor-denervated dogs. These results demonstrate that baroreceptor denervation increases the dipsogenic potency of intravenous angiotensin II and provides further support for the hypothesis that the dipsogenic action of intravenous angiotensin II is counteracted by the rise in blood pressure.

Median preoptic nucleus ablation does not affect angiotensin II-induced hypertension

1986 ◽  
Vol 251 (1) ◽  
pp. H148-H152
Author(s):  
G. D. Fink ◽  
C. A. Bruner ◽  
M. L. Mangiapane
Keyword(s):  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Cardiovascular Responses ◽  
Base Line ◽  
Ang Ii ◽  
Preoptic Nucleus ◽  
Water Excretion ◽  
Median Preoptic Nucleus ◽  
Induced Hypertension

Previous studies implicated the ventral median preoptic nucleus (MNPOv) in cardiovascular responses to circulating and intracerebroventricular angiotensin II (ANG II) and in normal cardiovascular and fluid homoeostasis. In the present experiments, chronically catheterized rats received continuous (24 h/day) intravenous infusions of ANG II (10 ng/min) for 5 days, and changes in mean arterial pressure, heart rate, water intake and urinary electrolyte and water excretion were determined daily. Three groups of rats were compared as follows: 1) sham-operated control rats (n = 12), 2) rats with 20-70% of the MNPOv ablated electrolytically (n = 6), and 3) rats with over 90% of the MNPOv ablated (n = 5). The organum vasculosum of the lamina terminalis was intact in all three groups. Base-line values of all measured variables were identical in the three groups on two control days preceding ANG II infusion and on two recovery days after infusion. During the administration of ANG II for 5 days, mean arterial pressure rose significantly (and similarly) in all three groups of rats; no other variable was significantly affected by ANG II infusion. These results suggest that neural pathways originating in, or passing through, the MNPOv region are not critical in the pathogenesis of ANG II-induced hypertension in the rat.

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.

Ovine fetal adaptations to chronically reduced urine flow: preservation of amniotic fluid volume

1996 ◽  
Vol 81 (6) ◽  
pp. 2588-2594 ◽  
Author(s):  
Stephanie E. Mann ◽  
Mark J. M. Nijland ◽  
Michael G. Ross
Keyword(s):  
Amniotic Fluid ◽  
Plasma Osmolality ◽  
Urine Osmolality ◽  
Urine Flow ◽  
Fluid Volume ◽  
Fetal Plasma ◽  
Arterial Blood ◽  
Amniotic Fluid Volume ◽  
Fetal Urine ◽  
Ovine Fetal

Mann, Stephanie E., Mark J. M. Nijland, and Michael G. Ross.Ovine fetal adaptations to chronically reduced urine flow: preservation of amniotic fluid volume. J. Appl. Physiol. 81(6): 2588–2594, 1996.—Adequate amniotic fluid (AF) volume is maintained by a balance of fetal fluid production (lung liquid and urine) and resorption (swallowing and intramembranous flow). Because fetal urine is the principle source of AF, alterations in urine flow and composition directly impact AF dynamics. Intra-amniotic 1-desamino-8-d-arginine vasopressin (DDAVP) is rapidly absorbed into fetal plasma and induces a marked fetal urinary antidiuresis. To examine the effect of intra-amniotic- DDAVP-induced fetal urinary responses on AF volume and composition, six chronically prepared ewes with singleton fetuses (gestation 128 ± 2 days) were studied for 72 h after a single intra-amniotic DDAVP (50-μg) injection. After DDAVP, fetal urine osmolality significantly increased at 2 h (157 ± 13 to 253 ± 21 mosmol/kg) and remained elevated at 72 h (400 ± 13 mosmol/kg). Urinary sodium (33.0 ± 4.5 to 117.2 ± 9.7 meq/l) and chloride (26.0 ± 2.8 to 92.4 ± 8.1 meq/l) concentrations similarly increased. AF osmolality increased (285 ± 3 to 299 ± 4 mosmol/kgH2O), although there was no change in fetal plasma osmolality (294 ± 2 mosmol/kg). Despite a 50% reduction in fetal urine flow (0.12 ± 0.03 to 0.05 ± 0.02 ml ⋅ kg−1 ⋅ min−1at 2 h and 0.06 ± 0.01 ml ⋅ kg−1 ⋅ min−1after 72 h), AF volume did not change (693 ± 226 to 679 ± 214 ml). There were no changes in fetal arterial blood pressures, pH,[Formula: see text], or[Formula: see text] after DDAVP. We conclude the following. 1) Intra-amniotic DDAVP injection induces a prolonged decrease in fetal urine flow and increases in urine and AF osmolalities. 2) Despite decreased urine flow, AF volume does not change. We speculate that, in response to DDAVP-induced fetal oliguria, reversed intramembranous flow (from isotonic fetal plasma to hypertonic AF) preserves AF volume.

A Non-inferiority Trial: Safety and Efficacy of Topical 1:1000 versus 1:10 000 Epinephrine in Sino-nasal Surgeries

2020 ◽  
pp. 000348942096282
Author(s):  
Cassie L. Dow ◽  
Anders W. Sideris ◽  
Ravjit Singh ◽  
Mitchell H. Giles ◽  
Catherine Banks ◽  
...  
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Nasal Passage ◽  
Hemodynamic Parameters ◽  
Hemodynamic Stability ◽  
Absolute Change ◽  
Significant Difference ◽  
Blood Pressures ◽  
Surgical Conditions

Objective: This study aimed to test the non-inferiority of topical 1:1000 epinephrine compared to topical 1:10 000 with regard to intraoperative hemodynamic stability, and to determine whether it produced superior visibility conditions. Methods: A single-blinded, prospective, cross-over non-inferiority trial was performed. Topical 1:1000 or topical 1:10 000 was placed in 1 nasal passage. Hemodynamic parameters (heart rate, systolic and diastolic blood pressures, and mean arterial pressure) were measured prior to insertion then every minute for 10 minutes. This was repeated in the contralateral nasal passage of the same patient with the alternate concentration. The surgeon graded the visualization of each passage using the Boezaart Scale. The medians of the greatest absolute change in parameters were compared using a Wilcoxon Rank-Signed test and confidence intervals were calculated using a Hodges-Lehman test. The non-inferiority margin was pre-determined at 10 bpm for heart rate and 10 mmHg for blood pressures. A Wilcoxon Rank-Signed test was used to assess superiority in visualization. Results: Thirty-two patients were enrolled and after exclusions, nineteen were assessed (mean age = 35.63 ± 12.49). Differences in means of greatest absolute change between the 2 concentrations were calculated (heart rate = 2.49 ± 1.20; systolic = −1.51 ± 2.16; diastolic = 2.47 ± 1.47; mean arterial pressure = 0.07 ± 1.83). In analyses of medians, 1:1000 was non-inferior to the 1:10 000. There was a significant difference (–0.58 ± 0.84; P = .012) in visualization in favor of topical 1:1000. Conclusion: Topical 1:1000 epinephrine provides no worse intraoperative hemodynamic stability compared to topical 1:10 000 but affords superior visualization and should be used to optimize surgical conditions.

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