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PubMed1995

Pre- and postjunctional effects of diadenosine polyphosphates in the guinea-pig vas deferens.

The pre- and postjunctional activities of a number of diadenosine polyphosphates were examined in the guinea-pig isolated vas deferens at the level of the membrane potential, using a modified sucrose-gap technique. P1,P3-Di(adenosine 5')triphosphate (Ap3A), P1,P4-di(adenosine 5')tetraphosphate (Ap4A) and P1,P5-di(adenosine 5')pentaphosphate (Ap5A) all caused concentration-dependent depolarization of the smooth muscle membrane. The potency order was: Ap5A > Ap4A > or = Ap3A. P1,P2-Di(adenosine 5')pyrophosphate (Ap2A) did not evoke depolarization even at the highest concentration tested (1 mM). All the dinucleotides caused a reduction in the amplitude of evoked excitatory junction potentials (e.j.ps). The potency order was: Ap5A = Ap4A > Ap3A > Ap2A. The depolarizations evoked by the dinucleotides were markedly reduced by the selective P2X-purinoceptor antagonist, pyridoxalphosphate-6-azophenyl-2',4'-disulphonic acid (PPADS, 10 microM), as was the amplitude of the fully facilitated e.j.p. The inhibition of the e.j.p. evoked by Ap3A and Ap2A was reduced by the P1-purinoceptor antagonist, 8-p-sulphophenyltheophylline (8-pSPT, 50 microM), but that evoked by Ap5A and Ap4A was not. Thus, Ap3A, Ap4A and Ap5A evoke depolarization of the guinea-pig vas deferens via P2X-purinoceptors, and additionally Ap2A and Ap3A exert a prejunctional effect via P1-purinoceptors. The prejunctional activity of Ap4A and Ap5A is mediated via an undefined purinoceptor, which is neither P1 nor P2X.

Animals↗
PubMed1993

Control of inositol polyphosphate-mediated calcium mobilization by arachidonic acid in pancreatic acinar cells of rats.

1. The patch-clamp technique of whole-cell current recording was applied to single, enzymatically isolated, rat pancreatic acinar cells to investigate the current responses evoked by internal perfusion of inositol polyphosphates (InsPx). The InsPx were included in the solution filling the recording pipette and inositol 1,4,5-trisphosphate (Ins(1,4,5)P3; 10 microM) evoked transient current responses generally of less than 1 min duration, inositol 2,4,5-trisphosphate (Ins(2,4,5)P3; 10 microM) evoked smaller current transients while inositol 1,3,4,5-tetrakisphosphate (InsP4; 10 microM) evoked no detectable current response. However, in the presence (in external bathing solution) of the phospholipase A2 inhibitor 4-bromophenacyl bromide (4-BPB; 8 microM) all three of the InsPx now evoked prolonged current responses lasting for several minutes. The current responses to all three InsPx were abolished by inclusion of the Ca2+ chelator EGTA (5 mM) in the internal, pipette-filling solution indicating that the responses are calcium dependent and reflect the effect of the InsPx in increasing intracellular Ca2+. Inositol 1,3,4,5,6-pentophosphate (InsP5) induced no current response when tested up to 20 microM in the presence or absence of 4-BPB. 2. The potentiating effect of 4-BPB on the InsPx-induced current responses was not mimicked by application of arachidonic acid (AA) oxidation inhibitors; indomethacin (20 microM), nordihydroguaiaretic acid (20 microM) or proadifen (SKF525A, 100 microM). The effects of 4-BPB were countered however, by the inclusion of 2 microM AA in the external solution. The results suggest that the 4-BPB potentiates the response by inhibiting the activity of phospholipase A2, thereby reducing the formation of AA. 3. In the presence of 4-BPB (8 microM) the InsPx-evoked responses were dose dependent with an increase in both the amplitude and speed of onset with increasing concentrations. In the presence of 4-BPB InsP4 was as efficient as Ins(1,4,5)P3 both in terms of speed of onset and amplitude of responses; the efficacy and dissociation constant (Kd) for both of these InsPx were the same at 1 microM and 45 nM respectively. Ins(2,4,5)P3 was always less effective, with an efficacy and Kd of 10 microM and 750 nM respectively. 4. If 4-BPB was applied after the current responses evoked by the InsPx were over, or if guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S) was included in the recording pipette then the phospholipase inhibitor gave rise to an additional, prolonged, current response.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetophenones↗
PubMed1996

Possible role of diadenosine polyphosphates as modulators of cardiac sensory-motor neurotransmission in guinea-pigs.

1. Isolated guinea-pig atria were used to study the neuromodulatory effect of diadenosine polyphosphates (APnA) on cardiac capsaicin-sensitive sensory-motor neurotransmission. 2. In the presence of atropine, guanethidine and propranolol, electrical field stimulation (EFS) of the atrial preparations evoked a positive inotropic response which is known to be mediated by release of calcitonin gene-related peptide (CGRP) from sensory-motor nerves. P1,P2-diadenosine pyrophosphate (AP2A), P1,P3-diadenosine triphosphate (AP3A), P1,P4-diadenosine tetraphosphate (AP4A), P1,P5-diadenosine pentaphosphate (AP5A) and P1,P6-diadenosine hexaphosphate (AP6A) inhibited in a concentration-dependent way (0.1-30 microM) cardiac responses to EFS. The inhibitory effect of APnA was mimicked by adenosine. 3. All the APnA tested had a direct negative inotropic effect, by reducing in a concentration-dependent manner the basal contractile tension. The inotropism of APnA was comparable to that of adenosine. 4. Both inhibition of cardiac responses to EFS and negative inotropism of AP2A, AP3A and AP4A were sensitive to the antagonism by the A1 adenosine receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX; 0.1-1 nM). The extent of antagonism of DPCPX for the APnA tested was comparable to that for adenosine. 5. Despite the direct negative inotropism, AP4A tested at the highest concentration used did not affect the cardiac responses to the neurotransmitter CGRP, applied exogenously. 6. These results have demonstrated that in isolated guinea-pig atria APnA inhibited sensory-motor neurotransmission, without affecting cardiac responses to exogenous CGRP. The effect of APnA was sensitive to antagonism by DPCPX, which suggests it operates via the activation of prejunctional A1 adenosine receptors. A postjunctional negative inotropism was also shown, mediated by myocardial A1 adenosine receptors.

Adenine Nucleotides↗
PubMed2002

Vasoactivity of diadenosine polyphosphates in human small mesenteric resistance arteries.

Diadenosine polyphosphates (ApnA) (n = 3-6) induced vasoconstrictions in isolated human mesenteric resistance arteries (hMRAs) mounted in a microvessel myograph (rank order of potency: Ap5A > Ap6A > Ap4A > Ap3A). The contractile effects of ApnA in hMRA were similar to their effects in rat MRA investigated previously. ATP, ADP, AMP, and adenosine had less contractile potency than ApnA, suggesting that the observed effects were not induced by the degradation products of ApnA. Ap4A- and Ap5A-induced vasoconstriction was inhibited by pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid (PPADS) (P2X purinoceptor antagonist) but not by ADP3'5' (P2Y purinoceptor antagonist). Thus, this purinergic vasoconstriction of hMRA seems to be P2X but not P2Y purinoceptor-mediated. In precontracted hMRA all ApnA caused vasorelaxations but (in contrast to rat MRA) the potencies of the ApnA did not differ significantly from each other. The ApnA degradation products had less vasorelaxing potency than ApnA, demonstrating that the vasorelaxations can be ascribed to the ApnA themselves. Ap5A-induced vasorelaxation of hMRA could neither be inhibited with ADP3'5' nor with PPADS, which reveals a decisive difference to the rat MRA where the inhibitory profile demonstrated the importance of the P2Y purinoceptor for Ap5A-induced vasorelaxation. However, Ap4A-induced vasorelaxation in hMRA could be inhibited by ADP3'5'. These findings show that Ap4A-induced vasorelaxation in hMRA is due to P2Y purinoceptor activation, that Ap5A evokes vasorelaxation in hMRA via another mechanism than Ap4A, and that data derived from the animal model cannot be simply transferred to human conditions.

Animals↗
PubMed2004

Protocols for regulation and study of diphosphoinositol polyphosphates.

The roles of diphosphoinositol polyphosphates (DIPs) in mammalian cell biology have been difficult to determine because of the lack of tools known to regulate their levels. I have determined a series of protocols that regulate these DIPs, and these can be used to further our understanding of these molecules. Sorbitol and sucrose significantly raised levels of bis-diphosphoinositol tetrakisphosphate ([PP]2-InsP4) but slightly lowered levels of diphosphoinositol pentakisphosphate (PP-InsP5) in DDT1 MF-2 cells. These effects correlate with the ability of hyperosmotic stress to interfere with protein trafficking described previously and suggest that [PP]2-InsP4 specifically impedes protein trafficking. The effects on [PP]2-InsP4 were not regulated by extracellular signal-regulated kinase or phospholipase D, as exemplified by the lack of effect of U0126 and butan-1-ol. I have also found that genistein potently and rapidly lowers levels of [PP]2-InsP4, whereas a similar inhibitor, herbimycin, was without effect. Thapsigargin, a sarcoplasmic-endoplasmic reticulum Ca(2+)-ATPase pump inhibitor previously shown to selectively lower PP-InsP5 after short-term treatment, also selectively raises PP-InsP5 after a longer treatment. The calmodulin inhibitors N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7) and chlorpromazine significantly lowered all higher inositol phosphates, as well as DIPs, whereas the calmodulin-dependent kinase inhibitors methyl 9-(S)-12-(R)-epoxy-1H-diindolo[1,2,3-fg:3',2',1'-kl]pyrrolo[3,4-i][1,6]benzodiazocine-2,3,9,10,11,12-hexahydro-10-(R)hydroxy-9-methyl-1-oxo-10-carboxylate (K-252a) and 2-[N-(2-hydroxyethyl)-N-(4-methoxybenzenesulfonyl)]amino-N-(4-chlorocinnamyl)-N-methylbenzylamine (KN-93) were without effect. W-7 and chlorpromazine also lowered levels of phosphatidylinositol 4,5-bisphosphate and ATP but greatly increased levels of phosphatidylinositol 4-phosphate. Trypan blue exclusion deemed that these doses were not cytotoxic. These results identify an increasing number of reagents that regulate DIP levels. Using these tools, and those described previously, we can further understand the roles of the DIPs in cell biology.

Animals↗
PubMed1999

A phospholipase C-dependent inositol polyphosphate kinase pathway required for efficient messenger RNA export.

In order to identify additional factors required for nuclear export of messenger RNA, a genetic screen was conducted with a yeast mutant deficient in a factor Gle1p, which associates with the nuclear pore complex (NPC). The three genes identified encode phospholipase C and two potential inositol polyphosphate kinases. Together, these constitute a signaling pathway from phosphatidylinositol 4, 5-bisphosphate to inositol hexakisphosphate (IP6). The common downstream effects of mutations in each component were deficiencies in IP6 synthesis and messenger RNA export, indicating a role for IP6 in GLE1 function and messenger RNA export.

Biological Transport↗
PubMed2002

Polyphosphate kinase from activated sludge performing enhanced biological phosphorus removal.

A novel polyphosphate kinase (PPK) was retrieved from an uncultivated organism in activated sludge carrying out enhanced biological phosphorus removal (EBPR). Acetate-fed laboratory-scale sequencing batch reactors were used to maintain sludge with a high phosphorus content (approximately 11% of the biomass). PCR-based clone libraries of small subunit rRNA genes and fluorescent in situ hybridization (FISH) were used to verify that the sludge was enriched in Rhodocyclus-like beta-Proteobacteria known to be associated with sludges carrying out EBPR. These organisms comprised approximately 80% of total bacteria in the sludge, as assessed by FISH. Degenerate PCR primers were designed to retrieve fragments of putative ppk genes from a pure culture of Rhodocyclus tenuis and from organisms in the sludge. Four novel ppk homologs were found in the sludge, and two of these (types I and II) shared a high degree of amino acid similarity with R. tenuis PPK (86 and 87% similarity, respectively). Dot blot analysis of total RNA extracted from sludge demonstrated that the Type I ppk mRNA was present, indicating that this gene is expressed during EBPR. Inverse PCR was used to obtain the full Type I sequence from sludge DNA, and a full-length PPK was cloned, overexpressed, and purified to near homogeneity. The purified PPK has a specific activity comparable to that of other PPKs, has a requirement for Mg(2+), and does not appear to operate in reverse. PPK activity was found mainly in the particulate fraction of lysed sludge microorganisms.

Anaerobiosis↗
PubMed1981

Stringent response of Bacillus stearothermophilus: evidence for the existence of two distinct guanosine 3',5'-polyphosphate synthetases.

Bacillus stearothermophilus reacted to pseudomonic acid-induced inhibition of isoleucine-transfer ribonucleic acid (RNA) acylation and to energy downshift caused by alpha-methylglucoside addition with accumulation of guanosine 3',5'-polyphosphates [(p)ppGpp] and restriction of RNA synthesis. In vitro studies indicated that (p)ppGpp was synthesized by two different enzymes. One enzyme, (p)ppGpp synthetase I, was present in the ribosomal fraction, required the addition of a ribosome-messenger RNA-transfer RNA complex for activation, and was inhibited by tetracycline and thiostrepton. It is suggested that (p)ppGpp synthetase I is comparable to the relA gene product from Escherichia coli and is responsible for (p)ppGpp accumulation during amino acid starvation. The other enzyme, (p)ppGpp synthetase II, was found in the high-speed supernatant fraction (S100). It functioned independently of ribosomes, transfer RNA, and messenger RNA and was not inhibited by the above-mentioned antibiotics. (p)ppGpp synthetase II is thought to be responsible for (p)ppGpp accumulation during carbon source downshift. The two enzymes differ in their Km values for adenosine triphosphate (ATP):2mM ATP for synthetase I and 0.05 mM ATP for synthetase II. They also have different molecular weights: apparent Mr of 86,000 (+/- 5,000) for synthetase I and 74,000 (+/- 5,000) for synthetase II.

Geobacillus stearothermophilus↗
PubMed1989

Glycogen-bound polyphosphate kinase from the archaebacterium Sulfolobus acidocaldarius.

Glycogen-bound polyphosphate kinase has been isolated from a crude extract of Sulfolobus acidocaldarius by isopycnic centrifugation in CsCl. Divalent cations (Mn2+ greater than Mg2+) stimulated the reaction. The enzyme does not require the presence of histones for its activity; it is inhibited strongly by phosphate and slightly by fluoride. The protein from the glycogen complex migrated in a sodium dodecyl sulfate-polyacrylamide gel as a 57-kilodalton protein band; after isoelectric focusing it separated into several spots in the pH range of 5.6 to 6.7.

Glycogen↗
PubMed2000

Inorganic polyphosphate in Vibrio cholerae: genetic, biochemical, and physiologic features.

Vibrio cholerae O1, biotype El Tor, accumulates inorganic polyphosphate (poly P) principally as large clusters of granules. Poly P kinase (PPK), the enzyme that synthesizes poly P from ATP, is encoded by the ppk gene, which has been cloned from V. cholerae, overexpressed, and knocked out by insertion-deletion mutagenesis. The predicted amino acid sequence of PPK is 701 residues (81.6 kDa), with 64% identity to that of Escherichia coli, which it resembles biochemically. As in E. coli, ppk is part of an operon with ppx, the gene that encodes exopolyphosphatase (PPX). However, unlike in E. coli, PPX activity was not detected in cell extracts of wild-type V. cholerae. The ppk null mutant of V. cholerae has diminished adaptation to high concentrations of calcium in the medium as well as motility and abiotic surface attachment.

Amino Acid Sequence↗
PubMed1976

Clinical experience with technetium-99m stannous polyphosphate for myocardial imaging.

Myocardial imaging with technetium-99m stannous polyphosphate was performed on 46 patients. Eleven patients had no cardiac disease, 22 had acute myocardial infarction, and 13 had stable arteriosclerotic heart disease. Distinct patterns of myocardial activity were noted: (1) the patients with no obvious cardiac disease showed no cardiac activity; (2) stable arteriosclerotic heart disease showed faint, ill-defined cardiac activity, primarily in the anterior or inferior aspect of the left ventricle; (3) acute myocardial infarction showed intense, focal, well-defined activity, with a shape that characterized the location of the infarct.

Acute Disease↗
PubMed1979

Estimation of myocardial infarct size in man using 99m Tc polyphosphate.

We have critically evaluated the use of 99m Tc polyphosphate to estimate myocardial infarct size. Optimum conditions were first defined with respect to infarct edge definition, and relative activity over infarct and bone and in blood pool. The scintigrams of 53 patients with acute transmural myocardial infarction were recorded under these defined constant conditions and analysed in various ways. Visual grading of infarct area or intensity correlated poorly with other indices of infarct severity. Computer-assisted measurements of above-background infarct uptake area or of total farct activity correlated well with clinical, electrocardiographic, and enzymatic measurements of infarct severity.

Adult↗
PubMed1978

Recharacterization of fungal dinucleoside polyphosphate (HS3).

Three polyphosphorylated dinucleosides given the pseudonyms of HS3, HS2, and HS1 that were erroneously described as diguanosine polyphosphates (LéJohn, H. B., Cameron, L. E., McNaughton, D. R. & Klassen, G. R. (1975) Biochem, Biophys, Res, Commun. 66, 460-467) have been repurified and partially recharacterized. They have proved to be extremely complex molecules; chemical (HCl and KOH hydrolysis), physical (ultraviolet-light spectral analysis and ion-exchange chromatography), and enzymic (nucleotide pyrophosphatase and bacterial alkaline phosphatase hydrolysis) studies showed that (i) all three HS compounds are uracil rich and (ii) only HS3 contains a purine nucleoside and glutamate. The partial structure of HS3 was deciphered as a moiety of ADP--sugar X--glutamate (the mode of attachment of glutamate is obscure) that is covalently linked to another moiety composed of UDP, mannitol, and four phosphates. Sugar X had chromatographic characteristics of ribitol, but the chromatographic isolate also contained a ninhydrin-sensitive entity presumed to be an amino group. Sugar X, THEREFore, may be an amino sugar polyol. Only the general chemical compositions of HS2 and HS1 were determined. Each contained two uridines and HS2 had 10 phosphates whereas HS1 had 12.

Adenosine Diphosphate↗
PubMed1975

99m-to-polyphosphate bone imaging in Legg-Perthes disease.

99m-Tc--polyphosphate bone imaging was useful in distinguishing Legg-Perthes disease from other childhood hip disorders in 40 patients. In 33 Legg-Perthes patients, imaging provided earlier and more accurate information concerning the extent of the necrotic and revascularization process involving the hip than radiographs alone. This advantage could both facilitate treatment selection and provide a more objective baseline from which to judge treatment results. Preliminary experience also suggests that the technique may offer some insight into the pathogenesis of Legg-Perthes disease.

Child↗
PubMed1976

Early detection of stress fractures using 99mTc-polyphosphate.

Clinical experience with 99mTc-polyphosphate scintigraphy in more than 200 patients with suspected stress fractures is presented. Stress fractures occur in bone which has been weakened as a result of accelerated physiological change induced by excessive muscular and mechanical activity. Unlike traumatic fractures, they are not accompanied by radiographic abnormality early in their course. Bone scintigraphy is sensitive enough to detect the physiological alterations found in stress fractures and was responsible for decreased morbidity in this series of patients due to early diagnosis.

Adolescent↗