Antidiuretic effect of acute morphine administration in the conscious rat

1982 ◽  
Vol 60 (2) ◽  
pp. 201-204 ◽  
Author(s):  
N. Wilson ◽  
J. Ngsee
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Diabetes Insipidus ◽  
Antidiuretic Hormone ◽  
Urine Flow ◽  
Conscious Rat ◽  
Antidiuretic Effect ◽  
Morphine Administration

Morphine was administered intravenously to normal and to Brattleboro (genetically deficient in antidiuretic hormone) rats. The injection caused a significant decrease in mean arterial pressure and urine flow in all animals, including those homozygous for diabetes insipidus. It is suggested that the antidiuretic effect of morphine may occur independently of ADH release.

scholarly journals Tyrosine kinase inhibitors modulate the ventilatory response to hypoxia in the conscious rat

1999 ◽  
Vol 87 (1) ◽  
pp. 363-369 ◽  
Author(s):  
Marc A. Czapla ◽  
Narong Simakajornboon ◽  
Gregory A. Holt ◽  
David Gozal
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Brain Stem ◽  
Tyrosine Phosphorylation ◽  
Minute Ventilation ◽  
Whole Body ◽  
Control Mechanisms ◽  
Conscious Rat ◽  
Adult Rats

Tyrosine kinases (TKs) exert multiple regulatory roles in neuronal activity and synaptic plasticity and could be involved in modulation of cardiovascular and respiratory control mechanisms within the dorsocaudal brain stem. To study this issue, the cardioventilatory responses to 1-μl microinjection within the dorsocaudal brain stem of either vehicle (Veh), the inactive TK inhibitor analog tyrphostin A1 (A1; 1 mM), or the active TK inhibitors genistein (Gen; 10 mM) and tyrphostin A25 (A25; 1 mM) were assessed by whole body plethysmography in unrestrained Sprague-Dawley adult rats. No changes in minute ventilation, heart rate, or mean arterial pressure occurred with Veh, A1, Gen, or A25 during room air breathing ( P not significant). However, Gen and A25 attenuated the peak hypoxic ventilatory responses (HVR) to 10% O2( P < 0.006 vs. Veh), whereas A1 did not modify HVR ( P not significant). HVR reductions by Gen and A25 were primarily due to diminished respiratory frequency enhancements ( P< 0.002). No changes in heart rate or mean arterial pressure responses occurred during hypoxia with TK inhibition. In addition, increases in tyrosine phosphorylation of the NR2A/B subunits, but not of the NR2C subunit, of the N-methyl-d-aspartate receptor occurred at 5, 30, and 60 min of hypoxia in the dorsocaudal brain stem and returned to baseline values at 120 min. We conclude that hypoxia induces tyrosine phosphorylation of the N-methyl-d-aspartate glutamate receptor, and TK inhibition within the dorsocaudal brain stem attenuates components of HVR in conscious rats.

scholarly journals Effects of serelaxin on renal microcirculation in rats under control and high-angiotensin environments

2018 ◽  
Vol 314 (1) ◽  
pp. F70-F80 ◽  
Author(s):  
Weijian Shao ◽  
Carla B. Rosales ◽  
Camila Gonzalez ◽  
Minolfa C. Prieto ◽  
L. Gabriel Navar
Keyword(s):  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Excretion Rate ◽  
No Synthase ◽  
Urine Flow ◽  
Ang Ii ◽  
Afferent Arterioles

Serelaxin is a novel recombinant human relaxin-2 that has been investigated for the treatment of acute heart failure. However, its effects on renal function, especially on the renal microcirculation, remain incompletely characterized. Our immunoexpression studies localized RXFP1 receptors on vascular smooth muscle cells and endothelial cells of afferent arterioles and on principal cells of collecting ducts. Clearance experiments were performed in male and female normotensive rats and Ang II-infused male rats. Serelaxin increased mean arterial pressure slightly and significantly increased renal blood flow, urine flow, and sodium excretion rate. Group analysis of all serelaxin infusion experiments showed significant increases in GFR. During infusion with subthreshold levels of Ang II, serelaxin did not alter mean arterial pressure, renal blood flow, GFR, urine flow, or sodium excretion rate. Heart rates were elevated during serelaxin infusion alone (37 ± 5%) and in Ang II-infused rats (14 ± 2%). In studies using the in vitro isolated juxtamedullary nephron preparation, superfusion with serelaxin alone (40 ng/ml) significantly dilated afferent arterioles (10.8 ± 1.2 vs. 13.5 ± 1.1 µm) and efferent arterioles (9.9 ± 0.9 vs. 11.9 ± 1.0 µm). During Ang II superfusion, serelaxin did not alter afferent or efferent arteriolar diameters. During NO synthase inhibition (l-NNA), afferent arterioles also did not show any vasodilation during serelaxin infusion. In conclusion, serelaxin increased overall renal blood flow, urine flow, GFR, and sodium excretion and dilated the afferent and efferent arterioles in control conditions, but these effects were attenuated or prevented in the presence of exogenous Ang II and NO synthase inhibitors.

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.

EVIDENCE THAT THE ANTIDIURETIC SUBSTANCE IN THE PLASMA OF CHILDREN WITH NEPHROGENIC DIABETES INSIPIDUS IS ANTIDIURETIC HORMONE

PEDIATRICS ◽  
1963 ◽  
Vol 32 (3) ◽  
pp. 384-388
Author(s):  
Malcolm A. Holliday ◽  
Charles Burstin ◽  
Jean Harrah
Keyword(s):  
Diabetes Insipidus ◽  
Antidiuretic Hormone ◽  
Nephrogenic Diabetes Insipidus ◽  
Water Deprivation ◽  
Jugular Vein ◽  
Urine Osmolality ◽  
Urine Flow ◽  
Antidiuretic Activity ◽  
Antecubital Vein ◽  
Assay Technique

The antidiuretic activity in the plasma of four children with nephrogenic diabetes insipidus was measured by a rat assay technique. The evidence presented to indicate that this activity was due to antidiuretic hormone (ADH) was as follows: (a) the activity was higher in jugular vein plasma than in femoral or antecubital vein plasma, (b) it was high when the children were thirsted and decreased when they drank water, (c) it was destroyed when the plasma was incubated with thioglycollate, and (d) it was ultrafilterable, and vasopressin (Pitressin), when injected, was distributed as though it was ultrafilterable. When the children were given vasopressin, there was no change in urine flow or osmolality, but plasma antidiuretic activity was higher than it was when water deprivation led to a reduction in urine flow and an increase in urine osmolality. The inference of these findings is that ADH is secreted normally in children with nephrogenic diabetes insipidus, it is ultrafilterable, but it is not a factor in modifying urine flow in response to dehydration.

Cooperative mechanisms of acute antidiuretic response to bendroflumethiazide in rats with lithium-induced nephrogenic diabetes insipidus

2010 ◽  
Vol 88 (12) ◽  
pp. 1191-1201 ◽  
Author(s):  
S. Mostafa Shid Moosavi ◽  
Masoud Haghani
Keyword(s):  
Diabetes Insipidus ◽  
Nephrogenic Diabetes Insipidus ◽  
Urine Volume ◽  
Free Water ◽  
Urine Flow ◽  
Water Reabsorption ◽  
Free Water Clearance ◽  
Urinary Osmolality ◽  
Antidiuretic Effect ◽  
Water Clearance

The exact mechanism underlying thiazides-induced paradoxical antidiuresis in diabetes insipidus is still elusive, but it has been hypothesized that it is exerted either via Na+-depletion activating volume-homeostatic reflexes to decrease distal delivery, or direct stimulation of distal water reabsorption. This study examined how these two proposed mechanisms actually cooperate to induce an acute bendroflumethiazide (BFTZ)-antidiuretic effect in nephrogenic diabetes insipidus (NDI). Anaesthetized rats with lithium (Li)-induced NDI were prepared in order to measure their renal functional parameters, and in some of them, bilateral renal denervation (DNX) was induced. After a 30 min control clearance period, we infused either BFTZ into 2 groups, NDI+BFTZ and NDI/DNX+BFTZ, or its vehicle into a NDI+V group, and six 30 min experimental clearance periods were taken. During BFTZ infusion in the NDI+BFTZ group, transiently elevated Na+ excretion was associated with rapidly increased urinary osmolality and decreased free water clearance, but Li clearance and urine flow declined in the later periods. However, in the NDI/DNX+BFTZ group, there was persistently elevated Na+ excretion with unchanged Li clearance and urine flow during the experimental period, while alterations in free water clearance and urinary osmolality resembled those in the NDI+BFTZ group. In conclusion, BFTZ initially exerted two direct effects of natriuresis–diuresis and stimulating free water reabsorption at the distal nephron in NDI, which together elevated Na+ excretion and urinary osmolality but kept the urine volume unchanged in the first hour. Thereafter, the resultant sodium depletion led to the activation of neural reflexes that reduced distal fluid delivery to compensate for BFTZ-induced natriuresis–diuresis which, in cooperation with the direct distal BFTZ-antidiuretic effect, resulted in excretion of urine with a low volume, high osmolality, and normal sodium.

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.

Extracellular Volume Expansion Inhibits Antidiuretic Hormone Increase during Positive End-Expiratory Pressure in Conscious Dogs

1993 ◽  
Vol 85 (5) ◽  
pp. 643-649 ◽  
Author(s):  
Gabriele Kaczmarczyk ◽  
Dinah Jörres ◽  
Rolf Rossaint ◽  
Martin Krebs ◽  
Volker Unger ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Atrial Natriuretic Peptide ◽  
Plasma Renin Activity ◽  
Antidiuretic Hormone ◽  
Natriuretic Peptide ◽  
Sodium Excretion ◽  
Extracellular Volume ◽  
Plasma Renin ◽  
Positive End Expiratory Pressure

1. This study in conscious dogs examined the effects of extracellular volume expansion on plasma antidiuretic hormone, atrial natriuretic peptide and aldosterone concentrations, plasma renin activity, and haemodynamic and renal responses during controlled mechanical ventilation with 20 cmH2O positive end-expiratory pressure. 2. Twenty experiments (10 controls, 10 expansion experiments with 03 ml min−1 kg−1 body weight of a balanced electrolyte solution given intravenously throughout) were performed in five trained, conscious, tracheotomized dogs over 4 h: first and fourth hour, spontaneous breathing; second and third hour, 20 cmH2O positive end-expiratory pressure. 3. In the control experiments positive end-expiratory pressure increased plasma antidiuretic hormone concentration from 1.4 + 0.2 to 10.0 + 3.3 pg/ml, plasma aldosterone concentration from 113 + 19 to 258 + 58 pg/ml and heart rate from 77 + 5 to 94 + 5 beats/min. Positive end-expiratory pressure did not change plasma atrial natriuretic peptide concentration (55 + 5 pg/ml), plasma renin activity (2.6 + 0.4 pmol of angiotensin I h−1 ml−1) and mean arterial pressure 103 + 3 mmHg). 4. In the expansion experiments, positive end-expiratory pressure did not change plasma antidiuretic hormone concentration (1.1 + 0.1 pg/ml), plasma aldosterone concentration (25 + 2 pg/ml), plasma atrial natriuretic peptide concentration (82 + 8 pg/ml), plasma renin activity (0.8 + 0.15 pmol of angiotensin I h−1 ml−1), heart rate (92 + 6 beats/min) and mean arterial pressure (111 + 4 mmHg). 5. In the control experiments, urine volume, sodium excretion and fractional sodium excretion remained in a low range during positive end-expiratory pressure, whereas potassium excretion increased. In the expansion experiments, urine volume, sodium excretion and fractional sodium excretion increased continuously. Glomerular filtration rate was decreased during positive end-expiratory pressure in the control experiments when compared with the expansion experiments (3.4 + 0.3 versus 3.9 + 0.2 ml min−1 kg−1 body weight). 6. Arterial blood gases and plasma osmolality did not change in either protocol. 7. It is suggested that the striking increase in antidiuretic hormone may play a part in the circulatory control mechanisms that maintain mean arterial pressure during positive end-expiratory pressure when the extracellular volume is not expanded.

THE VALUE OF RATS WITH HEREDITARY HYPOTHALAMIC DIABETES INSIPIDUS FOR THE BIOASSAY OF VASOPRESSIN

1967 ◽  
Vol 37 (3) ◽  
pp. 335-344 ◽  
Author(s):  
J. J. JONES ◽  
J. LEE
Keyword(s):  
Arterial Pressure ◽  
Diabetes Insipidus ◽  
Urine Volume ◽  
Urine Flow ◽  
Prolonged Administration ◽  
Urinary Osmolality ◽  
Daily Urine ◽  
Pituitary Glands ◽  
Hereditary Hypothalamic Diabetes Insipidus ◽  
Stimulation Of

SUMMARY The pituitary glands of 11 rats (six females and five males, weighing 140–200g.) with hereditary hypothalamic diabetes insipidus (DI) were found to contain oxytocin but no vasopressin. The DI rats could not always be distinguished from rats without diabetes insipidus (non-diabetes insipidus, NDI rats) by measurement of their daily urine volume. Stimulation of the neurohypophysis by fall in arterial pressure (haemorrhage, methacholine) or by nicotine, released vasopressin in NDI rats to produce a sustained antidiuresis, but in the DI rats there was only a transient fall in urine flow which did not outlast the hypotension. The DI rats were about twice as sensitive to vasopressin as NDI rats. As assay preparations they have the advantage that they cannot respond to vasopressin-releasing stimuli. Prolonged administration of Pitressin tannate in oil increased maximum urinary osmolality in DI rats, but failed to increase their sensitivity to intravenously injected vasopressin.

How we significantly reduced oesophagectomy leaks and the significance of Mean Arterial Pressure

2017 ◽  
Author(s):  
C Reissfelder ◽  
T Mees ◽  
S Schölch ◽  
A Remer ◽  
A Seifert ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure
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