scholarly journals The ATP4- receptor of rat mast cells

1980 ◽  
Vol 188 (3) ◽  
pp. 789-798 ◽  
Author(s):  
S Cockcroft ◽  
B D Gomperts
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Concentration Dependence ◽  
Free Acid ◽  
Histamine Secretion ◽  
Phosphatidylinositol Metabolism ◽  
Low Concentrations ◽  
Metabolite Leakage ◽  
High Concentrations ◽  
Rat Mast Cells

The concentration-dependence on exogenous ATP of activation and inhibition of mast-cell histamine secretion, phosphatidylinositol labelling and leakage of metabolites shows that all these functions are regulated by the free acid ATP4-. Maximal histamine secretion and phosphatidylinositol labelling occur with ATP4- at approx. 2 microM, but higher concentrations, which cause inhibition of secretion and phosphatidylinositol labelling, are required to maximize leakage of 32P-labelled metabolites. Both enhancement and inhibition of phosphatidylinositol labelling (due to low and high concentrations of ATP4- respectively) are rapid in onset; histamine secretion is characterized by a delay, especially at low concentrations of ATP4- (approx. 1 microM). Phosphatidylinositol labelling and histamine secretion are dependent on extracellular Ca2+. Metabolite leakage due to the presence of exogenous ATP4- is slow and does not require Ca2+. Of 18 analogues of ATP that were tested, only four were agonists for secretion, and only these four permitted leakage of 32P-labelled metabolites. It is argued that activation and inhibition of histamine secretion, phosphatidylinositol labelling and metabolite leakage are all initiated by ATP4- acting at the same receptor. For mast cells stimulated with ATP4- enhancement of phosphatidylinositol metabolism is not sufficient by itself to cause Ca2+-dependent secretion.

scholarly journals Effect of colchicine on rat mast cells.

1976 ◽  
Vol 71 (1) ◽  
pp. 182-195 ◽  
Author(s):  
D Lagunoff ◽  
E Y Chi
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Cell Shape ◽  
Marked Change ◽  
Polymyxin B ◽  
Inhibitory Effect ◽  
Cell Secretion ◽  
Histamine Secretion ◽  
Release Histamine ◽  
Rat Mast Cells

In the mast cell, a well-developed array of microtubules is centered around the centrioles. Complete loss of microtubules is observed when mast cells are treated with 10(-5) M colchicine for 4 h at 37 degrees C. The loss of ultrastructurally evident microtubules is associated with a marked change in the shape of mast cells from spheroids to highly irregular, frequently elongated forms with eccentric nuclei. In colchicine-treated cells the association of nucleus, Golgi apparatus, and centrioles is also lost. Mast cells exposed to 10(-5) M colchicine for 4 h at 37 degrees C retain 80% of their capacity to release histamine when stimulated by polymyxin B. Exocytosis is evident in stimulated cells pretreated with colchicine and lacking identifiable microtubules. When the conditions of exposure of mast cells to colchicine are varied with respect to the concentration of colchicine, the length of exposure, and the temperature of exposure, dissociation between deformation of cell shape and inhibition of histamine secretion is observed. These observations indicate that microtubules are not essential for mast cell histamine release and bring into question the assumption that the inhibitory effect of colchicine on mast cell secretion depends on interference with microtubule integrity.

Effect of flavone inhibitors of transport ATPases on histamine secretion from rat mast cells

Nature ◽  
1977 ◽  
Vol 265 (5595) ◽  
pp. 635-636 ◽  
Author(s):  
C. M. S. FEWTRELL ◽  
B. D. GOMPERTS
Keyword(s):  
Mast Cells ◽  
Histamine Secretion ◽  
Transport Atpases ◽  
Rat Mast Cells

Vascular responses to compound 48/80 in rat mesenteric vascular beds

2016 ◽  
Vol 94 (6) ◽  
pp. 620-626 ◽  
Author(s):  
Honghua Jin ◽  
Zhen Li ◽  
Shingo Takatori ◽  
Toshihiro Koyama ◽  
Xin Jin ◽  
...  
Keyword(s):  
Mast Cells ◽  
Ruthenium Red ◽  
High Concentration ◽  
Phase 3 ◽  
Vascular Effect ◽  
Vascular Responses ◽  
Endogenous Histamine ◽  
Low Concentrations ◽  
Vascular Beds ◽  
High Concentrations

A further investigation was performed on the vascular effect of endogenous histamine using the histamine releaser, compound 48/80, in rat mesenteric vascular beds with active tone. In preparations with intact endothelium, low concentrations of compound 48/80 (1.53 × 10−5 – 3 × 1.53 × 10−5 mg/mL) perfusion for 1 min only induced a small vasodilation. High concentrations of compound 48/80 (1.53 × 10−4 – 3 × 1.53 × 10−2 mg/mL) induced a biphasic vascular responses, an initial vasoconstriction followed a subsequent long-lasting vasodilation. The vasodilation induced by low concentrations of compound 48/80 and the vasoconstriction induced by high concentration of compound 48/80 was inhibited by olopatadine. However, cimetidine did not affect the responses induced by compound 48/80. Endothelium removal enlarged the compound 48/80-induced phase-2 vasoconstriction, while it attenuated the phase-3 vasodilation. Additionally, indomethacin and seratrodast significantly inhibited vasoconstriction but it did not affect the long-lasting vasodilation induced by high concentrations of compound 48/80. Ruthenium red inhibited the vasodilation induced by low concentrations and high concentrations of compound 48/80. These results suggest that the vasoconstriction induce by high concentrations of compound 48/80 is mediated by endogenous histamine released from mast cells. It is also suggested that thromboxane A2 released from mast cells is related to the vasoconstriction.

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