Endogenous opioids and electrolyte excretion after contralateral renal exclusion

1983 ◽  
Vol 244 (4) ◽  
pp. F392-F398 ◽  
Author(s):  
J. Ribstein ◽  
M. H. Humphreys
Keyword(s):  
Renal Mass ◽  
Opiate Receptors ◽  
Opiate Receptor ◽  
Endogenous Opioids ◽  
Subcutaneous Implantation ◽  
Electrolyte Excretion ◽  
Contralateral Kidney ◽  
Reflex Pathways ◽  
Ureteral Occlusion

Acute reductions in functioning renal mass result in increases in both sodium (U Na V) and potassium (U K V) excretion by the contralateral kidney (CK). We studied the role of endogenous opioids in this response. In control experiments acute unilateral nephrectomy (AUN) increased U Na V from 1,788 +/- 1,125 (SD) to 3,939 +/- 1,819 and U K V from 1,385 +/- 561 to 2,254 +/- 832 neq/min by the CK (P less than 0.005 for both); similar results occurred in rats undergoing acute unilateral ureteral occlusion (UUO). These increases occurred without overall change in GFR or mean arterial pressure. In rats receiving a continuous infusion of the opiate-receptor antagonist naloxone (0.3 mg . kg-1 . h-1) neither AUN nor UUO produced significant alterations in U Na V or U K V by the CK; naloxone infusion by itself did not alter GFR or basal rates of cation excretion. A separate group of rats was made tolerant to morphine by subcutaneous implantation of pellets containing 75 mg morphine base. In these rats, AUN also failed to produce any increase in U Na V or U K V by the CK. The results suggest that acute reductions in functioning renal mass produced by either AUN or UUO stimulate cation excretion by the remaining kidney through reflex pathways that involve opiate receptors.

Renal nerves and cation excretion after acute reduction in functioning renal mass in the rat

1984 ◽  
Vol 246 (3) ◽  
pp. F260-F265 ◽  
Author(s):  
J. Ribstein ◽  
M. H. Humphreys
Keyword(s):  
Glomerular Filtration Rate ◽  
Mean Arterial Pressure ◽  
Renal Mass ◽  
Filtration Rate ◽  
Renal Nerves ◽  
Potassium Excretion ◽  
Contralateral Kidney ◽  
Efferent Limb ◽  
Ureteral Occlusion

We evaluated the role of the renal nerves in the increased cation excretion by the contralateral kidney after acute unilateral nephrectomy (AUN) or unilateral ureteral occlusion (UUO) in anesthetized rats. Both AUN and UUO caused large increases in sodium (UNaV) and potassium excretion (UKV) by the control kidney without change in glomerular filtration rate or mean arterial pressure. Prior denervation of either the ipsilateral (experimental) kidney or the control kidney completely prevented the increase in UNaV and UKV after UUO. Prior denervation of either kidney also prevented the increase in UNaV after AUN. However, a significant kaliuresis persisted after AUN despite unilateral denervation although reduced in magnitude when compared with the increase in UKV after AUN with both kidneys innervated. These results indicate that the renal nerves play a major role in the excretory response of the control kidney after acute reduction in functioning renal mass. This role of the renal nerves may be through the activation of a renorenal reflex. The reflex is activated by afferents from the ipsilateral kidney; the efferent limb is composed of the renal nerves to the control kidney. This reflex can entirely account for the compensatory increase in cation excretion after UUO. However, a separate mechanism, not dependent on the renal nerves, contributes to UKV after AUN.

Endogenous opioids may mediate secondary damage after experimental brain injury

1987 ◽  
Vol 253 (5) ◽  
pp. E565-E574 ◽  
Author(s):  
T. K. McIntosh ◽  
R. L. Hayes ◽  
D. S. DeWitt ◽  
V. Agura ◽  
A. I. Faden
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Traumatic Injury ◽  
Opiate Receptors ◽  
Opiate Receptor ◽  
Endogenous Opioids ◽  
Secondary Brain Injury ◽  
Secondary Damage ◽  
Cord Injury

Although endogenous opioids have been implicated in the pathophysiology of spinal cord injury and brain ischemia, the role of specific opioid peptides and opiate receptors in the pathophysiology of traumatic brain injury remains unexplored. This study examined regional changes in brain opioid immunoreactivity and cerebral blood flow (CBF) after fluid-percussion brain injury in the cat and compared the effect of an opiate antagonist (Win 44,441-3 [Win-(-)]) with its dextroisomer Win 44,441-2 [Win-(+)] (which is inactive at opiate receptors) in the treatment of brain injury. Dynorphin A immunoreactivity (Dyn A-IR) but not leucine-enkephalin-like immunoreactivity accumulated in injury regions after traumatic injury; Dyn-IR increases also occurred predominantly in those areas showing significant decreases in regional CBF. Administration of Win-(-) but not Win-(+) or saline at 15 min after injury significantly improved mean arterial pressure, electroencephalographic amplitude, and regional CBF and reduced the severity and incidence of hemorrhage. Win-(-) also significantly improved survival after brain injury. Taken together, these findings suggest that dynorphin, through actions at opiate receptors, may contribute to the pathophysiology of secondary brain injury after head trauma and indicate that selective opiate-receptor antagonists may be useful in treatment of traumatic brain injury.

scholarly journals Impact of rotational stress on immunity parameters. Role of opiate receptors

2003 ◽  
Vol 49 (6) ◽  
pp. 56-58 ◽  
Author(s):  
S. V. Gein ◽  
T. A. Simonenko ◽  
S. P. Tendryakova
Keyword(s):  
Lymph Nodes ◽  
Considerable Increase ◽  
Opiate Receptors ◽  
Opiate Receptor ◽  
Delayed Type Hypersensitivity ◽  
Promoting Effect ◽  
Regional Lymph Nodes ◽  
The Impact ◽  
Stimulation Of

Experiments on non-inbred male mice used a model of rotational stress to examine the impact of 8-, p- к-opiate receptor blockade on antibody formation, delayed-type hypersensitivity (DTH), changes in the count of antibody-forming cells (AFC) and nucleated cells of lymph nodes and spleen during a local immune response. Rotational stress was found to cause a slightly pronounced inhibition of immune inflammation in DTH, a considerable increase in the count of AFC and nucleated cells in the regional lymph nodes, without changing the titers of antibodies from peripheral blood. Naloxone blockade of 8-, p- к-opiate receptors abolished these effects of stress. It has been suggested that abolishment of the promoting effect of rotational stress on the count of AFC and on the depression of DTH may be associated with the blockade of effects of ^-endorphin and met-enkephalin that act predominantly via stimulation of 8-receptors.

scholarly journals Neurohormones regulate T cell function.

1990 ◽  
Vol 171 (5) ◽  
pp. 1625-1633 ◽  
Author(s):  
W Heagy ◽  
M Laurance ◽  
E Cohen ◽  
R Finberg
Keyword(s):  
T Cell ◽  
Cell Function ◽  
Human Peripheral Blood ◽  
Opiate Receptors ◽  
Direct Interaction ◽  
Opiate Receptor ◽  
Endogenous Opioids ◽  
Terminal Sequence ◽  
Enkephalin Analogues ◽  
Cell Chemotaxis

In this communication we show that T cell locomotion is affected by direct interaction with neurohormones. Opioid peptides, including beta-END, MET-ENK, LEU-ENK, and related enkephalin analogues enhanced migration of human peripheral blood T lymphocytes. Activity was dependent on the peptide NH2-terminal sequence, stimulated by enkephalin analogues with specificity for classical delta or mu types of opiate receptor, and inhibited by the opiate receptor antagonist naloxone. Our studies suggest that such neuropeptides stimulate T cell chemotaxis by interaction with sites analogues to classical opiate receptors. We propose that the endogenous opioids beta-END, MET-ENK, and LEU-ENK are potent immunomodulating signals that regulate the trafficking of immune response cells.

Growth hormone, prolactin and cortisol nyctohemeral variations during naloxone-induced opiate receptor blockade in man

1982 ◽  
Vol 100 (3) ◽  
pp. 321-326 ◽  
Author(s):  
G. Delitala ◽  
M. Giusti ◽  
G. Rodriguez ◽  
G. Mazzocchi ◽  
S. Ferrini ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Bolus Injection ◽  
Opiate Receptors ◽  
Opiate Receptor ◽  
Normal Male ◽  
Opiate Antagonist ◽  
Endogenous Opioid Peptides ◽  
Endogenous Opioid ◽  
Blood Specimens

Abstract. To evaluate the role of endogenous opioid peptides in prolactin (Prl), growth hormone (GH) and cortisol neuroregulation, 50 mg of the opiate antagonist naloxone was infused over 24 h to 6 normal male volunteers. An additional naloxone dose (5 mg) was given iv as a bolus injection at 20.00 h. Blood specimens were collected hourly by means of a portable constant withdrawal pump. Naloxone failed to alter 24 h secretion of GH and Prl. The sleep-related GH and Prl rise was also unaffected by the opiate blocker. Moreover, naloxone failed to alter the circadian rhythm of cortisol and its 24 h concentration. The results do not suggest a major role of opiate receptors in spontaneous GH, Prl and cortisol secretion in man.

Interactions between the Endothelium-Derived Relaxing Factor/Nitric Oxide System and the Endogenous Opiate System in the Modulation of Cerebral and Spinal Vascular CO2 Responsiveness

2001 ◽  
Vol 21 (8) ◽  
pp. 937-944 ◽  
Author(s):  
Katalin Komjáti ◽  
Joel H. Greenberg ◽  
Martin Reivich ◽  
Peter Sándor
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Opiate Receptors ◽  
Opiate Receptor ◽  
Oxide System ◽  
Receptor Blockade ◽  
Relaxing Factor ◽  
Endogenous Opiate ◽  
Endothelium Derived Relaxing Factor

The role of the L-arginine-nitric oxide (NO) system, the role of the endogenous morphine-like substances (endorphins), and the possible interaction between these two systems in the modulation of regional cerebral and spinal CO2 responsiveness was investigated in anesthetized, ventilated, normotensive, normoxic cats. Regional cerebral blood flow was measured with radiolabeled microspheres in hypocapnic, normocapnic, and hypercapnic conditions in nine individual cerebral and spinal cord regions. General opiate receptor blockade by 1 mg/kg naloxone intravenously alone or NO synthase blockade by 3 mg/kg Nω-nitro-L-arginine-methyl ester (L-NAME) intravenously alone caused no changes in regional CO2 responsiveness. Combined administration of these two blocking agents in the very same doses, however, resulted in a strong potentiation, with a statistically significant reduction of the CO2 responsiveness observed. Separation of the blood flow response to hypercapnia and hypocapnia indicates that this reduction occurs only during hypercapnia. Specific μ and δ opiate receptors were blocked by 0.5 mg kg−1 IV β-funaltrexamine and 0.4 mg kg−1 IV naltrindole, respectively. The role of specific μ and δ opiate receptors in the NO–opiate interaction was found to be negligible because neither μ nor δ receptor blockade along with simultaneous NO blockade were able to decrease CO2 responsiveness. The current findings suggest a previously unknown interaction between the endothelium-derived relaxing factor/nitric oxide (EDRF/NO) system and the endogenous opiate system in the cerebrovascular bed during hypercapnic stimulation, with the phenomenon not mediated by μ or δ opiate receptors.

scholarly journals Opiate Receptors: An Introduction

1987 ◽  
Vol 15 (1) ◽  
pp. 27-37 ◽  
Author(s):  
J. J. Carmody
Keyword(s):  
Second Messengers ◽  
Opiate Receptors ◽  
Endogenous Opioids ◽  
Current Status ◽  
Anatomical Distribution ◽  
Functional Roles ◽  
Receptor Interactions ◽  
Main Target ◽  
Drug Receptor

Current status of opiate receptors and their agonists is reviewed — basic aspects of receptor theory, the importance of stereospecificity in drug-receptor interactions and the role of ‘second messengers’ in drug action. The three classes of endogenous opioids, originating from three distinct genes, are discussed: pro-opiomelanocortin, giving rise to β-endorphin, ACTH and various MSHs; pro-enkephalin, giving methionine enkephalin and leucine enkephalin; and prodynorphin; their anatomical distribution and the main classes of receptors with which they interact, the μ-receptor, with a high affinity for met-enkephalin and β-endorphin (as well as morphine and dynorphin A); the δ-receptor for which the primary ligand is leu-enkephalin; and the χ-receptor which is the main target for the dynorphins. Functional roles for endogenous opioids are considered. Essentially they are inhibitory to target neurones, depressing motor reflexes, baroreflexes and nociception. They also have roles in the response to physical and psychological stress.

Thymus peptides interacting with opiate receptors

1985 ◽  
Vol 110 (2) ◽  
pp. 284-288 ◽  
Author(s):  
Andrey A. Zozulya ◽  
Sergey Ph. Pschenichkin ◽  
Mikhail R. Shchurin ◽  
Jury N. Khomjakov ◽  
Ivan A. Besvershenko
Keyword(s):  
Membrane Fraction ◽  
Opiate Receptors ◽  
Opiate Receptor ◽  
Radioreceptor Assay ◽  
Endocrine Function ◽  
Receptor Ligands ◽  
Brain Membrane ◽  
Partial Agonists ◽  
Treatment Data

Abstract. The substances displacing labelled ligands from opiate receptors of the rat brain membrane fraction were found in the thymosin fraction 3 and acetoacid extract of the thymus by the radioreceptor assay. Comparison of the displacing activity of acetoacid extracts of perfused and non-perfused thymus and peripheral blood as well as an estimation of the blood content in the thymus allowed to conclude that blood does not participate in the ability of thymus preparations to bind to opiate receptors. On the basis of the enzymatic treatment data one can conclude that opiate receptor ligands present in thymus preparations are of peptide nature. The value of their sodium shift suggests that those peptides are partial agonists of morphine. The possible role of opioid peptides in the thymic endocrine function is discussed.

Role of endothelium-derived nitric oxide in hemodynamic adaptations after graded renal mass reduction

1993 ◽  
Vol 264 (6) ◽  
pp. R1254-R1259 ◽  
Author(s):  
K. A. Griffin ◽  
A. K. Bidani ◽  
J. Ouyang ◽  
V. Ellis ◽  
M. Churchill ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Renal Mass ◽  
Filtration Rate ◽  
Plasma Renin ◽  
Mass Reduction ◽  
Synthesis Inhibitor ◽  
Contralateral Kidney ◽  
Before And After ◽  
Renal Vascular

The mediator(s) of the adaptive increases in renal blood flow (RBF) and glomerular filtration rate (GFR) after renal mass reduction have not been identified. The present studies were designed to investigate the role of endothelium-derived nitric oxide (EDNO) in the hemodynamic adaptations after graded renal mass reduction. The experiments were performed in rats that had undergone a sham reduction in renal mass, uninephrectomy (UNX), or 5/6 NX (UNX plus excision of both poles of the contralateral kidney) 3-4 wk before. Measurements of RBF, GFR, renal vascular resistance (RVR), mean arterial pressure (MAP), and plasma renin concentration (PRC) were obtained before and after administration of the EDNO synthesis inhibitor NG-monomethyl-L-arginine (L-NMMA). L-NMMA (50 mg/kg bolus plus 500 micrograms.kg-1.min-1 infusion) led to significant (P < 0.01) and comparable increases in MAP (mmHg) (P < 0.01) in sham rats (117 +/- 6 to 154 +/- 6), UNX rats (112 +/- 5 to 139 +/- 7), and 5/6 NX rats (116 +/- 5 to 149 +/- 7). RVR increased significantly in all three groups (P < 0.01). The resultant decrease in RBF (ml.min-1.kg-1) was similar in sham rats (34.9 +/- 2.6 to 23.8 +/- 1.6), UNX rats (43.9 +/- 3.6 to 27.3 +/- 2.8), and 5/6 NX rats (34.6 +/- 2 to 22.3 +/- 1.6) (P < 0.01 for all groups).(ABSTRACT TRUNCATED AT 250 WORDS)

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