Influence of opioid peptides on release from vasopressin and oxytocin neurones of the hypothalamoneurohypophyseal system: effects of naloxone in the conscious rat

1990 ◽  
Vol 68 (5) ◽  
pp. 568-574 ◽  
Author(s):  
Savio W. T. Cheng ◽  
Edward F. O'Connor ◽  
William G. North
Keyword(s):  
Plasma Concentration ◽  
Opioid Peptides ◽  
Plasma Concentrations ◽  
Plasma Osmolality ◽  
Plasma Sodium ◽  
Endogenous Opioid ◽  
Salt Loading ◽  
Conscious Rats ◽  
Basal Plasma ◽  
Acute And Chronic Treatments

We examined the effects of acute and chronic treatments with naloxone on release of vasopressin and oxytocin from the hypothalamoneurohypophyseal system (HNS) in conscious, chronically instrumented Long–Evans rats. Plasma concentrations of vasopressin-associated neurophysin and oxytocin-associated neurophysin were evaluated before and during an intravenous infusion of 18% saline at 100 μL∙kg−1 body weight∙min−1 for 60 min. Acute treatment with naloxone (2.75 μmol/kg, intravenous) did not measurably alter basal plasma osmolality or vasopressin-associated neurophysin concentration, but it caused a three-fold rise in basal plasma oxytocin-associated neurophysin concentration (16 ± 2 to 46 ± 3 fmol/mL, p < 0.005). Chronic treatment with naloxone (13.75 μmol/day, subcutaneous pellets) increased plasma osmolality (292 ± 1 to 300 ± 2 mosmol/kg H2O, p < 0.01) by day 5, but it had no measurable effects on basal vasopressin- or oxytocin-associated neurophysin concentration. There were also no significant differences in plasma sodium concentration (144.8 ± 1.1 vs. 142.2 ± 1.4 mequiv./L) under both conditions. Acute and chronic treatments with naloxone accompanied by salt loading produced a five- and four-fold decrease in the rates that plasma concentration of vasopressin-associated neurophysin changed with plasma osmolality, compared with untreated salt-loaded control rats. For oxytocin secretion from the HNS, both treatments accompanied by salt loading substantially decreased the threshold for changes in relation to plasma osmolality; the rise in plasma concentration of oxytocin-associated neurophysin was similar at all levels of hyperosmotic stimulation. A strongly correlated relationship between plasma oxytocin-associated neurophysin and plasma osmolality (r = 0.739) found for control animals became poorly correlated following treatments (acute, r = 0.173; chronic, r = −0.079). Our results suggest that in conscious rats, endogenous opioid peptides enhance the secretion of vasopressin from neurones of the HNS in response to hyperosmotic stimulation but inhibit both basal and stimulated release of oxytocin.Key words: naloxone, vasopressin, oxytocin, neurophysin, conscious rats.

Tolerance and osmotic response to food deprivation and salt loading in the herbivorous non-drinking Moroccan Spiny-tailed lizard Uromastyx nigriventris (Sauria: Agamidae)

2021 ◽  
pp. 1-15
Author(s):  
Bendami Safaa ◽  
Znari Mohammed
Keyword(s):  
Water Deprivation ◽  
Plasma Osmolality ◽  
Condition Index ◽  
Plasma Sodium ◽  
Arid Environments ◽  
Salt Glands ◽  
Salt Loading ◽  
High K ◽  
Short Period ◽  
Herbivorous Species

Abstract Animals inhabiting arid environments use a variety of behavioural and physiological strategies to balance their water and salt budgets. We studied the effects of dehydration and salt loading on osmoregulatory capacities in a large herbivorous desert lizard, the Moroccan Spiny-tailed lizard Uromastyx nigriventris, the family Agamidae. These lizards select plants with a high K+ to Na+ ratio of 15 to 20, and like other herbivorous lizards, effectively eliminate the extra electrolyte load, mainly via a pair of active nasal salt glands, which exude the extra ions from blood. Here we present results of a series of laboratory experiments, which tested a five-week food and water deprivation and the excretory response of nasal salt glands, during a short period of five days, following salt loading by two separated injections of KCl or NaCl at a 5-day interval (4th and 9th days). During food-water deprivation, hypohydrated lizards lost 32% of their initial body mass with a substantial decrease of their Body Condition Index and the tail volume as an index of energy (fat and then potential metabolic water) storage. Plasma osmolality significantly increased by 20%. There were also significantly increased plasma sodium, chloride, and total protein concentrations. On the other hand, there was no significant decrease in the plasma glucose level. Most of the salt loaded lizards secreted far more K+ than Na+ via the nasal glands, even after NaCl loading. The K+/Na+ ratio decreased only after two to three repetitive NaCl injections but insufficient Na+ was eliminated. Two successive KCl injections were successfully eliminated, but daily natural average K+ administration induced progressive hyperkaliemia. These experimental data agreed with previous observations showing variations of plasma Na+ and K+ concentrations in free-living lizards. The nasal gland constitutes the main route of Cl− excretion but the Cl−/(Na+ + K+) ratio may vary according to observations in other herbivorous species.

Absence of negative feedback by oxytocin on release from magnocellular neurones in conscious rats

1992 ◽  
Vol 70 (1) ◽  
pp. 100-105 ◽  
Author(s):  
Savio W. T. Cheng ◽  
William G. North
Keyword(s):  
Negative Feedback ◽  
Plasma Concentrations ◽  
Plasma Osmolality ◽  
High Plasma ◽  
High Dose ◽  
Salt Loading ◽  
Significant Difference ◽  
And Control ◽  
The Relationship ◽  
Oxytocin Neurones

Peripheral administration of vasopressin (VP) was previously shown to exert a negative feedback influence on its own release and on the release of oxytocin (OT). In this study we examined the possible influence that OT has on the function of hypothalamic magnocellular neurones. Oxytocin was administered intraperitoneally and its effects on release from VP neurones and from OT neurones were determined as indexed by plasma concentrations of vasopressin-associated neurophysin ([VP-RNP]) and oxytocin-associated neurophysin ([OT-RNP]) under basal conditions and conditions of high plasma osmolality (Posm) induced by acute salt loading. Studies were performed on conscious, chronically instrumented Long-Evans rats. Oxytocin (1 nmol or 10 nmol) dissolved in 1 mL of 0.9% saline was administered intraperitoneally to animals 1 h before they received an intravenous infusion of hypertonic saline over 60 min at a rate designed to raise Posm by approximately 0.75 mosmol∙min−1. Intraperitoneal injection of vehicle or 1 nmol of OT did not significantly alter [VP-RNP], [OT-RNP], or basal Posm. Administration of 10 nmol OT also had no effect on [VP-RNP] or [OT-RNP], but this dose of peptide significantly lowered basal Posm (299 ± 2 to 290 ± 2 mosmol/kg H2O, p < 0.001). Both doses of OT did not significantly alter the responsiveness of VP neurones to hyperosmotic stimulation. The slopes of the relationship between the rise in [VP-RNP] (A[VP-RNP]) and the rise in Posm (ΔPosm) for the groups receiving pretreatment of 1 nmol OT (n = 5), 10 nmol OT (n = 7), and vehicle (n = 7) were similar (6.1 ± 1.4, r = 0.86; 5.1 ± 0.9, r = 0.91; and 6.6 ± 0.9 fmol∙mL−1∙mosmol−1∙kg−1, r = 0.93, respectively). For the 1-nmol dose of OT that generated plasma OT levels in the physiological range, the slopes of the relationship between the rise in [OT-RNP] (Δ[OT-RNP]) and ΔPosm over the period of salt loading for peptide-treated animals and control animals (39.5 ± 8.9, r = 0.89 vs. 23.4 ± 5.9, fmol∙mL−1∙mosmol−1∙kg−1, r = 0.93) indicated an increased responsiveness of OT neurones, but this difference was not significant (p < 0.1426). Higher plasma levels of OT were generated by administering the 10 nmol dose of OT, and the slopes of the relationship between Δ[OT-RNP] and ΔPosm for peptide-treated animals and control animals (13.9 ± 1.6, r = 0.96 vs. 23.4 ± 8.9 fmol∙mL−1∙mosmol−1∙kg−1, r = 0.93) suggested a decreased responsiveness of OT neurones, but again this difference was not significant (p < 0.1637). However, there was a significant difference in the rise in OT-RNP with plasma osmolality for rats receiving high versus low dose of peptide (p < 0.0475). Our data indicate that peripherally administered OT, unlike VP, does not exert a negative feedback influence on osmotically stimulated release from VP neurones and most probably OT neurones. However, it cannot be ruled out that the lack of modulation of magnocellular neurones by the high dose of OT could be due to the summation of a positive OT effect (since the 1-nmol group appeared to exhibit an enhancing effect) and of a negative VP effect as indicated by blood pressure increases and plasma dilution. OT also does not appear to have an influence on basal release from magnocellular neurones.Key words: neurophysins, oxytocin neurones, vasopressin neurones.

Changes in the hypothalamic contents of LHRH-I and -II and in pituitary responsiveness to synthetic chicken LHRH-I and -II during the progesterone-induced surge of LH in the laying hen

1990 ◽  
Vol 127 (3) ◽  
pp. 487-496 ◽  
Author(s):  
S. C. Wilson ◽  
R. A. Chairil ◽  
F. J. Cunningham ◽  
R. T. Gladwell
Keyword(s):  
Plasma Concentration ◽  
Pituitary Gland ◽  
Laying Hens ◽  
Plasma Concentrations ◽  
Posterior Hypothalamus ◽  
Anterior Hypothalamus ◽  
Significant Fall ◽  
Basal Plasma

ABSTRACT The contents of LHRH-I and -II in the anterior hypothalamus and posterior hypothalamus (including the mediobasal hypothalamus and median eminence) were measured at 90, 180 and 360 min after the i.m. injection of laying hens with progesterone. Whilst no changes were observed in the content of LHRH-I in the anterior hypothalamus, LHRH-I in the posterior hypothalamus tended to fall at 90 and 180 min after injection of progesterone in hens maintained on 16 h light:8 h darkness (16L:8D) and 8L:16D respectively. Pretreatment of laying hens with tamoxifen significantly increased the hypothalamic contents of LHRH-I and -II, raised the basal plasma concentration of LH and modified the LH response to progesterone injection. In hens in which tamoxifen prevented an increase in the plasma concentration of LH after progesterone injection, the content of LHRH-I in the posterior hypothalamus remained unchanged. In contrast, in hens in which progesterone stimulated a steep increase in LH within 90 min, there was a pronounced and significant fall in LHRH-I content of the posterior hypothalamus. No change in the hypothalamic content of LHRH-II was observed during the progesterone-induced surge of LH until plasma concentrations had attained maximal values or started to decline. Then, in hens maintained on 16L:8D, a significant fall in the content of LHRH-II in the anterior hypothalamus was found at both 180 and 360 min after injection with progesterone. Tests in vitro and in vivo of the responsiveness of the pituitary gland to synthetic LHRH-I and -II revealed no change at 90 min after injection of laying hens with progesterone, when plasma concentrations of LH were increasing, but a pronounced reduction when plasma LH concentrations were maximal or falling. These results suggest that LHRH-I mediates in the progesterone-induced increase in the plasma concentration of LH. Although the subsequent decline in plasma LH was associated with a reduced responsiveness of the pituitary gland to LHRH, a significant correlation between the contents of LHRH-I and -II in the anterior hypothalamus and a fall in the hypothalamic content of LHRH-II when plasma LH was maximal or declining allows the possibility of an involvement of this peptide in the neuroendocrine events preceding ovulation. Journal of Endocrinology (1990) 127, 487–496

Plasma vasopressin response to peripheral administration of angiotensin in conscious rats

1985 ◽  
Vol 248 (2) ◽  
pp. R249-R256 ◽  
Author(s):  
K. Yamaguchi ◽  
M. Koike ◽  
H. Hama
Keyword(s):  
Angiotensin Ii ◽  
Isotonic Saline ◽  
Plasma Osmolality ◽  
Plasma Sodium ◽  
Ang Ii ◽  
Mannitol Solution ◽  
Injection Volume ◽  
Conscious Rats ◽  
Plasma Vasopressin ◽  
Series Of Experiments

To assess a role for peripherally administered angiotensin II (ANG II) in regulating vasopressin (antidiuretic hormone, ADH) release, the effects on plasma ANG II and ADH of intraperitoneal injections of ANG II dissolved in various solutions were examined in conscious rats. Plasma ANG II and ADH were determined by radioimmunoassay using the trunk blood collected after decapitation. Injections of 150 mM NaCl containing ANG II (6, 12, or 24 micrograms X 2 ml-1 X 100 g body wt-1) caused dose-related increases in plasma ANG II 15 and 30 min after, but plasma ADH remained unchanged. The lack of effect on plasma ADH of the ANG II dissolved in isotonic saline was also confirmed in another series of experiments in which the solution with a higher ANG II concentration was loaded by much smaller injection volume (14.3 micrograms X 0.1 ml-1 X 100 g-1). However, when given together with 600 mM NaCl, ANG II (8 micrograms X 2 ml-1 X 100 g-1) significantly potentiated the plasma ADH response to the vehicle at 15, 30, and 60 min, without affecting those of plasma osmolality, sodium, and hematocrit. The elevations of plasma ANG II and osmolality brought about by the treatment were comparable with those previously observed in rats deprived of water for 46 h. ANG II was without effect on the plasma ADH responses to the intraperitoneal injections of hypertonic sucrose or mannitol solution that did not alter plasma sodium, although these solutions were equipotent to 600 mM NaCl in augmenting plasma ADH and osmolality.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Distinguishing Low and High Water Consumers—A Paradigm of Disease Risk

Nutrients ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 858 ◽  
Author(s):  
Lawrence E. Armstrong ◽  
Colleen X. Muñoz ◽  
Elizabeth M. Armstrong
Keyword(s):  
Disease Risk ◽  
Plasma Concentrations ◽  
Urine Volume ◽  
Plasma Osmolality ◽  
High Volume ◽  
High Water ◽  
Plasma Sodium ◽  
Reference Ranges ◽  
Dietary Recommendations ◽  
Tract Infections

A long-standing body of clinical observations associates low 24-h total water intake (TWI = water + beverages + food moisture) with acute renal disorders such as kidney stones and urinary tract infections. These findings prompted observational studies and experimental interventions comparing habitual low volume (LOW) and high volume (HIGH) drinkers. Investigators have learned that the TWI of LOW and HIGH differ by 1–2 L·d−1, their hematological values (e.g., plasma osmolality, plasma sodium) are similar and lie within the laboratory reference ranges of healthy adults and both groups appear to successfully maintain water-electrolyte homeostasis. However, LOW differs from HIGH in urinary biomarkers (e.g., reduced urine volume and increased osmolality or specific gravity), as well as higher plasma concentrations of arginine vasopressin (AVP) and cortisol. Further, evidence suggests that both a low daily TWI and/or elevated plasma AVP influence the development and progression of metabolic syndrome, diabetes, obesity, chronic kidney disease, hypertension and cardiovascular disease. Based on these studies, we propose a theory of increased disease risk in LOW that involves chronic release of fluid-electrolyte (i.e., AVP) and stress (i.e., cortisol) hormones. This narrative review describes small but important differences between LOW and HIGH, advises future investigations and provides practical dietary recommendations for LOW that are intended to decrease their risk of chronic diseases.

Relationship between oxytocin release and amplitude of oxytocin cell neurosecretory bursts during suckling in the rat

1987 ◽  
Vol 114 (2) ◽  
pp. 263-270 ◽  
Author(s):  
C. Meyer ◽  
M. J. Freund-Mercier ◽  
Y. Guerné ◽  
Ph. Richard
Keyword(s):  
Plasma Concentration ◽  
Direct Relationship ◽  
Plasma Concentrations ◽  
Pulsatile Release ◽  
Oxytocin Release ◽  
Anaesthetized Rats ◽  
Basal Plasma ◽  
Cell Firing ◽  
Basal Concentration

ABSTRACT Plasma concentrations of oxytocin and vasopressin were measured in relationship to oxytocin cell firing during suckling in urethane-anaesthetized rats. Preliminary experiments showed that plasma concentrations of oxytocin and vasopressin, which were increased immediately after anaesthesia, reverted to basal concentrations 3 h later. Moreover, it was found that exogenous oxytocin had entirely disappeared 5 min after i.v. bolus injections of known doses of oxytocin. Suckling did not modify the basal plasma concentration of oxytocin (14·6 ± 2·9 compared with 14·±61·5 pmol/l before suckling) except during a brief period immediately after neurosecretory bursts on oxytocin cells (37·8 ± 5·2 pmol/l; P < 0·001, n = 11). The plasma concentration of oxytocin did not differ significantly from the basal concentration 1·5 min later. The plasma concentration of vasopressin never varied. After two neurosecretory bursts of similar amplitude (total number of spikes during the burst) recorded on the same oxytocin cell, the variations in plasma concentration of oxytocin were also similar. When, for a given cell, the amplitude of neurosecretory bursts increased or decreased, the amount of oxytocin released changed in the same way. These data demonstrate (1) that suckling induces pulsatile release of oxytocin without vasopressin, and (2) a direct relationship between the amounts of oxytocin released and the amplitude of oxytocin cell neurosecretory bursts which argue in favour of simultaneous increases or decreases in the neurosecretory burst amplitudes on all oxytocin cells. J. Endocr. (1987) 114, 263–270

κ-Opioid modulation of vasopressin secretion in conscious rats

1991 ◽  
Vol 129 (3) ◽  
pp. 411-416 ◽  
Author(s):  
T. Wells ◽  
M. L. Forsling
Keyword(s):  
Plasma Concentration ◽  
Receptor Agonist ◽  
Plasma Concentrations ◽  
Endogenous Opioids ◽  
Inhibitory Influence ◽  
Conscious Rat ◽  
Opioid Receptor Agonist ◽  
Basal Plasma ◽  
Vasopressin Secretion ◽  
Prior Administration

ABSTRACT A series of studies has been performed in the conscious rat to investigate the effect of the intracerebroventricular (i.c.v.) administration of the selective κ-opioid receptor agonist, U50 488H, on arginine vasopressin (AVP) secretion stimulated by i.c.v. administration of hypertonic NaCl. Similarly, the effect of the i.c.v. administration of morphine and the i.v. administration of naloxone on AVP secretion was investigated. The response of AVP to an i.c.v. injection of hypertonic NaCl was potentiated by naloxone at a dose of 0·4 mg/kg, but a higher dose (1·2 mg/kg) was required to increase the basal plasma concentration of AVP. Prior treatment with U50 488H or morphine attenuated the increase in plasma concentrations of AVP stimulated by i.c.v. injection of hypertonic NaCl from 13·92±4·44 to 1·22±0·34 and 1·78±0·74 pmol/l respectively (n = 7; P<0·05). Prior administration of U50 488H also attenuated the potentiating effect of naloxone on AVP secretion stimulated by i.c.v. injection of hypertonic NaCl. These results indicate that basal AVP secretion is under tonic inhibitory control by dynorphin, and that μ-and κ-opioid receptors mediate an inhibitory influence of endogenous opioids on osmoreceptor-mediated AVP secretion. Journal of Endocrinology (1991) 129, 411–416

Function of vasopressinergic neurons in rats under conscious and anesthetized conditions

1985 ◽  
Vol 248 (2) ◽  
pp. E155-E161
Author(s):  
S. W. Cheng ◽  
W. G. North
Keyword(s):  
Plasma Osmolality ◽  
Sodium Concentration ◽  
Conscious State ◽  
Plasma Sodium ◽  
Salt Loading ◽  
Pentobarbital Sodium ◽  
Plasma Sodium Concentration ◽  
Rate Of Increase ◽  
The Relationship ◽  
Vasopressinergic Neurons

The responses of vasopressinergic neurons to acute salt loading and to graded hemorrhage were studied in rats under conscious and anesthetized conditions. Chronically cannulated rats were used in this study so that pre- and postanesthetic conditions could be studied in the same animals. Anesthesia induced by a combination of ketamine hydrochloride and pentobarbital sodium (Nembutal) did not cause a release of vasopressin-associated neurophysin (VP-RNP). In response to infusion of 18% saline, animals in the anesthetized state had significantly greater increases in plasma osmolality (Posmol) and plasma sodium concentration than animals in the conscious state. However, the rate of increase in plasma VP-RNP concentration ([VP-RNP]) as well as the relationship between [VP-RNP] and Posmol were not significantly different for the two states. Graded hemorrhage caused similar rates of increase in [VP-RNP] for animals under conscious and anesthetized conditions. These data suggest that anesthesia induced by ketamine plus pentobarbital sodium does not change the responsiveness of vasopressinergic neurons to acute salt loading and to graded hemorrhage.

Inhibitory effects of corticotrophin-releasing factor and β-endorphin on LH and FSH secretion in the lactating rat

1989 ◽  
Vol 120 (3) ◽  
pp. 509-515 ◽  
Author(s):  
K. Taya ◽  
S. Sasamoto
Keyword(s):  
Plasma Concentration ◽  
Opioid Peptides ◽  
Plasma Levels ◽  
Plasma Concentrations ◽  
Rapid Decrease ◽  
Significant Decline ◽  
Plasma Prolactin ◽  
Inhibitory Effects ◽  
Corticotrophin Releasing Factor ◽  
Significant Change

ABSTRACT The roles of corticotrophin-releasing factor (CRF) and β-endorphin in the suppression of LH and FSH secretion during lactation were investigated using ovariectomized lactating rats separated from their litters overnight. Within 1 h of returning the pups to their mothers a marked fall in plasma LH concentration and a large increase in plasma prolactin were noted. However, resuckling caused no significant change in plasma concentration of FSH until 12 h after the return of the litter but a significant decline occurred thereafter. Twenty-four hours after removal of the litter, a single i.v. injection of 200 μl anti-LHRH serum caused similar changes in plasma concentrations of LH and FSH observed in nursing rats during suckling. These results suggest that the suckling stimulus itself is responsible for the suppression of LH as well as FSH, via inhibition of the secretion of LHRH. Twenty-four hours after removal of the litter, a single intracerebroventricular (i.c.v.) injection of either 10 μg CRF or β-endorphin resulted in a rapid decrease in plasma LH. Only β-endorphin caused a marked increase in plasma levels of prolactin within 1 h whereas FSH was less affected by either hormone. Repeated i.c.v. administration of 10 μg CRF or β-endorphin at 6-h intervals caused a prolonged inhibition of LH as well as FSH secretion during 48 h, with β-endorphin being less effective than CRF. These results demonstrate that the suckling stimulus alone suppressed the secretion of both LH and FSH, and suggest that this effect may be mediated by the inhibition of LHRH secretion from the hypothalamus. They also suggest that the suckling-induced inhibition of LHRH may be primarily mediated by endogenous CRF and opioid peptides. Journal of Endocrinology (1989) 120, 509–515

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