scholarly journals Evidence that catecholamines stimulate renal gluconeogenesis through an α1-type of adrenoceptor

1980 ◽  
Vol 190 (1) ◽  
pp. 119-123 ◽  
Author(s):  
P Kessar ◽  
E D Saggerson
Keyword(s):  
Rat Kidney ◽  
Alpha Adrenoceptor ◽  
Adrenoceptor Antagonist ◽  
Renal Gluconeogenesis ◽  
Adrenoceptor Agonist ◽  
Alpha Agonist

1. Noradrenaline stimulates gluconeogenesis through an alpha-adrenoceptor in renal cortical tubule fragments from fed rats incubated with 5 mM-lactate. 2. The selective alpha 1-adrenoreceptor agonist methoxamine stimulated gluconeogenesis, but the selective alpha 2-adrenoceptor agonist clonidine was ineffective. 3. The selective alpha 1-adrenoceptor antagonist thymoxamine blocked the stimulatory effects on gluconeogenesis of noradrenaline and of oxymetazoline (a synthetic alpha-agonist). The selective alpha 2-adrenoceptor antagonist yohimbine was ineffective in this respect. 4. It is concluded that noradrenaline and oxymetazoline stimulate gluconeogenesis in rat kidney via an alpha 1-rather than an alpha 2-type of adrenoceptor.

scholarly journals Effect of compound D-600 (methoxyverapamil) on gluconeogenesis and on acceleration of the process by α-adrenergic stimuli in rat kidney tubules

1980 ◽  
Vol 190 (2) ◽  
pp. 283-291 ◽  
Author(s):  
E D Saggerson ◽  
C A Carpenter
Keyword(s):  
Renal Cortex ◽  
Rat Kidney ◽  
Sodium Lactate ◽  
Kidney Tubules ◽  
Alpha Adrenoceptor ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
Adrenoceptor Blocker ◽  
Glucose Formation ◽  
Stimulation Of

1. Tubule fragments were isolated from renal cortex of fed rats and glucose formation was measured after incubation with 5 mM-sodium lactate. 20 Compound D-600 (10-100 microM) decreased gluconeogenesis from lactate. This inhibition of the process by compound D-600 increased with increasing extracellular Ca2+ concentration, was overridden by noradrenaline and diminished by starvation for 24 h. 3. Inhibition of lactate-supported gluconeogenesis by compound D-600 was not prevented by the alpha 1-adrenoceptor antagonist thymoxamine. 4. Compound D-600 had little effect on gluconeogenesis from 2-oxoglutarate and increased gluconeogenesis from succinate. 5. Compound D-600 opposed stimulation of gluconeogenesis by noradrenaline or oxymetazoline (a selective alpha-adrenoceptor agonist) in a manner suggesting that compound D-600 is an alpha-adrenoceptor blocker. Oxymetazoline was more sensitive than noradrenaline to blockade by both compound D-600 and by the conventional alpha-adrenoceptor antagonist phentolamine. Noradrenaline became more sensitive to blockade by compound D-600 when extracellular Ca2+ was decreased. 6. Compound D-600 did not block stimulation of gluconeogenesis by angiotensin or cyclic AMP.

Ontogeny of alpha-adrenoceptor responses in renal vascular bed of sheep

1988 ◽  
Vol 254 (2) ◽  
pp. R277-R283 ◽  
Author(s):  
G. P. Matherne ◽  
K. T. Nakamura ◽  
J. E. Robillard
Keyword(s):  
Renal Vasoconstriction ◽  
Adult Sheep ◽  
Alpha Adrenoceptor ◽  
Adrenoceptor Antagonist ◽  
Low Concentrations ◽  
Adrenoceptor Agonist ◽  
Similar Dose ◽  
Nonpregnant Adult ◽  
Phenylephrine Infusion ◽  
Renal Vascular

The renal hemodynamic response to renal arterial infusions of guanabenz (alpha 2-adrenoceptor agonist) and phenylephrine (alpha 1-adrenoceptor agonist) were compared in conscious and chronically instrumented fetal (132-140 days gestation; term 145 days), newborn (6-15 days postnatal), and nonpregnant adult sheep. Phenylephrine produced similar dose-related decreases in renal blood flow velocity in all three groups at low concentrations (less than 1.8 X 10(-7) M) of drug in renal blood, whereas at the highest concentration adults demonstrated the most vasoconstriction and newborns the least (P less than 0.05 ANOVA). Responses to phenylephrine infusion during renal alpha 1-adrenoceptor blockade with prazosin were completely inhibited. Guanabenz produced greater renal vasoconstriction in adult sheep (P less than 0.05 ANOVA) at all concentrations (0.6 X 10(-6) to 8 X 10(-6) M) when compared with fetal and newborn sheep. Guanabenz-mediated vasoconstriction was not affected by alpha 1-adrenoceptor blockade with prazosin but was completely inhibited by the addition of an alpha 2-adrenoceptor antagonist idazoxan. Results of the present study demonstrate that renal vasoconstriction is mediated by both alpha 1- and alpha 2-adrenoceptors in fetal, newborn, and adult sheep. Moreover, these results suggest that renal alpha 1- and alpha 2-adrenoceptor-mediated vasoconstrictor responses mature at different rates.

scholarly journals Adrenergic inhibition of carbon dioxide excretion by trout red blood cells in vitro is mediated by activation of Na+/H+ exchange

1991 ◽  
Vol 157 (1) ◽  
pp. 367-380
Author(s):  
S. F. Perry ◽  
C. M. Wood ◽  
S. Thomas ◽  
P. J. Walsh
Keyword(s):  
Carbon Dioxide ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Beta Adrenoceptor ◽  
Alpha Adrenoceptor ◽  
Adrenoceptor Antagonist ◽  
Exchange Inhibitor ◽  
Adrenoceptor Agonist ◽  
Co2 Excretion

We have used a sensitive new technique to assess the mechanism(s) of adrenergic inhibition of rainbow trout (Oncorhynchus mykiss) red blood cell (RBC) carbon dioxide excretion in vitro. The effect was only apparent using blood acidified to simulate metabolic acidosis. Red blood cell CO2 excretion was inhibited in a dose-dependent manner by physiologically relevant concentrations of noradrenaline (10–1000 nmol l-1) or adrenaline (100–1000 nmol l-1). The beta-adrenoceptor antagonist propranolol abolished the inhibitory effect of adrenaline, whereas the alpha-adrenoceptor antagonist phentolamine was without effect. The action of noradrenaline on RBC CO2 excretion was mimicked by the beta-adrenoceptor agonist isoproterenol, but not by the alpha-adrenoceptor agonist phenylephrine. Therefore, adrenergic inhibition of CO2 excretion is mediated by RBC beta-adrenoceptors, presumably of the beta 1 subtype. The Na+/H+ exchange inhibitor amiloride effectively blocked adrenergic stimulation of Na+/H+ exchange (as indicated from measurements of pHe and RBC pHi) and entirely prevented the inhibition of CO2 excretion. Noradrenaline significantly reduced the rate of CO2 excretion even in the presence of the Cl-/HCO3- exchange inhibitor SITS. Therefore, adrenergic inhibition of CO2 excretion is accomplished via activation of RBC Na+/H+ exchange rather than by a direct inhibition of Cl-/HCO3- exchange. The observed relationship between CO2 excretion rates and the RBC transmembrane pH difference (pHe-pHi) and the occurrence of the inhibition only at low pHe provide further evidence of the linkage with RBC Na+/H+ exchange. We suggest that adrenergic activation of RBC Na+/H+ exchange impedes CO2 excretion by causing a rise in intracellular HCO3- levels concurrent with a reduction of intracellular PCO2. The net result is a reduced gradient for HCO3- entry into the RBC in conjunction with a diminution of the outwardly directed PCO2 gradient. Thus, the rate of formation of CO2 from the dehydration of plasma HCO3- is reduced and, in turn, a portion of this CO2 is not excreted but recycled through the red blood cell.

scholarly journals A Blunted Sympathetic Function and an Enhanced Nitrergic Activity Contribute to Reduce Mesenteric Resistance in Hyperthyroidism

2021 ◽  
Vol 22 (2) ◽  
pp. 570
Author(s):  
Laia Cros-Brunsó ◽  
Laura Camacho-Rodríguez ◽  
Ángel Martínez-González ◽  
Pablo Llévenes ◽  
Mercedes Salaices ◽  
...  
Keyword(s):  
Citrate Synthase ◽  
Purinergic Receptor ◽  
Body Weight Gain ◽  
Electrical Field Stimulation ◽  
Alpha Adrenoceptor ◽  
Adrenoceptor Antagonist ◽  
Sympathetic Function ◽  
Vasoconstrictor Response ◽  
Relevant Role ◽  
Male Wistar Rats

We aimed to determine whether an experimental model of hyperthyroidism could alter the function of sympathetic and nitrergic components of mesenteric innervation. For this purpose, male Wistar rats were divided into (1) control rats (CT) and (2) rats infused with L-Thyroxine (HT). Body weight gain and adipose tissue accumulation were lower in HT rats, while systolic blood pressure and citrate synthase activity in the soleus muscle were increased by HT. In segments from the superior mesenteric artery, the application of an electrical field stimulation (EFS) induced a vasoconstrictor response, which was lower in arteries from HT animals. The alpha-adrenoceptor antagonist phentolamine diminished EFS-induced vasoconstriction to a lower extent in HT arteries, while the purinergic receptor antagonist suramin reduced contractile response to EFS only in segments from CT. In line with this, noradrenaline release, tyrosine hydroxylase expression and activation and dopamine β hydroxylase expression were diminished in HT. The unspecific nitric oxide synthase (NOS) inhibitor L-NAME increased EFS-induced vasoconstriction more markedly in segments from HT rats. NO release was enhanced in HT, probably due to an enhancement in neuronal NOS activity, in which a hyperactivation of both PKC and PI3K-AKT signaling pathways might play a relevant role. In conclusion, perivascular mesenteric innervation might contribute to reduce the vascular resistance observed in hyperthyroidism.

Testosterone-augmented contractile responses to α1- and β1-adrenoceptor stimulation are associated with increased activities of RyR, SERCA, and NCX in the heart

2009 ◽  
Vol 296 (4) ◽  
pp. C766-C782 ◽  
Author(s):  
Sharon Tsang ◽  
Stanley S. C. Wong ◽  
Song Wu ◽  
Gennadi M. Kravtsov ◽  
Tak-Ming Wong
Keyword(s):  
Ventricular Myocytes ◽  
Left Ventricular ◽  
Contractile Responses ◽  
Adrenoceptor Antagonist ◽  
Cardiac Contractile ◽  
Plasmic Reticulum ◽  
Adrenoceptor Agonist ◽  
Intracellular Ca ◽  
Developed Pressure ◽  
Stimulation Of

We hypothesized that testosterone at physiological levels enhances cardiac contractile responses to stimulation of both α1- and β1-adrenoceptors by increasing Ca2+ release from the sarcoplasmic reticulum (SR) and speedier removal of Ca2+ from cytosol via Ca2+-regulatory proteins. We first determined the left ventricular developed pressure, velocity of contraction and relaxation, and heart rate in perfused hearts isolated from control rats, orchiectomized rats, and orchiectomized rats without and with testosterone replacement (200 μg/100 g body wt) in the presence of norepinephrine (10−7 M), the α1-adrenoceptor agonist phenylephrine (10−6 M), or the nonselective β-adrenoceptor agonist isoprenaline (10−7 M) in the presence of 5 × 10−7 M ICI-118,551, a β2-adrenoceptor antagonist. Next, we determined the amplitudes of intracellular Ca2+ concentration transients induced by electrical stimulation or caffeine, which represent, respectively, Ca2+ release via the ryanodine receptor (RyR) or releasable Ca2+ in the SR, in ventricular myocytes isolated from the three groups of rats. We also measured 45Ca2+ release via the RyR. We then determined the time to 50% decay of both transients, which represents, respectively, Ca2+ reuptake by sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) and removal via the sarcolemmal Na+/Ca2+ exchanger (NCX). We correlated Ca2+ removal from the cytosol with activities of SERCA and its regulator phospholamban as well as NCX. The results showed that testosterone at physiological levels enhanced positive inotropic and lusitropic responses to stimulation of α1- and β1-adrenoceptors via the androgen receptor. The increased contractility and speedier relaxation were associated with increased Ca2+ release via the RyR and faster Ca2+ removal out of the cytosol via SERCA and NCX.

Effects of α-adrenoceptor agonists and antagonists on thyroid hormone secretion

1985 ◽  
Vol 108 (2) ◽  
pp. 184-191 ◽  
Author(s):  
Bo Ahrén
Keyword(s):  
Thyroid Hormone ◽  
Dose Level ◽  
Hormone Secretion ◽  
High Dose ◽  
Inhibitory Effects ◽  
High Dose Level ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
Adrenoceptor Agonists

Abstract. The effects of various α-adrenoceptor agonists and antagonists on blood radioiodine levels were studied in mice pre-treated with 125I and thyroxine. The non-selective α-adrenoceptor agonist noradrenaline and the selective α1-adrenoceptor agonist phenylephrine both enhanced blood radioiodine levels. Noradrenaline was more potent than phenylephrine. Contrary, the selective α2-adrenoceptor agonist clonidine depressed basal levels of blood radioiodine. The non-selective α-adrenoceptor antagonist phentolamine and the selective α1-adrenoceptor antagonist prazosin both inhibited the noradrenaline-induced elevation of radioiodine levels, whereas the α2-adrenoceptor antagonist yohimbine had no such effect, except at a high dose level. All three α-adrenoceptor agonists, noradrenaline, phenylephrine and clonidine, inhibited the radioiodine response to TSH. In addition, TSH-induced increase in radioiodine levels was inhibited by prazosin, whereas yohimbine had no effect. Phentolamine inhibited the radioiodine response to TSH when given 2 h prior to TSH, whereas when given 15 min prior to TSH the response to TSH was potentiated by Phentolamine. It is concluded, that under in vivo conditions in the mouse, α1-adrenoceptor activation stimulates basal thyroid hormone secretion and inhibits TSH-induced thyroid hormone secretion. Further, α2-adrenoceptor activation inhibits basal thyroid hormone secretion. In addition, TSH-induced thyroid hormone secretion is inhibited by α1-adrenoceptor antagonism. Thus, α-adrenoceptors induce both stimulatory and inhibitory effects of thyroid function.

Actions of norepinephrine on rat hypoglossal motoneurons

1995 ◽  
Vol 74 (5) ◽  
pp. 1911-1919 ◽  
Author(s):  
M. A. Parkis ◽  
D. A. Bayliss ◽  
A. J. Berger
Keyword(s):  
Choline Chloride ◽  
Reversal Potential ◽  
Repetitive Firing ◽  
Inward Current ◽  
Hypoglossal Motoneurons ◽  
Beta Adrenoceptor ◽  
Adrenoceptor Antagonist ◽  
Perfusion Solution ◽  
Adrenoceptor Agonist ◽  
Firing Properties

1. We used conventional intracellular recording techniques in 400-microns-thick slices from the brain stems of juvenile rats to investigate the action of norepinephrine (NE) on subthreshold and firing properties of hypoglossal motoneurons (HMs). 2. In recordings in current-clamp mode, 50 or 100 microM NE elicited a reversible depolarization accompanied by an increase in input resistance (RN) in all HMs tested (n = 74). In recordings in single-electrode voltage-clamp mode, NE induced a reversible inward current (INE) accompanied by a reduction in input conductance. The average reversal potential for INE was -104 mV. The NE responses could be elicited in a Ca(2+)-free solution containing tetrodotoxin, indicating that they were postsynaptic. 3. The NE response could be blocked by the alpha-adrenoceptor antagonist prazosin, but not by the beta-adrenoceptor antagonist propranolol, and could be mimicked by the alpha 1-adrenoceptor agonist phenylephrine but not by the alpha 2-adrenoceptor agonist UK 14,304 or by the beta-adrenoceptor agonist isoproterenol when alpha-adrenoceptors were blocked. 4. Substitution of barium for calcium in the perfusion solution blocked the increase in RN in response to NE without completely blocking the depolarization. Replacement of sodium chloride with choline chloride in the barium-substituted perfusion solution blocked the remaining depolarization. 5. The neuropeptide thyrotropin-releasing hormone (TRH), which also depolarizes and increases the RN of HMs, occluded the response of HMs to NE. 6. NE altered HM firing properties in three ways: it always lowered the minimum amount of injected current needed to elicit repetitive firing, it increased the slope of the firing frequency versus injected current relation in 8 of 14 cells tested, and it increased the delay from the onset of the depolarizing current pulse to the first evoked spike in all cells tested. 7. We conclude that NE acts directly on alpha 1-adrenoceptors to increase the excitability of HMs. It does this by reducing a barium-sensitive resting potassium current and activating a barium-insensitive inward current carried primarily by sodium ions. A portion of the intracellular pathway for these actions is shared by TRH. In addition, there is evidence that NE alters HM firing patterns by affecting currents that are activated following depolarization.

scholarly journals Differential in vivo Sensitivity of Melanophores and Xanthophores to Catecholamines in Winter Flounder (Pseudopleuronectes Americanus Walbaum) Integumentary Patterns

1985 ◽  
Vol 114 (1) ◽  
pp. 649-659
Author(s):  
D. Burton
Keyword(s):  
Winter Flounder ◽  
Pseudopleuronectes Americanus ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
Albedo Change ◽  
Differential Responses

The catecholamines, adrenalin, dopamine and noradrenalin induce differential aggregation of melanophores in black-adapted winter flounder, Pseudopleuronectes americanus, paralleling patterning responses to albedo change. These differential responses to catecholamines suggest that the patterning mechanism in this species is largely dependent on a balance between neural aggregating and dispersing elements. The α-adrenoceptor agonist phenylephrine evokes paling in all pattern components in blackadapted flounder, whilst the α-adrenoceptor antagonist phentolamine darkens white-adapted flounders. The α-adrenoceptor agonist isoproterenol and the α-adrenoceptor antagonist propranalol have no effect on chromatophores of white-adapted flounder, but induce pallor in blackadapted flounder, which is interpreted as non specific. Noradrenalin elicits patterning responses in chromatically decentralized flounder, although the duration of pallor is shorter. The xanthophores, which are dispersed by a pituitary factor, will aggregate in response to high catecholamine doses.

Alpha-2 adrenoceptor agonist protects retinal function after acute retinal ischemic injury in the rat

2002 ◽  
Vol 19 (2) ◽  
pp. 175-185 ◽  
Author(s):  
RONALD K. LAI ◽  
TERESA CHUN ◽  
DAIN HASSON ◽  
STEVE LEE ◽  
FARROKH MEHRBOD ◽  
...  
Keyword(s):  
Ischemic Injury ◽  
Retinal Ischemia ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Retinal Cell ◽  
Brown Norway ◽  
Tunel Staining ◽  
Dependent Manner ◽  
Adrenoceptor Antagonist ◽  
Extracellular Signal ◽  
Adrenoceptor Agonist

Alpha-2 adrenoceptor agonists have previously been shown to enhance neuronal survival in an optic nerve mechanical injury model and to protect photoreceptors in a light-induced degeneration model. The purpose of this study was to examine the effect of the alpha-2 adrenoceptor agonist in a pressure-induced retinal ischemia model. Brown-Norway rats were treated systemically or topically with alpha-2 adrenoceptor specific agonist brimonidine. Retinal ischemia was induced by increasing the intraocular pressure to 110 mm Hg for 50 min. The effect of brimonidine on retinal ischemic injury was functionally assessed in the rats 7 d later using electroretinography (ERG). Ischemia-induced retinal cell death was studied using the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining. We found that brimonidine treatment significantly protected the retina from retinal ischemic injury in a dose- and time-dependent manner. This protection can be achieved either by systemic or topical application and can be blocked by pretreatment with the alpha-2 adrenoceptor antagonist, yohimbine. Using reverse transcription-polymerase chain reaction (RT-PCR) and Western blot analysis, we found that brimonidine can up-regulate the expression of basic fibroblast growth factor, bcl-2 and bcl-xl in the retina. The drug also can activate two major cell survival signaling pathways in the retina: the extracellular-signal-regulated kinases (ERKs) and phosphatidylinositol-3′ kinase/protein kinase Akt pathways. All these aforementioned factors may potentially contribute in mediating brimonidine's protective effect in this acute retinal ischemia model.

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