The phosphatidylinositol response of chondrocytes in culture

1989 ◽  
Vol 27 (3-4) ◽  
pp. 428-430 ◽  
Author(s):  
V. M. Baragi ◽  
D. T. Dudley ◽  
D. J. Schrier
Keyword(s):  
Phosphatidylinositol Response

scholarly journals Evidence for a role of phosphatidylinositol turnover in stimulus–secretion coupling. Studies with rat peritoneal mast cells

1979 ◽  
Vol 178 (3) ◽  
pp. 681-687 ◽  
Author(s):  
Shamshad Cockcroft ◽  
Bastien D. Gomperts
Keyword(s):  
Mast Cells ◽  
Concanavalin A ◽  
Immunoglobulin E ◽  
Histamine Secretion ◽  
Phosphatidylinositol Turnover ◽  
Phosphatidylinositol Response ◽  
Peritoneal Mast Cells ◽  
Stimulus Secretion Coupling ◽  
Rat Peritoneal Mast Cells

Histamine secretion and phosphatidylinositol turnover were compared in antigen-sensitized rat peritoneal mast cells stimulated with a number of different ligands. A small and variable increase in the incorporation of [32P]Pi and of [3H]inositol into phosphatidylinositol was observed when the cells were treated with immunoglobulin E-directed ligands (antigens and concanavalin A), and this was accompanied by a low amount of secretion (<10% of total cell histamine). In the presence of added phosphatidylserine, the addition of immunoglobulin E-directed ligands invariably led to an enhanced rate (approx. 4-fold) of labelling of phosphatidylinositol and, in the presence of Ca2+, this was accompanied by the secretion of histamine. The labelling of phosphatidylinositol and histamine secretion were also stimulated by chymotrypsin and compound 48/80. Whereas the phosphatidylinositol response did not require the presence of extracellular Ca2+, the secretion of histamine was either enhanced or dependent on extracellular Ca2+ (depending on the ligand used). The dependence on ligand concentration for the phosphatidylinositol response and histamine secretion were similar. The increased isotopic incorporation into phosphatidylinositol continued for about 1h although histamine secretion (elicited with concanavalin A) stopped within 2min. These results support the proposition that metabolic events involving phosphatidylinositol play a necessary intermediate role in the regulation of Ca2+ channels by ligand-activated receptors.

NONDEPOLARIZING MUSCLE RELAXANTS ATTENUATE CONTRACTILE RESPONSE AND PHOSPHATIDYLINOSITOL RESPONSE OF RAT TRACHEA

1998 ◽  
Vol 86 (Supplement) ◽  
pp. 457S
Author(s):  
S. Hashimoto ◽  
O. Shibata ◽  
A. Tsuda ◽  
S. Iwanaga ◽  
T. Makita ◽  
...  
Keyword(s):  
Contractile Response ◽  
Muscle Relaxants ◽  
Nondepolarizing Muscle Relaxants ◽  
Phosphatidylinositol Response ◽  
Rat Trachea

scholarly journals The relationship of phosphatidylinositol turnover to receptors and calcium-ion channels in rat parotid acinar cells

1981 ◽  
Vol 194 (2) ◽  
pp. 463-468 ◽  
Author(s):  
S J Weiss ◽  
J W Putney
Keyword(s):  
Membrane Permeability ◽  
Cholinergic Receptor ◽  
Phosphatidylinositol Turnover ◽  
Phosphatidylinositol Response ◽  
Gating Mechanism ◽  
32P Incorporation ◽  
Rat Parotid ◽  
Relationship Of ◽  
The Relationship ◽  
K Permeability

To help elucidate the possible role of phosphatidylinositol in the regulation of membrane permeability to Ca2+, the relationship in the rat parotid gland of phosphatidylinositol turnover to hormone receptor binding and to the hormone-mediated increase in K+ permeability (a Ca2+-dependent phenomenon) was investigated. The concentrations of adrenaline and substance P required to stimulate phosphatidylinositol turnover were found to be similar to those required for the Ca2+-mediated change in K+ permeability and for ligand binding. However, in the case of muscarinic (cholinergic) receptor stimulation, the phosphatidylinositol response was better correlated to the increase in membrane permeability to Ca2+, as determined by the change in K+ permeability, than to receptor occupation. Consistent with this relationship between the phosphatidylinositol response and Ca2+-channel activation were results obtained by simultaneous administration of maximal or submaximal concentrations of muscarinic and alpha-adrenergic agonists. The extent of 32P incorporation when stimulated by maximal concentrations of two agonists did not summate, but, rather, was intermediate between the response of either agonist alone. One interpretation for these observations is that the phosphatidylinositol response may not be related to receptor occupation or activation, but may be involved in the Ca2+-gating mechanism itself.

scholarly journals The effects of denervation on phosphatidylinositol-response in the rat vas deferens

1982 ◽  
Vol 32 ◽  
pp. 115
Author(s):  
Katsutoshi Goto ◽  
Tadaomi Takenawa ◽  
Takeshi Endo ◽  
Takao Arai ◽  
Tomoh Masaki
Keyword(s):  
Vas Deferens ◽  
Rat Vas Deferens ◽  
Phosphatidylinositol Response

scholarly journals Stimulation of phosphatidylinositol turnover in various tissues by cholinergic and adrenergic agonists, by histamine and by caerulein

1979 ◽  
Vol 182 (3) ◽  
pp. 669-676 ◽  
Author(s):  
Lynne M. Jones ◽  
Shamshad Cockcroft ◽  
Robert H. Michell
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Lacrimal Gland ◽  
Plasma Membranes ◽  
Partial Agonist ◽  
Muscarinic Agonist ◽  
Guinea Pig Ileum ◽  
Phosphatidylinositol Response ◽  
Muscarinic Cholinergic ◽  
Stimulation Of

Studies are reported of the biochemical and pharmacological characteristics of the stimulation of phosphatidylinositol metabolism that is produced in appropriate target tissues by stimulation of various receptors that use Ca2+ as their second messenger. (1) Muscarinic cholinergic and α-adrenergic phosphatidylinositol responses were observed in rat lacrimal gland, and a response to caerulein was detected in the longitudinal smooth muscle of guinea-pig ileum. (2) The muscarinic cholinergic phosphatidylinositol response of rat lacrimal gland, like that of several other tissues, is not dependent on the availability of extracellular Ca2+. (3) Three phosphatidylinositol responses, namely to histamine in guinea-pig ileum smooth muscle, to α-adrenergic stimulation in rat vas deferens and to muscarinic cholinergic stimulation in rat lacrimal gland, were all found to involve phosphatidylinositol breakdown. (4) The stereospecificity of the muscarinic receptor responsible for the phosphatidylinositol response of guinea-pig pancreas was tested by using the two stereoisomeric forms of acetyl-β-methylcholine; the S-isomer was very much more active than the R-isomer in provoking both phosphatidylinositol breakdown and its labelling with 32P, as it is in provoking other physiological responses such as contractility or secretion. (5) Pilocarpine, a muscarinic partial agonist, provoked a significantly smaller phosphatidylinositol breakdown in rat parotid fragments than did carbamoylcholine, a potent muscarinic agonist. (6) All of these results are consistent with, but do not prove, a previously offered hypothesis that suggests that phosphatidylinositol breakdown is a reaction essential to stimulus–response coupling at a variety of cell-surface receptors that mobilize Ca2+ from and through the plasma membranes of target tissues.

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