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Biomedical subjects

G Hertting

Publications and source records attributed to G Hertting.

At least 109 records · Page 6Linked to original sources
PubMed1984

Identification of mechanisms involved in the modulation of release of noradrenaline in the hippocampus of the rabbit in vitro.

The modulation of the electrically-evoked release of noradrenaline by various possible neurotransmitters or neuromodulators in the hippocampus was studied in the dorsal part of the hippocampus of the rabbit. Slices of this tissue were preincubated with [3H]noradrenaline and superfused with a medium containing 30 microM cocaine. The evoked overflow of tritium was calcium-dependent, tetrodotoxin-sensitive and subject to modulation by presynaptic alpha 2-autoreceptors. Drugs with affinity for beta-adrenoceptors (up to 1 microM), muscarinic (up to 10 microM), nicotinic (up to 100 microM), GABA- (up to 1000 microM), glutamate- (up to 100 microM) and prostaglandin-receptors (up to 1 microM) did not show any modulatory influence on the evoked release of noradrenaline. In contrast, morphine (1 microM) and fentanyl (1 microM) significantly reduced the evoked overflow; this effect was antagonized by naloxone (10 microM), which, given alone, was ineffective. Apomorphine (1 microM) reduced the release of noradrenaline in the absence, and increased it in the presence, of 0.1 microM haloperidol; haloperidol (0.1 microM), given alone was ineffective. From these results it is concluded that, in addition to the well-known alpha 2-autoreceptor mechanism, presynaptic opiate-, D2- and probably D1-receptors might modulate the release of noradrenaline in the hippocampus.

Animals↗
PubMed1984

Changes in cyclooxygenase activity and prostaglandin profiles during monoamine metabolism in rat brain homogenates.

The effect of different monoamine oxidase (MAO) substrates on the endogenous prostaglandin(PG) and thromboxane (TX) biosynthesis in rat brain homogenates was studied. In the absence of MAO substrates the following pattern of arachidonic acid metabolites was found: PGD2 greater than PGF2 alpha greater than TXB2 greater than PGE2 greater than or equal to 6ketoPGF1 alpha. Phenylethylamine(PEA) stimulated the cyclooxygenase activity 1.5-fold (expressed as the sum of the products formed), without altering the product profile. Tyrosine(Tyr) caused a twofold increase in cyclooxygenase activity and slightly modified the product composition (PGD2=PGF2 alpha greater than PGE2 greater than TXB2 greater than 6ketoPGF1 alpha). In the presence of noradrenaline(NA) there was a threefold stimulation of cyclooxygenase activity. The increase of PGF2 alpha was more pronounced than that of the other metabolites (PGF2 alpha greater than PGD2 greater than TXB2 greater than PGE2 greater than 6ketoPGF1 alpha). alpha-Methylnoradrenaline(alpha metNA ) (not a substrate for MAO but bearing the catechol group) altered the PG pattern in the same way as NA, but without enhancing the cyclooxygenase activity. PEA or Tyr when administered together with alpha metNA produced a NA-like effect both on the cyclooxygenase activity and on the product profile. The increase in cyclooxygenase activity was abolished by pargyline or by catalase, independently of the activator system used. The results support the hypothesis that NA-stimulation of brain PG (and TX) formation is mediated by H2O2 formed during the degradation of the amine via MAO. The role of the catechol group in protection of the cyclooxygenase against inactivation and in the changes of product composition, as well as the possible significance of the coupling between arachidonate and monoamine metabolism is discussed.

Amines↗
PubMed1984

Anticonvulsive effects of endogenous prostaglandins formed in brain of spontaneously convulsing gerbils.

Seizures were induced in a strain of epileptic gerbils by moderate environmental stress. Concentrations of five different cyclooxygenase products (PGD2, PGF2 alpha, PGE2, 6-keto-PGF1 alpha and thromboxane B2) were measured in brain by specific radioimmunoassays before and at different time intervals after the onset of clonic-tonic convulsions. All prostanoids markedly increased subsequent to the convulsions. Maximal concentrations were reached after about 15 min. The major compound detected was PGD2, followed by PGF2 alpha and lower concentrations of the other cyclooxygenase products. Indomethacin completely prevented the convulsion-induced formation of prostanoids. Fifteen min after a first seizure almost all animals proved to be protected against a second convulsion. Indomethacin pretreatment markedly reduced the number of convulsion-resistant animals. These findings are compatible with the hypothesis that endogenous prostaglandins exert anticonvulsive effects.

Animals↗
PubMed1984

The importance of endogenous prostaglandins other than prostacyclin, for the modulation of contractility of some rabbit blood vessels.

Helically cut strips of rabbit aorta, extrapulmonary artery, coeliac artery, and femoral artery were set up in organ baths. Contractions of the strips by noradrenaline and angiotensin II were recorded isotonically. The release of prostaglandins 6-keto-PGF1 alpha, E2, F2 alpha, D2 and thromboxane B2 from the strips was measured by means of sensitive and specific radioimmunoassays. All blood vessels released a characteristic pattern of cyclo-oxygenase products. Prostacyclin (PGI2, measured as 6-keto-PGF1 alpha) was the major compound formed, followed by smaller amounts of PGE2 and traces of PGF2 alpha, PGD2 and thromboxane A2 (measured as thromboxane B2). The pulmonary and the femoral artery had comparatively high abilities to synthesize PGE2. Contractions induced by noradrenaline increased prostaglandin release from the pulmonary artery but not from the other blood vessels. Angiotensin II-induced contractions were accompanied by a marked prostaglandin release from the coeliac artery. After angiotensin II, prostaglandin release was also enhanced in the pulmonary artery, but remained essentially unchanged in the aorta and femoral artery. Arachidonic acid markedly increased the levels of all prostaglandin formed. Indomethacin inhibited the formation of all prostaglandins below the detection limits of the respective radioimmunoassays. Indomethacin treatment induced a qualitatively similar shifting of the concentration-response curves of noradrenaline and angiotensin II in some vessels: the concentration-response curves remained unchanged for the aorta, were slightly shifted to the left of the pulmonary artery, were markedly shifted to the left for the coeliac artery, and were shifted to the right for the femoral artery. 7 Exogenous PGI2 strongly and concentration-dependently inhibited contractions induced by the approximate EC50 of noradrenaline in the coeliac artery, but was without effect on the other three preparations. PGE2 had no effect on noradrenaline-induced contractions of the aorta, inhibited those of the pulmonary and the coeliac artery, but markedly potentiated those of the femoral artery. PGF2 alpha significantly enhanced contractions of the femoral artery, but increased contractions of the other preparations were not significant. PGD2 was without effect on any preparation. 8 In conclusion, the contractility of the aorta does not seem to be modulated substantially by prostaglandins. The major prostanoid regulating the tone of the coeliac artery was found to be PGI2. The contractility of the pulmonary and especially the femoral artery is probably not modulated by PGI2 but rather by PGE2. 9 These observations suggest that in certain blood vessels, prostaglandins other than PGI2 are important endogenous modulators of contractility.

Angiotensin II↗
PubMed1984

Adrenocorticotropin and beta-endorphin release from rat adenohypophysis in vitro: inhibition by prostaglandin E2 formed locally in response to vasopressin and corticotropin-releasing factor.

The present study examined the involvement of prostaglandins (PGs) in the mechanisms of ACTH and beta-endorphin release from rat anterior pituitary quarters incubated in vitro. Various cyclooxygenase inhibitors (indomethacin, diclofenac, flurbiprofen) had no effect on basal release of ACTH-like or beta-endorphin-like immunoreactivity (beta-EI), but enhanced ACTH-immunoreactivity/beta-EI release upon stimulation by arginine-vasopressin (AVP) or synthetic ovine corticotropin-releasing factor [CRF-(1-41)]. The lowest effective concentration of indomethacin was just sufficient to prevent PG synthesis. Indomethacin was similarly active after blockade of the phosphodiesterase by 3-isobutyl-1-methylxanthine. When added to the incubation media in concentrations up to 1 microM, PGE2, D2, F2 alpha, or prostacyclin (PGI2) did not alter basal beta-EI release; however, with stimulation by AVP or CRF-(1-41), PGE2 but not PGD2, F2 alpha, or I2 inhibited beta-EI release by about 60%. The concentrations of PGE2 in the incubation media, as measured by RIA, were somewhat higher than those of any other cyclooxygenase product (PGD2, F2 alpha, 6-keto-PGF1 alpha, thromboxane B2). Upon stimulation by AVP or CRF-(1-41), the concentrations of PGE2 increased, whereas those of PGD2 or F2 alpha remained unchanged. The release of beta-EI stimulated by high potassium concentration was not enhanced by indomethacin, although this release was sensitive to inhibition by PGE2. We conclude that PGE2 is formed locally subsequent to binding of the neurohormones and may act as a negative feedback-modulator of vasopressin's and CRF-(1-41)'s activity in the anterior pituitary gland.

1-Methyl-3-isobutylxanthine↗
PubMed1983

Effect of neonatal treatment with monosodium glutamate on vasopressin release during foot shock stress in the rat.

Several lines of evidence indicate that beta-endorphin inhibits the release of vasopressin during foot shock-induced stress in the rat. This study was to evaluate the relative importance of the hypothalamic versus the pituitary pool of beta-endorphin. Neonatal treatment with monosodium glutamate (MSG) reduced drastically the content of beta-endorphin-like immunoreactivity (beta-EI) of hypothalamus but not the beta-EI concentration in the pituitary; the content of vasopressin in the hypothalamus and the pituitary was not altered by MSG treatment. MSG treatment had no effect on the plasma vasopressin response to inescapable electric foot shock stress, when compared to controls. Naloxone enhanced vasopressin release during stress both in MSG-treated rats and in controls. These results suggest that hypothalamic beta-endorphin is not involved in the control of vasopressin release during foot shock-induced stress in the rat.

Animals↗
PubMed1983

Effects of intracerebroventricular administration of prostaglandin D2 on behaviour, blood pressure and body temperature as compared to prostaglandins E2 and F2 alpha.

The present work examined some central nervous actions of prostaglandin D2 (PGD2), which is the most prevalent prostaglandin in rodent brain. The effects of PGD2 were compared with those of PGE2 and PGF2 alpha. The prostaglandins were administered intracerebroventricularly (ICV) to conscious rats using the method of Herman (1970). All three prostaglandins studied produced depressive behavioral effects, causing obvious sedation at doses of 2.0 micrograms and 20.0 micrograms ICV. PGD2 and PGE2 significantly reduced spontaneous motor activity at doses of 2.0 micrograms and 20.0 micrograms ICV. PGF2 alpha was less effective; only 20.0 micrograms significantly inhibited motor activity. At a dose of 20.0 micrograms ICV all three compounds were shown to block convulsions induced by pentylenetetrazol. PGD2, the most effective prostaglandin in this respect, was still slightly anticonvulsive at a dose of 2.0 micrograms ICV. PGF2 alpha hat the weakest anticonvulsive potency. PGE2 and PGF2 alpha (2.0 micrograms and 20.0 micrograms ICV) caused a marked hypertensive effect, whereas PGD2 at the same dose levels only produced a small increase in blood pressure. PGE2 and PGF2 alpha (2.0 micrograms and 20.0 micrograms) also exerted marked pyrogenic actions. The effects of PGD2 on body temperature were variable. When given at a dose of 20.0 micrograms ICV, it caused slight hyperthermia whereas a lower dose (2.0 micrograms ICV) induced a moderate fall in body temperature. These findings suggest a relationship between the actions of the different prostaglandins on blood pressure and body temperature.

Animals↗
PubMed1983

Increase in brain prostaglandins during convulsions is due to increased neuronal activity and not to hypoxia.

The levels of prostaglandin D2 (PGD2) and prostaglandin F2 alpha (PGF2 alpha), being the major prostaglandins formed in mouse brain in vivo were determined using a radioimmunological technique. Under basal conditions, they were less than 8.49 ng/g for PGD2 and less than 3.76 ng/g for PGF2 alpha. During seizures, induced by the centrally acting convulsant pentylenetetrazol, cerebral concentrations of both prostaglandins were markedly enhanced as compared to basal conditions. The seizure evoked increase in brain prostaglandins could be attributed to the enhanced neuronal activity. If convulsions were induced with the spinal cord convulsant strychnine no increase in brain prostaglandins was seen although the occurring hypoxia was probably very similar. Therefore, hypoxia does not seem to play a significant role in the prostaglandin increase. The effect of pentylenetetrazol on cerebral prostaglandins was independent of the mechanical convulsions induced by the drug. Muscle relaxed mice showed the same increase in cerebral prostaglandins as convulsing mice. Muscle relaxation alone had no influence on prostaglandin formation in brain. These data indicate that the increased neuronal activity induced by centrally acting convulsants is likely to be the sole cause for the rise in cerebral prostaglandins. Brain hypoxia, another known stimulus of prostaglandin synthesis, does not seem to play an important role during convulsions.

Animals↗
PubMed1982

Metabolism of 6-ketoprostaglandin F1 alpha and prostacyclin to 6,15-diketo-13,14-dihydroprostaglandin F1 alpha-like material in cats and rabbits.

Using previously described radioimmunoassays for 6-ketoprostaglandin F1 alpha and 6,15-diketo-13,14-dihydroprostaglandin F1 alpha, plasma levels of these two products of degradation of prostacyclin (prostaglandin I2) were monitored in cats and rabbits. It was shown that both exogenous prostaglandin I2 and 6-ketoprostaglandin F1 alpha could be rapidly converted to 6,15-diketo-13,14-dihydroprostaglandin F1 alpha immunoreactivity, 6-ketoprostaglandin F1 alpha to an even somewhat larger extent. This difference in conversion could be explained by competing mechanisms which could delay or hinder the access of prostaglandin I2 to the sites of metabolism by 15-hydroxyprostaglandin dehydrogenase. The 6-ketoprostaglandin F1 alpha and 6,15-diketo-13,14-dihydroprostaglandin F1 alpha immunoreactivities were further characterized in two different thin-layer chromatographic systems and were shown to co-chromatograph exclusively with their respective standards. Similar results were obtained when tritium-labeled prostaglandin I2 or 6-ketoprostaglandin F1 alpha were infused into cats. Extracts of plasma samples taken at different time intervals after the infusion were submitted to thin-layer chromatography. The radioscans of the chromatograms showed two consistent peaks, one co-chromatographing with authentic 6-ketoprostaglandin F1 alpha and the other one with 6,15-diketo-13,14-dihydroprostaglandin F1 alpha. After infusion of 6-ketoprostaglandin F1 alpha the conversion to the 6,15-diketo-13,14-dihydro-prostaglandin F1 alpha-like product occurred somewhat faster than after infusion of prostaglandin I2. We conclude that, under in vivo conditions in the two species investigated, 6-ketoprostaglandin F1 alpha can be rapidly and effectively metabolized by 15-hydroxyprostaglandin dehydrogenase.

6-Ketoprostaglandin F1 alpha↗
PubMed1982

Role of vasopressin in the ACTH response to isoprenaline.

The present study investigated whether or not the beta-sympathomimetic amine isoprenaline, given systemically to conscious rats, influences corticotrophin (ACTH) release and if so, what could be the role of vasopressin in this response. Isoprenaline (i.m.) elevated plasma ACTH-like immunoreactivity (ACTHi) in a time- and dose-dependent manner. The highest dose of isoprenaline used (240 microgram/kg) raised plasma ACTHi about six fold. Most of the ACTHi co-migrated with porcine ACTH-(1-39) on Sephadex G-50 column chromatography. The beta-receptor antagonist propranolol abolished the increase in plasma ACTHi induced by isoprenaline, as did dexamethasone pretreatment. The increase in plasma ACTHi following isoprenaline (120 microgram/kg) injection was diminished by about 35% in rats congenitally lacking vasopressin (Brattleboro rats), when compared to normal rats. The vasopressin analogue, [1-deaminopenicillamine, 2-(O-methyl)tyrosine]-arginine-vasopressin, almost completely prevented the rise in plasma ACTHi provoked by i.v. injection of arginine vasopressin and diminished by about 40% the isoprenaline-(120 microgram/kg)-caused ACTHi release. However, this vasopressin analogue had no effect in Brattleboro rats. These results indicate that isoprenaline, given systemically, stimulates the release of pituitary ACTH and this response appears to be mediated in part by vasopressin acting as an ACTH-releasing factor.

Adrenocorticotropic Hormone↗
PubMed1982

Potential anticonvulsive properties of endogenous prostaglandins formed in mouse brain.

The levels of 5 different prostanoids (PGD2, PGF2 alpha, PGE2, TXB2 and 6-keto-PGF1 alpha) formed in whole mouse brain in vivo were measured by specific radioimmunoassays. Basal concentrations were found to be very low (few ng/g wet weight). A marKed increase occurred during convulsions induced by either pentylenetetrazole or by electroconvulsive shock. Under both conditions the major cyclooxygenase product detected was PGD2, followed by PGF2 alpha and lower concentrations of the other prostanoids. The non-steroidal anti-inflammatory drugs flurbiprofen, indomethacin, and diclofenac dose-dependently inhibited the pentylenetetrazole-induced formation of prostaglandins. Concomitantly these 3 compounds dose-dependently increased the acute toxicity of pentylenetetrazole (decrease in LD50). Conversely, if levels of cerebral prostaglandins were enhanced by a preceding electroshock, the toxicity of pentylenetetrazole was significantly reduced (increase in LD50), and the time of onset of clonic seizures was markedly prolonged. Both the effect on the latency time and the LD50 could be reversed if the cerebral prostaglandin synthesis was prevented by indomethacin, or if the time interval between the electroshock and pentylenetetrazole administration was extended, so that the electroshock-stimulated prostaglandin concentrations had declined to basal levels again. These findings indicate that endogenous prostanoids formed in mouse brain during convulsions might possess anticonvulsive properties.

Animals↗
PubMed1982

Vasopressin and beta-endorphin release after osmotic and non-osmotic stimuli: effect of naloxone and dexamethasone.

The purpose of this study was to determine whether or not vasopressin release in response to various stimuli in the conscious rat is controlled by endogenous opioid peptides, in particular beta-endorphin. Naloxone (1 mg.kg-1 i.m.) promoted vasopressin release in response to both an angiotensin II infusion (500 ng . kg-1 . min-1) or an isosmolar, nonhypotensive hypovolaemia achieved by polyethylene glycol injection (PEG, 20% solution i.p.); however, naloxone was without effect when vasopressin release was induced by hypertonic saline injection (2.5% solution i.p.) or a severe fall in arterial blood pressure following trimethidinium (10 mg . kg-1 i.m.) induced ganglionic blockade. Vasopressin release was accompanied by an increase in plasma beta-endorphin-like immunoreactivity (beta-EI) following an angiotensin II infusion of PEG administration, but not after hypertonic saline or trimethidinium injection. Dexamethasone pretreatment (0.5 mg . kg-1 twice i.p.) prevented the increase in plasma beta-EI following an angiotensin II infusion or PEG administration. The simultaneous angiotensin II- or PEG-induced increase in vasopressin release was unaffected or potentiated, respectively, by the glucocorticoid. In contrast, vasopressin release in response to hypertonic saline or trimethidinium injection was significantly inhibited by dexamethasone. We conclude that an inhibitory control by endogenous opiates is involved in some, but not all of the different pathways leading to vasopressin release. The results obtained do not prove but can be reconciled with the proposal that hypophyseal beta-endorphin is the compound responsible.

Animals↗
PubMed1982

Role of dopamine receptors in the modulation of acetylcholine release in the rabbit hippocampus.

Modulation of acetylcholine release was studied in slices of the rabbit hippocampus preincubated with 3H-choline and then continuously superfused with a medium containing 10 mumol/l hemicholinium-3. Electrical field stimulation of the superfused slices elicited an increase in tritium outflow, which was tetrodotoxin-sensitive and largely calcium-dependent. Stimulus-evoked acetylcholine release in the rabbit hippocampal slices was modulated by presynaptic muscarinic autoreceptors, as has been shown previously for the rat hippocampus. Drugs with affinity for alpha- and or beta-adrenoceptors did not affect the evoked overflow of tritium from rabbit hippocampal slices. In contrast, the dopamine receptor agonist apomorphine (0.1 or 1 mumol/l) and exogenous dopamine (1 or 10 mumol/l) significantly reduced the evoked outflow by about 10 or 20%, respectively. This effect was antagonized by haloperidol (0.01 mumol/l) but not by phentolamine (1 mumol/l). Attempts to enhance (using nomifensine 10 mumol/l) or reduce (using haloperidol, up to 1 mumol/l; or bretylium, 1 mmol/l for 5 min) endogenous dopaminergic transmission in the hippocampal slices did not affect stimulation evoked acetylcholine release. In conclusion, presynaptic dopamine receptors modulating acetylcholine release are present in the rabbit hippocampus, but they seem not to be of physiological significance.

Acetylcholine↗
PubMed1982

Are presynaptic dopamine autoreceptors and postsynaptic dopamine receptors in the rabbit caudate nucleus pharmacologically different?

Slices of the rabbit caudate nucleus were preincubated with [3H]dopamine or [3H]choline and then superfused and stimulated electrically. Apomorphine reduced the stimulation-evoked overflow of tritium over the same concentration range, independently of whether slices had been pre-incubated with [3H]dopamine or with [3H]choline. Each of three antagonists--molindone, sulpiride and metoclopramide--increased the evoked overflow of tritium over the same concentration range in experiments with [3H]dopamine and those with [3H]choline. For each antagonist, the pA2 values against apomorphine obtained in [3H]dopamine experiments and in [3H]choline experiments were very similar. This study is a functional in vitro approach to receptor characterization, as opposed to radioligand binding studies or in vivo investigations. The results show that the dopamine receptor agonist apomorphine and three antagonists are unable to distinguish between the presynaptic, release-inhibiting dopamine autoreceptors and those postsynaptic dopamine receptors which, when activated, depress the release of acetylcholine. Although there are certainly more dopamine receptors in the caudate nucleus, these two physiologically important groups seem to be closely related.

Acetylcholine↗
PubMed1982

Rapid and effective conversion of 6-keto-prostaglandin F1 alpha to 6,15-diketo-13, 14-dihydro-prostaglandin F1 alpha-immunoreactive material in vivo.

Pentobarbitone-anaesthetized cats were injected i.v. with equal doses of prostacyclin and 6-keto-PGF1 alpha. Subsequently the time course of plasma levels of 6-keto-PGF1 alpha-immunoreactivity (i.r.) and 6,15-diketo-13, 14-dihydro-PGFi alpha-i.r. was determined in arterial blood by specific radioimmunoassays. Injection of both prostacyclin and 6-keto-PGF1 alpha resulted in short lasting peaks of 6-keto-PGF1 alpha-i.r. with maxima after 1 min, which rapidly declined. After injection of prostacyclin plasma 6,15-diketo-13, 14-dihydro-PGF1 alpha-i.r. increased to about one third of the height of the 6-keto-PGF1 alpha-peak and the maximum was reached after 6 min. On the other hand after administration of the same dose of 6-keto-PGFi alpha 6,15-diketo-13, 14-dihydro-PGF1 alpha-i.r. rose to about the same level as the 6-keto-PGF1 alpha-immunoreactive peak and the maximum was already attained after 2 min. When 6,15-diketo-13, 14-dihydro-PGF1 alpha itself was injected no increase in 6-keto-PGF1 alpha-i.r. was seen, whereas the 6,15-diketo-13, 14-dihydro-PGFi alpha-i.r. markedly increased, reaching its maximum after 1 min. These data indicate that in the cat in vivo 6-keto-PGF1 alpha can be rapidly metabolized to a 6,15-diketo-13, 14-dihydro-PGF1 alpha-like compound. The smaller conversion of prostacyclin as compared to 6-keto-PGF1 alpha could be explained by differences in compartmentalization of the two prostaglandins.

6-Ketoprostaglandin F1 alpha↗
PubMed1982

Synaptosomal calcium uptake systems: prostaglandins are probably not involved in the regulation of calcium fluxes into and within the nerve endings.

45Ca2+ uptake measurements were performed on intact and osmotically lysed synaptosomes from rat brain to study the possible influence of prostaglandins (PGs) on Ca2+ movements into and within the nerve endings. The K+-induced 45Ca2+ uptake of intact synaptosomes was not influenced by several inhibitors of PG synthesis. 45Ca2+ uptake in lysed synaptosomal preparations was promoted by ATP and seemed to be largely attributable to mitochondria, as it was inhibited by mitochondrial poisons. This Ca2+ uptake was strongly reduced by PG synthesis inhibitors but also by PG precursor fatty acids. Both PG synthesis inhibitors and precursors, according to their relative efficacy in blocking Ca2+ uptake, were able to induce Ca2+ efflux from preloaded intrasynaptosomal organelles. The PGs E2, F2 alpha, D2, and thromboxane B2 were without effect on 45Ca2+ uptake in lysed synaptosomal preparations. On the basis of our results it does not seem likely that PGs influence Ca2+ availability by modulating Ca2+ fluxes into or within the nerve endings. The observed inhibitory effects of PG synthesis inhibitors and precursors on the intrasynaptosomal Ca2+ uptake might be due to unspecific impairment of mitochondrial functions.

2,4-Dinitrophenol↗
PubMed1982

Release of beta-lipotropin- and beta-endorphin-like material induced by angiotensin in the conscious rat.

1 The influence of the renin-angiotensin system on plasma beta-endorphin-like immunoreactivity (beta-EI) was investigated in the conscious rat by use of a radioimmunoassay for beta-endorphin without prior extraction.2 Intravenous infusion of angiotensin I, II or (des-1-Asp)angiotensin II (angiotensin III) caused a dose-dependent increase in plasma beta-EI, angiotensin III infusion being less effective than angiotensin I or II. The plasma adrenocorticotrophin (ACTH) levels too were elevated by angiotensin II. The receptor antagonist, saralasin, prevented the angiotensin II-induced beta-EI release as did dexamethasone pretreatment.3 Both the release of beta-EI and the pressor response to angiotensin I were abolished by the converting enzyme inhibitor, captopril (SQ 14225). In contrast, captopril did not affect the action of angiotensin II.4 In view of the appreciable cross-reactivity of beta-lipotropin (beta-LPH) in our assay, plasma beta-EI was analysed by Sephadex G-50 chromatography. In plasma extracts of angiotensin II-infused rats, immunoreactivity corresponding to human beta-endorphin comprised about 49% of the total immunoreactivity, whereas 51% co-migrated with human beta-LPH.5 The increase in plasma levels of beta-EI elicited by angiotensin II was diminished by about 35% in rats with a hereditary absolute lack of vasopressin (Brattleboro rats), when compared to normal rats.6 These results suggest that the renin-angiotensin system can stimulate the secretion of beta-LPH and beta-endorphin with ACTH from rat anterior pituitary. One link in mediating the response appears to be vasopressin. The physiological function remains to be defined.

Angiotensin I↗