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At least 739 records · Page 41Linked to original sources
PubMed1977

Vasoactive properties of prostaglandin compounds on the in vitro human basilar artery.

The action of six prostaglandins A1, E1, (A2, E2, F1 alpha, F2 alpha) on in vitro human basilar artery circumferential strips was evaluated to assess relative vasoreactivity. Degree of contraction was compared with 5-hydroxytryptamine (5-HT), hitherto the most active in this laboratory. The three most vasoactive prostaglandins were E1, E2, and F2, alpha. The three PGs giving highest magnitude of response were F1 alpha, F2 alpha, and E2. Most were more active when compared to 5-HT. Vasodilation did not occur. Because of their vasoconstrictive qualities, prostaglandins may participate in arterial vasospasm. It is postulated that prolonged vasoconstriction may lead to vasospasm and that the latter may result from one or more autacoids acting along or synergistically.

Basilar Artery↗
PubMed1996

Non-neurogenic electrically evoked relaxation in canine airway muscle involves action of free radicals on K+ channels.

Cyclopiazonic acid (selective blocker of the internal Ca+2 pump) evoked tonic contraction in canine bronchial smooth muscle (BSM) and tracheal smooth muscle. This contraction was biphasic, including an initial component that was relatively insensitive to blockade of Ca+2 influx (e.g., removal of external Ca+2; nifedipine; hyperpolarization using lemakalim) followed by a component that was sensitive to all such interventions. In BSM, but not in tracheal smooth muscle, electrical field stimulation (EFS) evoked relaxations that were not affected by interventions designed to prevent release of autacoids from nerve endings or the epithelium, Na+/Ca+2 exchange or Ca(+2)-ATPase activities (internal or plasmalemmal). EFS evoked little or no relaxant response in carbachol-precontracted BSM in the presence of propranolol. After Ca+2 was replaced with Sr+2, however, carbachol evoked comparable contraction after which EFS evoked non-neurogenic relaxations. We found that the EFS-evoked relaxations were abolished by TEA or high KCI, were reduced significantly by charydotoxin or quinine, were reduced partially by ouabain and were unaffected by removal of external K+, by apamin or by glybenclamide. In addition, the relaxations were reduced significantly by the free radical scavenger N-acetylcysteine, were mimicked by H2O2 but were unaffected by superoxide dismutase or catalase. These observations suggest that the cyclopiazonic acid-evoked contraction involves pharmacomechanical coupling mechanisms (i.e., Ca(+2)-release) initially, followed by electromechanical coupling (i.e., voltage-dependent Ca+2 influx). After depletion of the internal Ca+2 store (e.g., by cyclopiazonic acid or Sr+2), EFS is able to evoke in BSM (but not in tracheal smooth muscle) relaxations that seem to involve opening of K+ channels (including those of the large-conductance Ca(+2)-dependent type) by EFS-liberated free radicals.

Animals↗
PubMedDate not supplied

Vanadate and cardiovascular system.

Rats were given 1, 10, 40, or 100 ppm of vanadium in drinking water for seven months, while rabbits received 1 ppm of vanadium (as sodium metavanadate, NaVO3) in drinking water for twelve months. Rats developed arterial hypertension through complex effects of vanadium on central neurogenic pathways, central and periferal catecholaminergic mechanisms, specific autacoidal systems (kallikrein-kinin, reninangiotensin-aldosterone, enkephalin ones), and effectors (vessels and heart). The above effects of vanadium were in part confirmed in the rabbits which, however, did not show arterial hypertension since the increase of vascular resistance was counteracted by a reduction of both cardiac inotropism and cardiac output. Vanadium was accumulated in tissues as vanadyl; higher levels were found in the bone and in the kidney, but relevant amounts were determined in aorta, heart and brain. There was evidence, in the rabbits, that vanadium reduces synthesis and/or release of nitric oxide, the endothelium-derived vasodilating factor, likely through a reduced formation from bradykinin. The functional, analytical and morphological results obtained in this study show that chronic exposure to vanadium induces arterial hypertension by mechanisms only in part related to the levels and times of exposure, and to the species.

Animals↗
PubMed1996

[An ultrastructural study of the apical cytoskeleton of the epithelial cells in the frog bladder with an ADH-dependent and an ADH-independent increase in osmotic permeability].

Immunocytochemical methods of electron and confocal microscopy were applied for studying the primembrane actin cytoskeleton in the frog urinary bladder granular cells, following the two actions: under the increased vasopressin-induced water permeability, and following autacoid removal by multiple changes of the Ringer solution around the serosa. In both cases similar changes have been revealed in the structure of the apical cytoskeleton and, in addition, a decrease in the density of its actin filament distribution was noticed.

Animals↗
PubMed1996

[Cardioactive hormones: bradykinin].

Kinins are autacoids affecting B2-receptors of many organs. They are involved in autocrine and paracrine mechanisms which are crucial in organ protection. Because of rapid degradation their effects are only short acting. Therefore, inhibition of degradation by ACE-inhibitors increases their pharmacological effects, and is of significant importance for therapy of cardiovascular diseases. Blood pressure lowering and cardioprotective effects are most important and can be explained by actions on the endothelium. The participation of kinins in blood pressure decrease during ACE inhibitor treatment can be estimated from animal experiments at about 50%. With respect to regression of cardiovascular hypertrophy or increase in insulin sensitivity their participation might be even more significant. The role of kinins in cardiovascular diseases as a pathophysiologic correlate has to be elucidated in further investigations.

Angiotensin-Converting Enzyme Inhibitors↗
PubMedDate not supplied

Expression of nitric oxide synthase in human peripheral blood mononuclear cells and neutrophils.

It has been clearly demonstrated in rodents that nitric oxide (NO) plays an important role in host defense and immunity. However, evidence that human leukocytes express inducible nitric oxide synthase (iNOS) or its products has been inconclusive and a source of controversy. We report that iNOS could not be detected in human monocytes, HL-60 cells, neutrophils, and T cells by Western blotting analysis (< or = 10 pg) or by radiolabeled L-arginine-to-L-citrulline conversion (< or = 20 pmol L-citrulline) under conditions sufficient to induce iNOS in the rodent system and in human hepatocytes, which include activation with cytokines, endotoxins, and/or chemoattractants. However, sensitive methods such as RT-PCR and Northern blot analysis show "constitutively expressed" iNOS mRNA from human monocytes, neutrophils, Jurkat cells, and HL-60 cells. This iNOS mRNA is 4.4 kb and is similar to that seen in human hepatocytes and rodent macrophages. In spite of the constitutive expression of mRNA in neutrophils and the lack of detectable NOS activity (based on Western blotting and L-arginine-to-L-citrulline conversion assay), stimulation of human neutrophils unit FMLP in vitro induced the ADP-ribosylation of an intracellular NO target, glyceraldehyde-3-PO4 dehydrogenase (GAPDH), in a NO-dependent manner. These studies indicate that low levels of NOS protein are expressed in neutrophils (and perhaps T cells and monocytes) and produce NO following stimulation. The data indicate that, in addition to its phagocytic and tumoricidal activity. NO may also function as an autacoid signaling molecule within the cells.

Adenosine Diphosphate Ribose↗
PubMed1997

Arachidonic acid derivatives and renal function in liver cirrhosis.

Prostaglandins (PGs) are arachidonic acid (AA) derivatives via the PG endoperoxyde H synthase (PGHS) complex. Two PGHS isoforms have been recognized, constitutive (PGHS-1) and inducible (PGHS-2), respectively. Within the kidney, vascular endothelium mainly produces PGI2; the whole glomerulus synthesizes several prostanoids, the predominant AA metabolite in humans being PGI2; tubules and medullary interstitial cells produce mainly PGE2. Renal PGs modulates the action of other hormones and autacoids involved in the regulation of renal hemodynamics, glomerular filtration and the renal handling of sodium and water. Renal PGs are, at least in part, excreted into urine. Measurement of urinary PGs or their metabolites has been found to provide a reliable estimation of basal as well as stimulated PG synthesis. Patients with cirrhosis of the liver show an increased renal synthesis of vasodilating PGs, as indicated by the high urinary excretion of PGs and/or their metabolites. Administration of nonsteroidal anti-inflammatory drugs (NSAIDs) to these patients causes a profound reduction in renal blood flow and glomerular filtration rate, a reduction in sodium excretion, and an impairment of free water clearance. These data clearly indicate that the increased renal synthesis of vasodilating PGs has a relevant role in maintaining renal hemodynamics, sodium and water excretion in a clinical setting characterized by a reduction of effective plasma volume and a striking activation of the major vasoconstricting systems, namely the renin-angiotensin-aldosterone, the sympathetic nervous system, and vasopressin. Patients with hepato-renal syndrome have a reduced renal synthesis of vasodilating PGE2 in the setting of a striking activation of endogenous vasoconstrictors and a maintained or increased renal production of thromboxane A2. Therefore, an imbalance between vasoconstricting systems and the renal vasodilator PGE2 was proposed to explain the renal failure observed in this condition. The urinary excretion of 2-3-dinor 6-keto-PGF1 alpha, an index of systemic PGI2 synthesis, is increased in patients with cirrhosis and hyperdynamic circulation, thus raising the possibility that systemic synthesis of PGI2 may contribute to the arterial vasodilatation of these patients. Finally, administration of exogenous prostanoids to patients with cirrhosis is not effective either in ameliorating renal function or in preventing the deleterious effect of NSAIDs.

Animals↗
PubMed1997

Induction of cyclooxygenase-2 by parathyroid hormone in human osteoblasts in culture.

OBJECTIVE: Parathyroid hormone (PTH) induced bone resorption by osteoclasts depends on the presence of osteoblasts. PTH induced production of prostaglandins by osteoblasts and induction of bone resorption by prostaglandins suggest that these autacoids may be implicated in the effects of PTH on bone. Our objective was to determine if the increase in prostaglandin production induced in human osteoblasts by PTH is due to an increase in cyclooxygenase-2 (COX-2) expression. METHODS: Primary cultures of human osteoblasts were obtained from specimens of trabecular bone. Confluent cells were treated with PTH, dexamethasone or compound NS-398, a specific COX-2 inhibitor. The concentration of prostaglandin E2 (PGE2) in the supernatants was determined by radioimmunoassay and COX-2 mRNA levels evaluated by Northern blot. RESULTS: PTH induced COX-2 mRNA expression and PGE2 production. These effects were time and concentration dependent and were inhibited by dexamethasone. Compound NS-398 reduced PGE2 production to the same extent as dexamethasone, and neither compound had an additive effect on this variable. CONCLUSION: These results show that PTH induces COX-2 expression in human osteoblasts in culture and suggest that this isoenzyme is the main factor in the control of prostaglandin synthesis in these experimental conditions.

Cells, Cultured↗
PubMedDate not supplied

[Study of the efficacy of prostaglandins and prostacyclin in decrease of osmotic permeability of the frog urinary bladder].

Washout of autacoids using a repeated change of serosal Ringer solution of the frog urinary bladder was accompanied by a pronounced rise in the osmotic water permeability. A decrease in the osmotic water permeability was achieved by addition at the serosal Ringer solution of different eikosanoids at concentrations of 10(-10)-10(-6) M. According to efficiency of the recovery of the low osmotic water permeability, the substances studied showed the following order: prostaglandin E1 > prostaglandin > E2 > prostaglandin F2 alpha > (prostaglandin I2). The data obtained indicate a role of the endogenous prostaglandin production in maintaining of the low osmotic water permeability.

Alprostadil↗
PubMed1980

Slow-reacting substances and their structural elucidation.

For more than forty years since their discovery, the structure of a group of closely related materials known collectively as slow-reacting substances has been unknown. These substances are released from a variety of tissues in response to immunological or non-immunological stimulation. A slow-reacting substance is believed to be implicated in hypersensitivity reactions such as asthma; in order to fully understand its bronchoconstrictor role, the structural elucidation of these materials has been a necessary (albeit difficult) task. Studies on both immunologically generated slow-reacting substance of anaphylaxis (SRS-A) and other slow-reacting substances (SRSs) have indicated a precursor role for arachidonic acid in their biosynthesis; this, coupled with enzymic and chemical activity destruction data, gave an insight into the structure of these moieties. In order to define the structure of these materials homogeneous SRS-A was required; a purification scheme was developed relying on the high resolution separative capability of reverse-phase high pressure liquid chromatography, resulting in extensively purified SRS-A. It was then possible to demonstrate that SRS-A possessed a characteristic ultraviolet spectrum, allowing us for the first time to define a major structural moiety in the molecule (conjugated triene). To complement studies on, and to act as a model for the more pathologically relevant SRS-A, a slow-reacting substance was produced from rat basophilic leukaemia (RBL-1) cells. The structure of this biologically active species has been determined by mass spectrometric examination of the intact molecule as a derivative, together with analytical protein chemical studies, and shown to be the novel peptidolipid 5-hydroxy-6-cysteinylglycinyl-7,9,11,14-eicosatetraenoic acid.

Animals↗
PubMed1985

Substance P-like immunoreactivity is present in the central nervous system of Limulus polyphemus.

The distribution of substance P-like immunoreactivity (substance P-li) in the central nervous system of Limulus polyphemus was studied by using indirect immunocytochemical techniques. Six bilaterally symmetrical pairs of cell clusters in the circumesophageal connectives and the subesophageal mass contain substance P-li. Two of those pairs are the source of a system of efferent fibers that is involved in the expression of circadian rhythms of photosensitivity by the lateral eye. Substance P-li-containing cells were also observed scattered along the length of the circumesophageal connectives, which contain abundant stained fibers and some terminals. Substance P-li fibers leave through the ventral and dorsal nerves of the posterior circumesophageal ring. The neuropil of the subesophageal mass contains an abundance of stained terminals. Immunoreactive fibers can be seen throughout the length of the two longitudinal connectives of the ventral cord, in discrete fiber tracts in the lateral edges of the interganglionic connectives, and in the dorsal and ventral nerves of abdominal ganglia 1-4. Each of these ganglia contains three pairs of substance P-immunoreactive cell body clusters: an anterolateral, a medial longitudinal, and a medial posterior cluster. Substance P-li fibers entering through the ventral (posterior) nerves form very distinctive fascicles in each side of the ganglia, giving off fibers throughout their length. The neuropil is filled with immunoreactive terminals distributed homogeneously. The anterolateral clusters of the abdominal ganglia may be involved in cardioregulation. The six pairs of clusters in the posterior circumesophageal ring, and perhaps some of those in the abdominal ganglia, are believed to constitute a neurosecretory system, projecting to multiple targets throughout the organism. This system is postulated to modulate various sensory inputs and motor activity, and could be driven by a circadian clock, as well as by other systems responsible for integrated organismic responses.

Animals↗
PubMed1982

Release of platelet-activating factor (PAF-acether) and leukotrienes C and D from inflammatory macrophages.

Macrophages (M phi) isolated from the peritoneal cavity of C57BL/6 mice were either untreated or treated with various eliciting agents (thioglycollate, sodium caseinate) or with an activating agent bacillus Calmette Guérin (BCG). The various populations were assessed for their ability to release platelet-activating factor (PAF-acether), an ether phospholipid mediator, and slow-reacting substance (SRS), a lipoxygenase arachidonic acid derivative. PAF-acether was recovered in higher amounts form BCG M phi than from resident M phi, whereas elicited M phi exhibited a marked decreased ability to release this mediator. Such variations were only quantitative as evidenced by the similar enzyme sensitivity and high pressure liquid chromatography (HPLC) retention times of the various PAF-acether-containing supernatants. Resident, BCG- and sodium caseinate-induced M phi released similar amounts of SRS, whereas thioglycollate M phi exhibited once again a marked decreased ability to release this mediator. Comparing retention times on HPLC of resident and BCG M phi SRS with those of synthetic leukotrienes C and D, molecular variations were noted. Even though both M phi populations released higher amounts of leukotrienes C than D, the D/C ratio was higher in BCG M phi than in resident M phi. These results show that different environmental factors can influence the release of PAF-acether and leukotrienes from M phi.

Animals↗
PubMed1998

Identification of one tachykinin- and two kinin-related peptides in the brain of the white shrimp, Penaeus vannamei.

This paper reports the purification of three myotropic neuropeptides from the white shrimp Penaeus vannamei. The central nervous systems of 3500 shrimps were extracted in an acidified solvent, after which four to five HPLC column systems were used to obtain pure peptides. A cockroach hindgut muscle contraction bioassay was used to monitor all collected fractions. The pure peptides were submitted to Edman degradation based automated microsequencing. Mass spectrometry and chemical synthesis confirmed the sequences. Ala-Pro-Ser-Gly-Phe-Leu-Gly-Met-Arg-NH2 (Pev-tachykinin, 934.1 Da) belongs to the tachykinin family with identified members in all vertebrate classes and some invertebrate classes: arthropods, annelids and molluscs. A very specific Pev-tachykinin antiserum was developed, which labels 4 neurosecretory cells in the brain. Ala-Ser-Phe-Ser-Pro-Trp-Gly-NH2 (Pev-kinin 1, 749.8 Da) and Asp-Phe-Ser-Ala-Trp-Ala-NH2 (Pev-kinin 2, 694.7 Da) are the first crustacean kinins. Pev-kinin 2 is the first kinin with a Trp-Ala-NH2 instead of a kinin-typical Trp-Gly-NH2 carboxyterminus.

Animals↗
PubMed2001

Down-regulation and recovery of endothelin-1 binding and signaling in rat cardiomyocytes.

Down-regulation and recovery of endothelin (ET) receptors and of ET-dependent phosphoinositide-specific phospholipase C (PI-PLC) signaling was examined in cultured cardiomyocytes from neonatal rats. Three hours treatment with 5 nM ET-1 decreased surface receptors to 30%, and transduction to 19%, of their respective time-zero values. After extensive washing and a 3 h recovery period surface receptors returned to 74% of the time-zero value, with concomitant recovery of signal transduction to 75% of the time-zero value. The recovery of PI-PLC signaling in these cells is in contrast with a previous report, but consistent with recovery of the receptor complement.

Animals↗
PubMed1979

Slow-reacting substance of anaphylaxis: studies on purification and characterisation.

We have demonstrated the role of arachidonic acid and lipoxygenase in the genesis of SRS-A and the possible role of lipoxygenases in its metabolism. SRS-A has been purified in microgram quantities together with closely related material. We have identified 5,12 di-hydroxy-6, 8, 10, 14 eicosatetranenoic acid released by antigen challenge, and which we feel is related to SRS-A. Further structural work is in progress.

Animals↗
PubMed1987

Behavioural effects of intrathecally injected tachykinins in rats with peripheral nerve transection.

The effect of unilateral sciatic nerve transection on behavioural responses produced by intrathecal administration of substance P (SP), neurokinin A, eledoisin and physalaemin was investigated in the rat. The injection of SP (3 nmol/rat) into the subarachnoid space was followed by reciprocal scratching, biting and licking of the fore- and hind-limbs. There was no observable difference in the behavioural response to SP between rats with nerve transection and sham operated rats at 5 days after operation. Whereas at 10, 20, and 30 days after nerve transection the response to SP was significantly increased as compared with sham operated rats. This phenomenon was also observed with neurokinin A (1.5, 3.0 and 6.0 nmol/rat), eledoisin (0.05 and 0.10 nmol/rat) and physalaemin (0.05 and 0.10 nmol/rat) at 10 days after operation. Ipsilateral depletion of SP from the lumbar (L4-L6) spinal cord was observed at 5, 10, 20, and 30 days after the unilateral transection of the sciatic nerve. These results suggest that sciatic nerve transection may produce an increased response to tachykinins through an enhanced sensitivity of tachykinin receptors in the lumbar cord.

Animals↗