Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Angiotensin II (AII), injected intracerebroventricularly, has been shown to antagonize opioid analgesia. The mechanism for this was obscure. In the neuroblastoma X glioma NG 108-15 hybrid cell line, the K(+)-induced increase in [Ca2+]i can be suppressed by the delta opioid agonist [D-Pen2, D-Pen5]enkephalin (DPDPE) at 0.01-1 microM, an effect completely reversed by the opioid antagonist naloxone. Angiotensin II (AII) at concentrations of 0.1 and 1 microM mobilized free Ca2+ from an intracellular pool, and this effect was antagonized by the AII receptor antagonist saralasin. All (1 microM) had no significant effect on the increase in [Ca2+]i induced by K+, but it blocked the suppressive effect of DPDPE on the K(+)-induced [Ca2+]i increase. The results indicate that mobilization of intracellular calcium may underlie the anti-opioid effect of AII.
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PMID:Mobilization of calcium from intracellular store as a possible mechanism underlying the anti-opioid effect of angiotensin II. 150 24

Cholecystokinin octapeptide (CCK-8) and angiotensin I (AI) have been shown in behavioral studies being endogenous antiopioid substrates (AOS). To assess their antiopioid mechanism at postreceptor level, we observed the effects of the three opioids and the two AOS on 45Ca uptake of the rat spinal synaptosomal preparations. Morphine, Dyn A and DPDPE at concentrations of 10 nmol/L to 1 mumol/L, produced a mild suppression of 45Ca uptake of synaptosomal preparations from ventral spinal cord. CCK-8 showed a mild suppression only at a concentration of 1 mumol/L. In synaptosomes prepared from dorsal spinal cord, Dyn A but not morphine or DPDPE, produced a strong inhibition of 45Ca uptake which was blocked by nor-BNI, a kappa receptor antagonist, at 1 mumol/L. While CCK-8 (10 nmol/L to 1 mumol/L) also suppressed 45Ca uptake, it could antagonize the suppressive effect induced by Dyn A. In contrast to CCK-8, AI (10 nmol/L to 1 mumol/L) influenced neither on synaptosomal 45Ca uptake, nor on Dyn A suppression of 45Ca uptake. The results presented above fit very well with our behavioral studies, i.e., CCK-8 antagonized opioid analgesia in both the brain and the spinal cord, whereas AI antagonized opioid analgesia in the brain but not in the spinal cord. It is therefore concluded that antagonism of the opioid suppression of synaptosomal 45Ca uptake might be one of the mechanisms for the antiopioid activity of CCK-8 and AI.
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PMID:[Effects of dynorphin A and CCK-8 on synaptosomal 45Ca uptake of the rat spinal cord]. 198 24

Ovarian follicular fluid (FF) of a number of species contain regulatory peptides secreted by granulosa cells or by autonomic nerve terminals. In this report we demonstrate the presence of authentic (HPLC-verification) angiotensin II and III as well as of substance P (SP) in human FF obtained from hMG stimulated infertile patients undergoing in vitro fertilization. Angiotensin II/III (AII/III), estradiol (E2) and progesterone concentrations increase with the size of the follicles. SP concentrations did not vary significantly in FF of various sizes. These peptide concentrations in FF are about 10-fold higher than those measured in the serum of the same patients. Attempts to correlate SP, AII/III, E2 and progesterone concentrations in the individual FF with the ability of an oocyte to be fertilized, failed. Neither AII/III, SP, E2 nor progesterone concentrations were different in these subclasses of FF. Follicles of patients punctured under general anesthesia contained significantly more SP than follicles of patients which had lumbar analgesia. AII/III concentrations were the same in FF of both treatment groups. The presence of angiotensin II and III in FF in increasing concentrations depending on the maturity of the follicle and the inability of general anesthesia to affect the AII/III concentrations suggests that this peptide is produced within the ovary.
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PMID:Angiotensin II/III and substance P in human follicular fluid obtained during IVF: relation of the peptide content with follicular size. 245 91

Behavioral observations have repeatedly shown that the analgesic effect of morphine can be antagonized by intracerebroventricular injection of angiotensin I (A I), although mechanisms underlying the action were obscure. Since a prevention of Ca2+ uptake into the nerve terminals was considered as one of the mechanisms for morphine analgesia, we examined the effect of A I and morphine on the 45Ca uptake by rat brain synaptosomal preparations. Morphine of 10(-8)-10(-6) mol/L produced a dose-related suppression on synaptosomal 45Ca uptake, which was completely reversed by the opioid antagonist naloxone of 10(-6) mol/L. A I of 10(-8)-10(-6) mol/L, on the contrary, enhanced 45Ca uptake. This effect was totally abolished by saralasin, a A I antagonist, at 10(-6) mol/L. When synaptosomal preparations were incubated in a mixture of morphine (10(-6) mol/L) and A I (10(-8)-10(-6) mol/L), the effect of morphine was almost completely reversed. The results suggest that the distinct effect of A I may account for, at least in part, the antagonistic effect of A I on morphine analgesia.
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PMID:[Antagonistic effects of angiotensin II and morphine on synaptosomal calcium uptake]. 276 44

Angiotensin II (AII), arginine vasopressin (AVP) and prolactin (PRL) were measured by radioimmunoassay in plasma and cerebrospinal fluid (CSF) in concurrent daily samples from conscious unrestrained steers. Packed cell volume, [Na+] and osmolality were also measured from these samples. Salt appetite was assessed during a 5-min daily session of operant conditioning. Food and water was always available. Unilateral parotid duct fistulation was effected under xylazine analgesia and halothane/O2 anaesthesia. To prevent a sodium deficit developing from loss of [Na+] in the extruded saliva, 0.3 M NaHCO3 was available ad libitum so that each animal could ingest sufficiently to balance the salivary loss. A week later epidural cannulae were implanted in the cisternae magna using the same anaesthesia. Three days afterwards when the saliva [Na] was 78 mmol/1, the 0.3-M NaHCO3 supplement was withdrawn for 7 days so that sodium deficiency developed to a degree which evoked salt appetite. When the NaHCO3 supplement was restored ad libitum, all aspects of [Na+] deficiency and salt appetite were completely ameliorated within 2-3 days. Packed cell volume increased and body weight decreased (p less than 0.05) during depletion, but rapidly returned to normal on day 2 of repletion. Both plasma and CSF osmolality were reduced during depletion as were plasma [Na+] (p less than 0.01) and CSF [Na+] (p less than 0.001). From a basal value of 64.7 +/- 9.35 fmol/ml on day 0, plasma AII increased to 229.2 +/- 46.65 fmol/ml (p less than 0.001) on day 3, prior to the onset of salt appetite on days 4-7. In marked contrast to plasma AII during sodium depletion, CSF AII was unchanged during salt appetite. There was no correlation between plasma and CSF AII during behavioural salt appetite.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relation of endogenous systemic and brain angiotensin II, arginine vasopressin and prolactin with the genesis of salt appetite in cattle. 284 67

The central effect of angiotensin II on the analgesic action of morphine in mice was investigated using the tail-pinch and hot plate tests. Angiotensin II (0.1-10 pmol), given intracerebroventricularly (i.c.v.), had no effect on the nociceptive sensitivity but did produce a dose-dependent attenuation of the morphine-induced analgesia. A specific angiotensin II antagonist, Saralasin (1 pmol), which in itself had no analgesic effect, significantly potentiated the morphine-induced analgesia. These results suggest that angiotensin II probably plays the physiological role of an anti-opioid substance in pain-modulating systems in the brain.
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PMID:Intracerebroventricular administration of angiotensin II attenuates morphine-induced analgesia in mice. 408 Jan 8

Polypeptides are endogenous agents, involved in the regulation of many physiologic functions and the pathogenesis of several diseases. Polypeptide antagonists form a group of new chemical entities which may provide valid therapeutic agents. Some polypeptides (angiotensin, kinins) are released through the action of proteolytic enzymes (renin, kallikreins) and act as hormones or autacoids; others (substance P, neurotensin) are synthetized by nervous cells to serve as neurotransmitters or neuromodulators. The main homeostatic role of the renin-angiotensin system is to uphold high systemic arterial blood pressure. Overproduction of renin and insufficient checking of renin secretion are among the most common causes of arterial hypertension. Several forms of arterial hypertension (neurovascular, idiopathic) benefit from a reduction in renin-angiotensin system activity. This is achieved either through decreasing renin secretion, by inhibiting conversion of angiotensin I into angiotensin II, or through blocking the peripheral actions (at the receptor sites) of angiotensin II. Renin secretion is very significantly reduced by beta-blocking agents (propranolol); conversion of angiotensin I into angiotensin II is inhibited by teprotide, captopril and their derivatives; peripheral actions of angiotensin II are blocked by saralasin. Bradykinin and related agents produce vasodilation, increase vascular permeability and stimulate pain fibers. Kinins thus reproduce the cardinal features of inflammation and are held to be mediators of the inflammatory reaction. The substance P neuropeptide is found in the brain and bowel; it may act as a transmitter of the sensation of pain at the spinal cord and central nervous system sites. Among other effects outside of the brain, substance P is a potent vasodilator and inhibits renin secretion. Neurotensin is a neuropeptide which produces hypothermia, muscular relaxation and analgesia. Outside of the brain, this peptide is involved in the regulation of gastric secretion, intestinal motility and insulin and glucagon secretion. The vasoactive intestinal peptide, found in certain cholinergic nerve endings, is a large peptide which inhibits gastric secretion, intestinal motility and vascular tone.
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PMID:[Polypeptides and antagonists]. 620 6

Paired maternal venous (MV) before (P1) and after (P2) general anesthesia, cord venous (CV) and cord arterial (CA) blood was taken from two groups of primagravid women, one delivered vaginally and the other by elective lower segment Caesarian section (ELSCS). ACTH, Cortisol (CoSol) Aldosterone (Aldo) Plasma Renin Activity (PRA) Plasma Renin Concentration (PRC) Angiotensin II (AII) Solium (N alpha) and Potassium [K]+ were measured in both study groups. Of the various hormones studied, all but cortisol were raised in the P2 sample with only ACTH and AII achieving significant increase. A number of significant positive correlations was found between P1 and P2 samples as well as between the hormones themselves. Four of the vaginally delivered group received epidural analgesia and demonstrated significantly higher levels of ACTH and CoSol in the CV sample. A comparison of the studied variables between the two groups showed a significant decrease in the ELSCS group of ACTH and CoSol in the MV sample, of ACTH, CoSol, PRC in the CV sample, and of CoSol in the CA sample. Of all the parameters, studied, only [K]+ together with Aldo was found to be elevated in the CV sample of the ELSCS group but only [K]+ achieved significant increase.
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PMID:The effects of anesthesia and mode of delivery on the parameters of the renin-angiotensin system. 630 54

Using the tail-flick method in 45 rats with a chronic cannula stereotaxically implanted in the third ventricle, a rapid onset, dose related and short lasting analgesia was obtained after intracerebroventricular injection of Ang II 10-15 ng/kg or renin 0.03-0.1 U. Analgesic effects of the endogenous and exogenous Ang II are prevented by naloxone--1 mg/kg i.p. The inhibition of serotonin synthesis with PCPA--400 mg/kg/day i.p. for five days as well as the serotonin-receptor block with ketanserin 0.1 mg/kg i.p. partially prevent analgesic effects of Ang II and renin intracerebral administration. The increase of the pain perception threshold after infusing into the brain Ang II or renin points out a new functional consequence of the possible opioid participation in the central effects of renin-angiotensin system.
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PMID:Possible opioid participation in the analgesic effects of the renin-angiotensin system. 641 96

MOR-1 encodes a mu receptor. In an effort to establish the relationship of this cloned opioid receptor with ingestive behavior and analgesia in rats, the present study examined the actions of four antisense oligodeoxynucleotides aimed at exons 1 (AS1), 2 (AS2), 3 (AS3) and 4 (AS4) of the MOR-1 clone, as well as a mismatch antisense sequence (MS1). Rats were administered intracerebroventricular injections (10 micrograms/2 microliters) of each of the oligodeoxynucleotides on days 1, 3 and 5. Body weight and spontaneous food and water intake were monitored daily. In addition, 2-deoxy-D-glucose (2DG)-induced hyperphagia, central Angiotensin II (ANG-II) induced hyperdipsia and central morphine analgesia were examined 24 h following the last antisense injection. AS1, AS2, AS3 and AS4 each significantly reduced body weight (7-17 g), food intake (8-13 g) and water intake (11-23 ml), while the vehicle or MS1 conditions significantly increased weight (9-20 g) and produced smaller reductions (2-4 g) in food intake. None of the AS probes altered the magnitude of either 2DG-induced hyperphagia or ANG-II-induced hyperdipsia. Central morphine analgesia was reduced by pretreatment with AS1 and AS4, but not AS2, AS3 or MS1. The sensitivity of general feeding to all four exons suggest that the receptor responsible for this action is encoded by the MOR-1 clone. The differences between feeding and morphine analgesia raise the possibility that these two actions are mediated through different mu receptor subtypes. Our results also demonstrate the viability of the in vivo antisense technique in modulating opioid-mediated ingestive responses.
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PMID:Antisense oligodeoxynucleotides against the MOR-1 clone alter weight and ingestive responses in rats. 878 66


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