Role of transmitters in mediating hypothalamic control of electrolyte excretion

1977 ◽  
Vol 55 (5) ◽  
pp. 1143-1154 ◽  
Author(s):  
M. Morris ◽  
S. M. McCann ◽  
R. Orias
Keyword(s):  
Sodium Excretion ◽  
Adrenergic Receptors ◽  
Male Rats ◽  
Intraventricular Injection ◽  
Urinary Volume ◽  
Electrolyte Excretion ◽  
Hypothalamic Control ◽  
Adrenergic Blocker ◽  
Β Receptor

Changes in urinary volume and electrolyte excretion were monitored after the injection of cholinergic and monoaminergic drugs into the third cerebral ventricle of conscious male rats made diuretic by an intravenous infusion of 5% dextrose. A natriuretic and kaliuretic response was induced by the intraventricular injection of norepinephrine (NE) or carbachol, whereas dopamine (DA) had no effect. The β-receptor stimulator isoproterenol (ISO) induced an antinatriuretic and antikaliuretic effect.Intraventricular injection of the α-adrenergic blocker phentolamine abolished the natriuretic response to NE and carbachol and to intraventricular hypertonic saline (HS). By contrast, the β-adrenergic blocker propranolol induced a natriuresis and kaliuresis when injected alone and an additive effect when its injection was followed by NE or HS. Propranolol potentiated the natriuretic response to carbachol. Cholinergic blockade with atropine diminished the response to NE and blocked the natriuretic response to HS. It is suggested that sodium receptors in the ventricular wall can modify renal sodium excretion via a stimulatory pathway involving cholinergic and α-adrenergic receptors and can inhibit sodium excretion via a tonically active β-receptor pathway.

scholarly journals The role of pneumoperitoneum in the glomerular filtration in an experimental model with 2/3 reduction of the renal mass

2017 ◽  
Vol 39 (1) ◽  
pp. 89
Author(s):  
Marco Aurélio Valadão ◽  
Djalma José Fagundes ◽  
Willian Cesar Cavazana ◽  
Gabriel Jorge Fagundes
Keyword(s):  
Renal Function ◽  
Glomerular Filtration ◽  
Renal Mass ◽  
Inulin Clearance ◽  
Male Rats ◽  
Urinary Volume ◽  
Co2 Pneumoperitoneum ◽  
Wistar Male Rats ◽  
Better Than

Objective: To evaluate the influence of the CO2 pneumoperitoneum in the glomerular filtration in a rat model with a 2/3 reduction of renal parenchyma. Methods: Adult Wistar male rats (n = 50) were subjected to right nephrectomy and a 2/3 ligature of the renal left vascular branch. Animals were randomly distributed as follows: GI (n = 10) - simulated, GII (n = 20) –8 mm Hg pneumoperitoneum, and GIII (n = 20) –15 mm Hg pneumoperitoneum. After two (GIIA and GIIIA) and three (GIIB and GIIIB) hours of insufflation, and one hour of disinsufflation, they were evaluated for the following aspects: mean blood pressure (MBP), microhematocrit, urinary volume and inulin clearance. Results: The microscopic aspects showed signs of glomerulosclerosis that caused proteinuria. Renal function with8 mm Hg pneumoperitoneum after two hours of disinsufflation (Δ% = 202.68) was better than after three hours (Δ% = 10.89). With15 mm Hg pneumoperitoneum, the renal function was damaged by both procedures, that is, two (Δ% = -3.57) and three hours (Δ% = -3.25). Conclusion: Inulin clearance evidenced renal insufficiency in the model with a 2/3 reduction of renal mass, and depending on both the increase of the exposure time and the pressure intensity, it can be more intensified. 

Urine Reinfusion Diuresis and Natriuresis in Rats: Role of Water, Electrolytes and Urea

1979 ◽  
Vol 57 (2) ◽  
pp. 187-193
Author(s):  
R. A. Norman ◽  
T. G. Coleman ◽  
P. R. Kastner
Keyword(s):  
Flow Rate ◽  
Sodium Excretion ◽  
Infusion Rate ◽  
Ringer Solution ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Urinary Volume ◽  
Natriuretic Factors

1. The purpose of this study was to determine the role of reinfused water, electrolytes and urea in the diuresis and natriuresis of urine reinfusion. 2. Three groups of rats underwent 5 h of urine reinfusion. The first group served as a control, and during urine reinfusion the urinary volume and sodium excretion increased to 10 or 12 times control values. 3. In a second group, urine reinfusion was followed by 2 h of infusion of Ringer solution at a rate equal to the urine flow rate; 71% of the diuresis and 75% of the natriuresis resulting from urine reinfusion were maintained. 4. In a third group, urine reinfusion was followed by infusion of Ringer solution with urea added. The infusion rate was equal to urine flow rate and the concentration of urea was equal to that in the urine; 98% of the diuresis and 102% of the natriuresis were maintained. 5. These results indicate that the majority of urine-reinfusion diuresis and natriuresis is due to reinfused volume and electrolytes, and the remainder, in these experiments at least, could be explained by the reinfused urea. Therefore there was no need to postulate additional urinary natriuretic factors to explain the results of urine reinfusion.

β-Adrenergic regulation of Na+ uptake by larval zebrafish Danio rerio in acidic and ion-poor environments

2012 ◽  
Vol 303 (10) ◽  
pp. R1031-R1041 ◽  
Author(s):  
Yusuke Kumai ◽  
Mellissa A. R. Ward ◽  
Steve F. Perry
Keyword(s):  
Danio Rerio ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Receptor Agonist ◽  
Acidic Water ◽  
Adrenergic Systems ◽  
Β Receptor ◽  
Β Adrenergic Receptors ◽  
Adrenergic Receptor Agonist

The potential role of adrenergic systems in regulating Na+ uptake in zebrafish ( Danio rerio) larvae was investigated. Treatment with isoproterenol (a generic β-adrenergic receptor agonist) stimulated Na+ uptake, whereas treatment with phenylephrine (an α1-adrenergic receptor agonist) as well as clonidine (an α2-adrenergic receptor agonist) significantly reduced Na+ uptake, suggesting opposing roles of α- and β-adrenergic receptors in Na+ uptake regulation. The increase in Na+ uptake associated with exposure to acidic water (pH = 4.0) was attenuated in the presence of the nonselective β-receptor antagonist propranolol or the β1-receptor blocker atenolol; the β2-receptor antagonist ICI-118551 was without effect. The stimulation of Na+ uptake associated with ion-poor water (32-fold dilution of Ottawa tapwater) was unaffected by β-receptor blockade. Translational gene knockdown of β-receptors using antisense oligonucleotide morpholinos was used as a second method to assess the role of adrenergic systems in the regulation of Na+ uptake. Whereas β1- or β2B-receptor knockdown led to significant decreases in Na+ uptake during exposure to acidic water, only β2A-receptor morphants failed to increase Na+ uptake in response to ion-poor water. In support of the pharmacology and knockdown experiments that demonstrated an involvement of β-adrenergic systems in the control of Na+ uptake, we showed that the H+-ATPase-rich (HR) cell, a subtype of ionocyte known to be a site of Na+ uptake, is innervated and appears to express β-adrenergic receptors (propranolol binding sites) at 4 days postfertilization. These data indicate an important role of adrenergic systems in regulating Na+ uptake in developing zebrafish.

Uterine β-adrenergic receptors in allogeneic and syngeneic pregnancy

1994 ◽  
Vol 72 (5) ◽  
pp. 456-462 ◽  
Author(s):  
Maria Elena Sales ◽  
Enri S. Borda
Keyword(s):  
Cyclic Amp ◽  
Binding Sites ◽  
Adrenergic Receptors ◽  
Binding Assay ◽  
Binding Assays ◽  
Receptor Affinity ◽  
Number Of Binding Sites ◽  
Β Receptor ◽  
Β Adrenergic Receptors

Two different mechanisms of regulation in uterine β-adrenergic receptors in allogeneic pregnancy (AP) and syngeneic pregnancy (SP) are described in this work. Firstly we noted changes in β-adrenergic sensitivity to isoproterenol in AP, while in SP differences in uterine reactivity to isoproterenol were found. In binding assays with the β-antagonist [3H]dihydroalprenolol, changes in β-receptor affinity were seen in AP, while in SP the maximal number of binding sites is altered. In addition, there are differences in uterine concentrations of cyclic AMP in both types of pregnancies as well as in the nucleotide response to isoproterenol. The differences in the reactivity and expression of uterine β-adrenoceptors in both types of pregnancies may be due to a distinctive immunological role of the semiallogeneic fetus in AP.Key words: β-adrenoceptors, cyclic AMP production, uterus, contractility, binding assay, syngeneic pregnancy, allogeneic pregnancy.

Effects of acute NaCl, KCl and KHCO3 loads on renal electrolyte excretion in humans

1992 ◽  
Vol 83 (5) ◽  
pp. 567-574 ◽  
Author(s):  
Marjolijn van Buren ◽  
Ton J. Rabelink ◽  
Herman J. M. van Rijn ◽  
Hein A. Koomans
Keyword(s):  
Sodium Excretion ◽  
Plasma Potassium ◽  
Acid Excretion ◽  
Potassium Salts ◽  
Electrolyte Excretion ◽  
Specific Effects ◽  
Identical Manner ◽  
Natriuretic Effect ◽  
Nacl Load

1. Potassium salts increase sodium excretion in humans. To define the role of the potassium ion in this effect, we compared the effects of equimolar single oral loads of 100 mmol of NaCl and KCl on renal electrolyte excretion in seven healthy subjects. In a second group (n = 7), we infused equimolar loads of NaCl or KCl (0.75 mmol/kg in 2 h). 2. In both experiments the KCl load quickly increased plasma potassium and aldosterone concentrations and potassium and sodium excretion to a maximum by 2 h after the load, whereas the NaCl load had no such effect. 3. In a third group (n = 7) we compared the effects of single oral loads of KCl and KHCO3 (1 mmol/kg), to assess the role of the anion in the natriuretic effect of potassium salts. 4. KCl and KHCO3 transiently stimulated urinary excretion of potassium and sodium in an identical manner. 5. We also followed the changes in acid excretion over time. Whereas both KCl and KHCO3 loading decreased acid excretion, this effect was greater after KHCO3 loading. Interestingly, acid excretion did not decrease further after the first collection hour after the potassium load, although the plasma potassium concentration was still increasing. 6. From these data we conclude (1) that increased excretion of sodium, potassium and chloride and decreased excretion of protons after administration of potassium salts are the specific effects of the potassium component; (2) that potassium also appears to have secondary, indirect effects on proton excretion, the mechanism of which remains to be clarified.

scholarly journals ANG II-related myocardial damage: role of cardiac sympathetic catecholamines and β-receptor regulation

1998 ◽  
Vol 275 (2) ◽  
pp. H534-H541 ◽  
Author(s):  
Jeffrey R. Henegar ◽  
Dean D. Schwartz ◽  
Joseph S. Janicki
Keyword(s):  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Myocardial Damage ◽  
Sympathetic Neuron ◽  
Receptor Regulation ◽  
Ang Ii ◽  
Receptor Density ◽  
Β Receptor ◽  
Acute Nature

The objectives of this study were 1) to determine whether ANG II-induced myocardial damage (ANG Dam) is mediated via the β1-adrenergic receptor, 2) to elucidate whether adrenal medulla or cardiac sympathetic neuron catecholamines are responsible for ANG Dam, and 3) to determine whether the lack of damage after 3 days of elevated ANG II levels is due to β1-receptor downregulation. To this end, ANG II was administered to rats 1) that were treated with a β-receptor blocker, 2) after adrenal medullectomy and/or cardiac sympathectomy, and 3) for 3 or 8 days. ANG II caused both myocyte necrosis and coronary vascular damage after adrenal medullectomy but not after cardiac sympathectomy. There was a 38 and 55% decrease in β-receptor density after 3 and 8 days, respectively, of ANG II infusion, and an upregulation to control levels 5 days after a 3-day ANG II infusion was stopped. We conclude that cardiac sympathetic neuron catecholamines are responsible for ANG Dam and that the acute nature of this damage is associated with a downregulation of β1-adrenergic receptors.

The role of interaction between orexin receptors and β2 adrenergic receptors in basolateral amygdala in dentate gyrus synaptic plasticity in male rats

2021 ◽  
Vol 177 ◽  
pp. 164-171
Author(s):  
Seyedeh Kebria Noorani ◽  
Vida Hojati ◽  
Esmaeil Akbari ◽  
Simin Ehsani ◽  
Takeshi Sakurai ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Dentate Gyrus ◽  
Adrenergic Receptors ◽  
Basolateral Amygdala ◽  
Male Rats ◽  
Orexin Receptors

Renal interstitial hydrostatic pressure during verapamil-induced natriuresis

1992 ◽  
Vol 262 (3) ◽  
pp. R432-R436 ◽  
Author(s):  
J. P. Granger ◽  
M. J. Solhaug
Keyword(s):  
Angiotensin Ii ◽  
Hydrostatic Pressure ◽  
Sodium Excretion ◽  
Fractional Excretion ◽  
Electrolyte Excretion ◽  
Filtration Fraction ◽  
Fractional Excretion Of Sodium ◽  
Induced Hypertension ◽  
Renal Vascular

Infusion of calcium antagonists results in significant increases in sodium excretion, an effect that is exacerbated in hypertensive animals. The mechanism responsible for the increase in sodium excretion has not been elucidated. The purpose of this study was to determine the role of renal interstitial hydrostatic pressure (RIHP) in mediating increases in sodium excretion produced by the calcium antagonist verapamil. Changes in renal hemodynamics and electrolyte excretion were examined in response to an intrarenal infusion of verapamil (100 micrograms/min) in normal dogs and in dogs with angiotensin II-induced hypertension. Infusion of verapamil in normal dogs increased renal blood flow by 18% and had no effect on glomerular filtration rate. Renal vascular resistance and filtration fraction both decreased in response to verapamil. Absolute (5.1 +/- 2.3 to 176 +/- 45.8 mueq/min) and fractional excretion of sodium (0.21 +/- 0.13 to 7.36 +/- 3.12%) also increased significantly. Despite renal vasodilation, the natriuresis was not associated with significant increases in RIHP (6.4 +/- 0.9 to 5.8 +/- 0.9 mmHg). Infusion of verapamil into dogs with angiotensin II hypertension resulted in a natriuresis (4.2 +/- 1.6 to 338.7 +/- 78.3 mueq/min) that was much greater than under normal conditions. Although the renal vasodilation was significantly higher in the angiotensin II-hypertensive dogs, the enhanced natriuresis in these animals was not associated with increases in RIHP. The results of this study indicate that increases in RIHP are not responsible for the natriuresis produced by verapamil in normal or angiotensin II-hypertensive dogs.

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