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PubMed1987

Changes in the biological activity of autacoids during passage through the human perfused fetoplacental lobule.

Changes in the biological activities of a number of autacoids after a single passage through the human perfused fetoplacental lobule have been assessed by bioassay, whilst recording fetal vascular resistance. Bradykinin did not affect vascular resistance, but its biological activity on the superfused bioassay tissues fell by approximately 98%, whereas des-Asp1-angiotensin I activity increased at least 80-fold and the vascular resistance rose. All these effects were inhibited by captopril. Angiotensin II increased vascular resistance but its activity on the bioassay tissues was not changed. 5-Hydroxytryptamine activity was reduced by 67-90% and resistance to flow was not affected. The activities of prostaglandins D2, E2, and F2 alpha were slightly reduced. Prostaglandins D2 and F2 alpha caused vasoconstriction, their maximum effects being greater than those of either of the angiotensins. The TxA2-mimetic U46619 was approximately 90 times more potent than PGF2 alpha, as a vasoconstrictor, but the maximal effects were comparable. Thus, autacoid activity can be reduced, augmented or not affected during passage through the human perfused fetal placental vasculature.

Angiotensin I↗
PubMed1997

Autacoids mediate coronary vasoconstriction induced by nitric oxide synthesis inhibition.

Inhibition of nitric oxide (NO) synthesis results in coronary vasoconstriction. Using a Langendorff rat heart preparation, we tested the hypothesis that this vasoconstriction is caused by the unopposed effect of the autacoids prostaglandin H2 (PGH2) or thromboxane A2 (TxA2) or both through a mechanism that involves oxygen free radicals. The vasoconstriction induced by NO synthesis inhibition was studied with two different NO synthase inhibitors, N(omega)-nitro-L-arginine methyl ester (L-NAME) and N(omega)-monomethyl-L-arginine (L-NMMA). We found that the decrease in coronary flow (CF) induced by L-NAME (from 19.3 +/- 0.9 to 13.2 +/- 0.9 ml/min; p < 0.001) and L-NMMA (from 20.1 +/- 0.4 to 15.0 +/- 0.3 ml/min; p < 0.001) was completely blocked by the cyclooxygenase inhibitor indomethacin. A different cyclooxygenase inhibitor (ibuprofen), a PGH2/TxA2-receptor antagonist (SQ29548), and a TxA2 synthase inhibitor (CGS 13080) also completely abolished the vasoconstrictor effect of L-NAME, suggesting that this vasoconstriction is mediated by TxA2. Two different scavengers of superoxide radical anions (O2-), the enzyme superoxide dismutase (SOD) and a cell-permeable SOD mimic, 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl (Tempol), also blocked the vasoconstriction induced by NO synthesis inhibition. In contrast, catalase, which inactivates hydrogen peroxide (H2O2), failed to do so, indicating that O2- is needed for the vasoconstrictor effect of L-NAME, whereas H2O2 is not. To determine whether O2- acts on the conversion of PGH2 to TxA2 or at the receptor or postreceptor level, we studied whether the vasoconstriction induced by exogenous PGH2 or the TxA2 receptor agonist U46619 is blocked by scavengers of O2-. CF decreased by 50% with PGH2 (from 21 +/- 2.1 to 10.6 +/- 5.8 ml/min; p < 0.01), and this decrease was abolished by SOD and Tempol but not catalase. However, SOD had no effect on the vasoconstriction induced by U46619, which decreased CF by 45% (from 17.3 +/- 2.5 to 9.5 +/- 1.8 ml/min; p < 0.01). In addition, PGH2 increased the release of TxB2 (the stable metabolite of TxA2) in the coronary effluent (from 5.1 +/- 1.2 to 136.1 +/- 11.8 pg/ml/min). The release of TxB2 was significantly lower in hearts treated with SOD (76.8 +/- 14.2 pg/ml/min) and CGS (65.7 +/- 13.9 pg/ml/min). We conclude that the coronary vasoconstriction induced by inhibition of NO synthesis is the result of the unopposed effect of the autacoid TxA2 through activation of its receptor, and that O2- is necessary for conversion of PGH2 to TxA2.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1989

The evocation of rumination in sheep by the close-arterial injection of catecholamines, cholinergic drugs, autacoids and gastrointestinal hormones into the forestomach.

The effect of alpha-2 adrenoreceptor agonists, cholinergic drugs, autacoids and some gastrointestinal hormones upon the evocation of rumination in sheep when injected by close-arterial injection into the forestomach was examined. Apart from adrenaline, noradrenaline, dopamine and xylazine only one alpha-2 agonist (BHT933) evoked rumination effectively. Acetylcholine, neostigmine, the gastrointestinal hormones and the autacoids examined did not evoke rumination consistently. Tyramine did not usually evoke rumination and guanethidine injected before adrenaline did not prevent the latter from evoking rumination. The evocation of rumination by catecholamines does not appear to involve sympathetic, cholinergic or non-sympathetic non-cholinergic neurones in the enteric nervous system to activate the nervous sensory receptors involved in the reflex evocation of rumination.

Animals↗
PubMed1984

Effects of vasoactive autacoids on the human umbilical-fetal placental vasculature.

Studies have been made of the effects of autacoids on vascular tone of the human perfused fetal umbilical vein and placental lobule. The thromboxane A2 (TxA2)-mimetic substance U46619, 5-hydroxytryptamine and bradykinin were powerful constrictors of the vein. Prostaglandins E2 (PGE2), F2 alpha (PGF2 alpha), adrenaline, noradrenaline, histamine and angiotensin II were much less potent. Venoconstriction caused by U46619, bradykinin and 5-hydroxytryptamine was reduced during inhibition of phospholipase A2 with mepacrine. Responses to U46619 were also reduced after inhibition of cyclo-oxygenase with indomethacin whereas those to bradykinin and 5-hydroxytryptamine were potentiated. In the placenta U46619 was the most potent vasoconstrictor, bradykinin, 5-hydroxytryptamine, angiotensin II, PGE2 and PGF2 alpha being 10-100 times less active. Responses to U46619 were reduced by either mepacrine or indomethacin. Arachidonic acid caused umbilical venoconstriction but vasodilatation in the placenta. Both effects were reduced by indomethacin. Prostacyclin (PGI2) caused vasodilatation in both preparations. It is suggested that TxA2 in the placenta and TxA2, 5-hydroxytryptamine and bradykinin in the umbilical vein could contribute to control of vascular smooth muscle tone. Their vasoconstrictor effects are partly indirect and affected by the concomitant local release of eicosanoids. The results add support to previous conclusions that these autacoids may normally have important influences on blood flow in the fetal extra-corporeal circulation. Agents inhibiting their synthesis, eg non-steroidal anti-inflammatory agents, should only be prescribed during pregnancy with these facts in mind.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed2006

The role of autacoids and the autonomic nervous system in cardiovascular responses to radio-frequency energy heating.

Among the potential effects of exposure to high levels of radio-frequency energy (RFE) (which includes microwaves), an increase in body temperature is the primary consequence. Release of autacoids and activity of the autonomic nervous system may influence (or be directly responsible for) some of the physiological changes that occur in conjunction with this hyperthermia. The main focus of this review is the interaction of autacoids and the autonomic nervous system with cardiovascular changes during heating. Differences between environmental and RFE-induced heating (such as rate of temperature change and degree of skin vs. core heating) may be important when considering these effects. Antihistamines exhibited no beneficial effect on circulatory collapse during RFE-induced heating. The serotonergic blocker methysergide decreased survival time in rats during terminal RFE exposure, despite no effects on heart rate (HR) or blood pressure. Although blockade of platelet-activating factor resulted in lower HR before RFE exposure, there was a lack of effect on the subsequent increase in HR during heating. Nitric oxide did not contribute to the hypotension that occurs due to rapid heating by RFE exposure. There have been either no or very limited studies of effects of prostaglandins, bradykinin, or angiotensin on RFE-induced heating responses. beta-Adrenoceptor antagonism with propranolol resulted in significantly decreased survival times and lower final colonic temperatures during RFE exposure. A lack of effects of nadolol on survival time and temperature, coupled with its poor ability to traverse the blood-brain barrier, suggests that central beta-adrenergic stimulation rather than peripheral stimulation may alter thermoregulation. Effects of the autonomic nervous system (as studied by adrenoceptor blockade) on potassium changes during heating have not been fully investigated. Such changes could be important in animals' responses to RFE and other modalities of heating, and should be studied in future.

Adrenergic alpha-Antagonists↗
PubMed2003

In vitro effects of hormones and autacoids on the activity of acid phosphatase in the lysates of endotoxin-activated rat peritoneal and bronchoalveolar macrophages.

Peritoneal and bronchoalveolar macrophages activated in vitro by endotoxin, exhibit alterations in the acid phosphatase activity of cell lysates when certain hormones or autacoids are present in the culture medium. They also show morphological changes concerning general appearance and acid phosphatase cytochemistry. Certain agents known to increase the intracellular levels of cyclic AMP, such as dopamine and prostaglandin E2, decreased this enzyme activity in the lysates of peritoneal macrophages. Adrenalin had no effect on this activity at 14 hours, but was found to increase the activity in the culture medium at the initial hours of incubation. Glucagon decreased whereas insulin increased acid phosphatase activity in bronchoalveolar macrophages. Serotonin or histamine, known to activate phospholipase C, increased this activity in peritoneal or bronchoalveolar macrophages. The results of this study, taken together with previously published data (Kondomerkos et al., 2003), suggest that hormones and autacoids may control certain parameters of macrophage activation including acid phosphatase activity.

Acid Phosphatase↗
PubMed2005

[Study of autacoids role in the regulation of circadian rhythm of the human renal function].

The circadian rhythm of urine formation was studied in younger (27 +/- 8 yr) and aged (76 +/- 3 yr) males. In 11 younger healthy examined persons a decrease of diuresis during the night as compared with the day time was due to a rise of solute free water reabsorption. In 31 aged males the change of the urine formation rhythm with increase of the nocturnal diuresis is based on a rise of osmolal clearance combined with an increase of the solute free water reabsorption. It is shown that blockade of autacoid secretion leads to normalization of the diuresis circadian rhythm. In 10 aged men, nocturia was due to a decrease of vasopressin secretion which resulted in a decrease of the solute free water reabsorption and an increase of diuresis. The obtained data are considered as an evidence for the role of renal autacoids, alongside with vasopressin, in regulation of the circadian rhythm of the kidney function.

Adult↗
PubMed1986

Autacoids and some mediators in allergic and non allergic forms.

The aim of this review is that to examine some among the most important mediators involved in the onset of autacoid-mediated allergic and non-allergic symptomatology. Autacoids, such as histamine and arachidonic acid derivatives (leukotrienes and prostaglandins), mediators derived from cell membrane, such as PAF-acether and other cell-derived mediators, such as PF4, are described. Special importance is given to the respective pharmacological actions and to the mechanisms by which these actions are performed (receptors, antagonisms, synergism) from whose complexity systemic reactions might ensue. Furthermore, a part of this study is dedicated to the complex interactions among biochemical systems of the body such as Kinins, Coagulation, Fibrinolysis and Enzymatic Activity Mediators that can interfere with these interactions and support some pathologies. Besides, a chapter is devoted to Neurogenic Inflammation and therefore to Substance P and other neuropeptides.

Animals↗
PubMed1993

A proposed autacoid mechanism controlling mastocyte behaviour.

Evidence is provided here supporting the existence of a novel autacoid mechanism negatively modulating mast cell behaviour in response to noxious stimuli in vivo; hence, the denomination "autacoid local inflammation antagonism" (ALIA). In particular, as lipid amides of the N-acylethanolamine type have been reported to accumulate in tissues in degenerative inflammatory conditions, we examined whether these N-acylated lipids could exert regulatory effects on mast cell activation in vivo. The results reported show that both long- and short-chain N-acylethanolamines, when systemically administered, are effective in reducing mast cell degranulation induced by local injection of substance P in the ear pinna of developing rats. These and other data suggest that the endogenous production of N-acylethanolamines may constitute a local autocrine/paracrine response for the negative feedback control of mast cell responses to various activating signals. Such a process may be of physio-pathological relevance in the regulation of functional neuro-immune-mast cell interactions.

Animals↗
PubMed1986

Autacoid binding to serum proteins. Interaction of platelet activating factor (PAF) with human serum alpha-1-acid glycoprotein (AAG).

Platelet activating factor (PAF; 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine) is a potent bioactive phospholipid released from platelets, neutrophils, basophils and macrophages that has been proposed as a mediator of anaphylaxis, acute lung injury and other disorders. Specific factors which stabilize PAF and/or regulate PAF activity in body fluids are largely unknown. As part of a general autacoid-serum protein binding screen, the platelet activating factor-alpha-1-acid glycoprotein (PAF-AAG) interaction was indirectly characterized by examining the ability of PAF to displace propranolol from AAG. Both PAF and its deacetylated metabolite (lyso-PAF), at 20 microM, doubled the fraction unbound of propranolol (0.4 microM) from purified human AAG (20 microM). None of the other autacoids that were studied (epinephrine, serotonin, spermidine, putrescine, leu-enkephalin or phenethylamine) exhibited any propranolol displacement activity. Scatchard analysis indicated that PAF competitively displaced propranolol from AAG, causing the apparent affinity constant for propranolol-AAG to decrease from 1.8 X 10(5) M to 6.9 X 10(4) M. PAF behaved qualitatively like chlorpromazine (a documented inhibitor of propranolol binding to AAG), but PAF was less effective at displacing propranolol. The apparent binding to AAG may help stabilize and transport extracellular PAF. Furthermore, the interaction of PAF and AAG suggests that serum AAG, which fluctuates in a number of diseases, may function to regulate PAF activity during acute and chronic disease states.

Binding, Competitive↗
PubMed1991

Effect of autacoid modulation on N-(3,5-dichlorophenyl)succinimide (NDPS) and NDPS metabolite nephrotoxicity.

N-(3,5-Dichlorophenyl)succinimide (NDPS) is an agricultural fungicide which has been shown to induce acute tubular necrosis. The purpose of the present study was to determine if creatinine clearance was altered early in the development of NDPS nephrotoxicity. This study also examined the effect of autacoid modulation on the renal effects induced by NDPS and two metabolites of NDPS, N-(3,5-dichlorophenyl)-2-hydroxysuccinimide (NDHS) and N-(3,5-dichlorophenyl)-2-hydroxysuccinamic acid (NDHSA). In one set of experiments, male Fischer 344 rats (4 rats/group) were administered a single intraperitoneal (i.p.) injection of NDPS (1.0 mmol/kg) or vehicle and creatinine clearance was determined at 3 and 6 h post-treatment. NDPS administration resulted in a marked decrease in creatinine clearance at both time points. In a second set of experiments, rats (4-8 rats/group) were pretreated with the cyclooxygenase inhibitor indomethacin (3.0 or 5.0 mg/kg, i.p.) or the thromboxane synthase inhibitor dazmegrel (20 mg/kg, i.p.) 1 h before the i.p. administration of NDPS (0.2 or 0.4 mmol/kg), NDHS (0.05 or 0.1 mmol/kg), NDHSA (0.05 or 0.1 mmol/kg) or vehicle. Indomethacin pretreatment potentiated the nephrotoxic potential of NDPS and its two metabolites, while dazmegrel pretreatment attenuated NDPS nephrotoxicity without marked effects on NDHS or NDHSA nephropathy. These results indicate that renal hemodynamic changes occur early in the development of NDPS nephrotoxicity and that autacoids are important modulators of NDPS- and NDPS metabolite-induced renal effects.

Animals↗
PubMed1999

Role of autacoids in cardiovascular colapse in anaphylactic shock in anaesthetized dogs.

OBJECTIVE: In anaphylactic shock (AS), the relative effects of the autacoids including histamine, prostaglandins (prost), and leukotrienes (leuk) on causing cardiovascular collapse and the extent to which receptor blocking agents and pathway inhibitors may prevent this collapse are not clear. METHODS: In randomized design, we investigated whether blockade of histamine H1, H2, and H3 receptors or inhibition of the cyclooxygenase (cyclo) and lipoxygenase pathways (lipox) prevented AS in ragweed sensitized dogs. Seven dogs were studied under pentobarbital anesthesia in which the treatment studies were approximately 2 weeks apart. RESULTS: During H1 receptor blockade, the decreases in blood pressure and cardiac output otherwise observed in AS were attenuated (P < 0.05) and the release of prost, thromboxanes, and leuk were reduced as compared with nontreatment studies. Cyclo inhibition also attenuated cardiovascular collapse and mediator release in AS, but the other treatments showed no effects. CONCLUSION: H1 receptor blockade and cyclo may attenuate cardiovascular shock in AS. These agents inhibit autacoid release from mast cells in addition to any specific receptor blocking and pathway inhibition effects.

Analysis of Variance↗
PubMed1992

Release of contracting autacoids by aortae of normal and atherosclerotic rabbits.

The aim of our study was to examine the release of various lipid and peptide contracting autacoids by aortae of normal and atherosclerotic rabbits. Leukotriene (LT) E4, an enzymatic derivative of LTC4, thromboxane (Tx) B2, and endothelin-1 (ET-1) were measured by radioimmunoassay techniques in aortic preparations of normal and cholesterol-fed rabbits. Intact aortae of normal rabbits incubated with the calcium ionophore A23187 for 1 h at 37 degrees C released LTE4 and TxB2 (22 +/- 3.5 and 14.8 +/- 2 pg/mg of tissue, respectively, mean +/- SEM, n = 33). Removal of aortic endothelium was associated with a significant reduction in LTE4 (44%) and TxB2 (58%) release. In aortic preparations from cholesterol-fed rabbits, the release of LTE4 was significantly enhanced (41 +/- 8 pg/mg of tissue, mean +/- SEM, n = 27) whereas TxB2 was not significantly altered. No detectable amounts of ET-1 were measured after 1 h of incubation. However, at 4 h, an endothelium-dependent release of ET-1 from normal aortae was demonstrated. In atherosclerotic aortae, ET-1 release was significantly higher than in controls (10 +/- 1.3 vs. 5 +/- 0.5 pg/cm2, mean +/- SEM, n = 16). We conclude that enhanced formation of vasoconstrictor autacoids may contribute to altered vasomotion of atherosclerotic blood vessels.

Animals↗
PubMed1982

Autonomic and autacoid activity in antigen-sensitized and control ovine pulmonary vein and artery.

Spirally cut strips of ovine pulmonary vein and artery were studied in isolated organ baths and their responses to selected autacoid and autonomic agents were compared. In addition blood vessels taken from horse plasma-sensitized sheep were compared with their respective controls. Pulmonary vein and artery exhibited qualitative and quantitative differences in their autacoid and autonomic reactivity. Veins were more sensitive in responding with contractions to histamine (HIST) and carbachol (CARB) when compared with arteries. Responses of these vessels differed qualitatively to 5-Hydroxytryptamine (5HT); phenylephrine (PE) and adrenaline (ADR): arteries responded with strong contraction and veins with relaxations. Isoproterenol (ISOP) effectively relaxed veins but was either without effect or produced 10%-15% relaxations of precontracted arterial strips. Phentolamine competitively antagonized ADR and PE-induced contractile responses of arteries while on veins, ISOP and PE dose-response curves (DRCs) were shifted to the right in the presence of propranolol. Mepyramine inhibited venous and arterial responses to HIST. Comparisons between sensitized and non-sensitized sheep vasculature revealed a significant (P less than 0.05) decrease in the activity of spasmolytic agonists on veins, i.e. relaxant actions of 5HT, PE and ISOP were significantly impaired. In addition the activity of 5HT to contract pulmonary artery was significantly (P less than 0.05) increased when compared with controls. Present investigation suggests: (i) the predominance of H1-histaminergic receptors in ovine pulmonary vasculature; (ii) the preponderance of alpha and beta-adrenergic receptors in pulmonary artery and vein, respectively; (iii) that antigenic sensitization exaggerates the pathological state by causing a decrease in spasmolytic activity with a parallel increase in spasmogenic activity.

Animals↗
PubMed1998

Autacoid interactions in the regulation of blood flow in the human placenta.

1. Interactions between autacoids may play important roles in the regulation of blood flow in the foetal placenta. In order to investigate this aspect of placental haemodynamics, human normal-term placentae were perfused in vitro and the responses of the foetal vessels to various combinations of vasoactive agents were determined. 2. Vasoconstriction responses to 5-hydroxytryptamine (5-HT) were potentiated in the presence of endothelin-1 (ET-1), the thromboxane A2-mimetic U46619 and a nitric oxide synthase inhibitor, N-nitro-L-arginine (NOLA), but not in the presence of angiotensin II. 3. N-Nitro-L-arginine caused vasoconstriction of the perfused placenta and indomethacin attenuated this effect and blocked the potentiation of the 5-HT response by NOLA. 4. Indomethacin did not affect ET-1-induced pressure increases and infusion of U46619 had no effect on release of ET-like immunoreactivity into the foetal placental circulation. 5. The present study provides evidence of interactions between several autacoids in human perfused placentae in vitro. These interactions may play important roles in foetal placental haemodynamics in normal or pathological situations.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1992

Involvement of renal autacoids in the direct effects of mixed amino acids on the kidney.

A pharmacological approach has been employed to investigate the involvement of renal autacoids in the direct effect of amino acids on the isolated rat kidney. The increase in renal perfusate flow induced by 6 mM mixed amino acids was inhibited by sulpiride, a dopamine antagonist. The change in GFR induced by 6 mM mixed amino acids was abolished by L-nitro-arginine methyl ester, an inhibitor of nitric oxide biosynthesis and partially inhibited by either sulpiride or indomethacin. It is concluded that several autacoids may mediate the direct effect of amino acids on the kidney with dopamine being primarily involved in hyperperfusion and nitric oxide involved primarily in hyperfiltration.

Amino Acids↗
PubMedDate not supplied

A model of cytosolic calcium regulation and autacoids production in vascular endothelial cell.

A model of vascular endothelial cell is proposed to describe the mechanisms by which cytosolic calcium (Cai) is modulated and endothelium-derived relaxing factor (EDRF) and prostacyclin (PGI2) are released when the cell is stimulated by agonist. The intracellular Ca2+ store of the model cell is comprised of a superficial (sc) and a deep (dc) compartment. The dc Ca2+ content is refilled by the sc whose [Ca2+] is the same as extracellular Ca2+. Inositol (1,4,5)-trisphosphate (IP3) produced by agonist modifies the dc permeability which discharges its Ca2+ to the cytosol. The increase of Cai induces Ca2+ released from the sc. Ca(2+)-activated K+ current hyperpolarises the cell. The raised Cai releases PGI2 in the presence of IP3 while EDRF is released by Cai. The model explains satisfactorily the Ca2+ transient and autacoids production of the aortic endothelial cell without the need of calcium influx from extracellular space. The cytoplasmic Ca2+ oscillations observed in human endothelial cell from umbilical veins were reproduced by the model. Production of EDRF by the artery due to increase in pressure was also simulated.

Autacoids↗
PubMed1979

Reactivity of isolated canine bronchus and pulmonary blood vessels to autonomic, autacoid agents and antigen.

Adult dogs were sensitized to horse plasma. Reactivity of isolated bronchus and pulmonary blood vessels to antigen and some selected autonomic and autacoid agents were studied. Pulmonary veins contracted to bradykinin, 5-HT, PGF2alpha, PGE2, histamine, carbachol and antigen (Schultz-Dale reaction). Pulmonary arterial strips contracted to 5-HT and histamine, but only weakly to horse plasma. Bronchial strips contracted to carbachol, 5-HT, histamine and horse plasma, relaxed to isoprenaline, PGE1 and PGE2. Subsequent antigen challenge produced 'desensitization'. Allowing the tissues to 'rest' for 1 and 2 h resulted in partial 'recovery' of the anaphylactic response. This investigation suggests that the contractions of sensitized pulmonary vein and bronchus to specific antigen may contribute to the patho-physiology of pulmonary hypersensitivity in dogs.

Anaphylaxis↗