Tension response of mammalian muscle to intra-arterial acetylcholine

1960 ◽  
Vol 198 (3) ◽  
pp. 507-510 ◽  
Author(s):  
Peter T. Rowley ◽  
Jay B. Wells ◽  
Richard L. Irwin

Using isometric tension recording of the tibialis anterior muscle of the cat, the response to intra-arterial acetylcholine injection was studied and compared to the response to electrical stimulation of the nerve. The amount of acetylcholine, the rate of injection and the volume of diluent injected are interrelated factors in the production of tension. Regardless of the amount and concentration of the acetylcholine injected, the contractile response of the muscle has a slower rate of rise and a longer duration than the response from single maximal impulse stimulation to the nerve and a maximal tension less than from a tetanic neural stimulation. The dose-response relationship between the injected acetylcholine and the resultant tension and its modification by curare are described. The steep portion of the dose-response curve was found to occur in most experiments between 0.5 and 6.0 µg. A method of supplying blood to the muscle is described which provides more reliable intermittent arterial occlusion during injection.

1982 ◽  
Vol 52 (5) ◽  
pp. 1363-1367 ◽  
Author(s):  
A. R. Leff ◽  
N. M. Munoz ◽  
B. Alderman

Because isometric systems differ substantially from methods of measuring airway smooth muscle tone that depend on airway diameter, we determined the sensitivity and significance of data derived from these different methods in 20 anesthetized dogs. The airway contractile response was measured directly from an isometric tracheal segment in situ and simultaneously as pulmonary resistance (RL) and dynamic compliance (Cdyn). The contractile response to intravenous (iv) methacholine (MC) (2.6 X 10(-11) to 2.6 X 10(-6) mol/kg) and norepinephrine (NE) (1.2 X 10(-11) to 1.2 X 10(-6) mol/kg) was measured in dose-response studies of beta-blocked and ganglion-blocked animals. A statistically significant change in isometric tracheal tension was first observed at 2.6 X 10(-10) mol/kg iv MC and 1.2 X 10(-9) mol/kg iv NE. Statistically significant changes in Cdyn and RL did not occur at doses less than 10(-8) mol/kg for either agonist. Substantial increase in isometric tracheal tension (greater than 10 g force/cm) occurred before any change in RL or Cdyn. These finding indicate that change in isometric tension reflects parallel changes in RL and Cdyn. For NE and MC, tracheal tension is a more sensitive and selective measurement of airway contraction than RL or Cdyn.


1990 ◽  
Vol 79 (3) ◽  
pp. 273-278 ◽  
Author(s):  
Robin G. Woolfson ◽  
Lucilla Poston

1. Using a myograph to measure isometric tension, we have looked at the action of NG-monomethyl-l-arginine on the endothelium-dependent relaxation of human subcutaneous resistance arteries. 2. NG-Monomethyl-l-arginine, the novel inhibitor of endothelium-derived relaxing factor synthesis, caused concentration-dependent but only partial inhibition of maximal relaxation induced by acetylcholine in human subcutaneous resistance arteries. 3. The inhibitory action of NG-monomethyl-l-arginine on acetylcholine-induced maximal relaxation was partially reversed by incubation of the arteries in equimolar concentrations of l-arginine and NG-monomethyl-l-arginine. Subsequent incubation in l-arginine led to further reversal, but this was no greater than with incubation in physiological saline. 4. A component of acetylcholine-induced relaxation was sensitive to indomethacin, suggesting that this response is mediated by prostanoids as well as by endothelium-derived relaxing factor. 5. NG-Monomethyl-l-arginine did not increase the tension of resting human subcutaneous resistance arteries. NG-Monomethyl-l-arginine did enhance the contractile response to noradrenaline, possibly due to inhibition of release of endothelium-derived relaxing factor resulting from stimulation of α2-adrenoreceptors on the endothelial cells.


1992 ◽  
Vol 262 (5) ◽  
pp. L574-L581 ◽  
Author(s):  
W. E. Finkbeiner ◽  
J. H. Widdicombe ◽  
L. Hu ◽  
C. B. Basbaum

The role of adenosine 3',5'-cyclic monophosphate (cAMP) and protein phosphorylation during beta-adrenergic receptor stimulation of bovine tracheal gland serous cells was investigated in vitro. Isoproterenol, a beta-adrenergic agonist, increased the secretion of 35S-labeled molecules. Intracellular cAMP levels were increased within 1 min after stimulation of bovine tracheal gland serous cells with isoproterenol. The dose-response relationship for isoproterenol-stimulated generation of cAMP correlated with the dose-response relationship for isoproterenol-stimulated secretion of 35S-labeled molecules. The phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine potentiated both isoproterenol-evoked secretion of 35S-labeled molecules and the production of intracellular cAMP, and the beta-adrenergic receptor antagonist propranolol completely blocked both effects. The secretory response of the cells to isoproterenol could be mimicked by the cAMP analogues 8-bromoadenosine 3',5'-cyclic monophosphate and dibutyryl adenosine 3',5'-cyclic monophosphate. Activity of cAMP-dependent kinase was measured in soluble and particulate cell extracts. cAMP effected the state of phosphorylation of proteins associated with the soluble but not the particulate fraction. These studies are consistent with the hypothesis that beta-adrenergic stimulation of secretion from bovine tracheal gland serous cells occurs via a cAMP-mediated pathway and that one of the molecular events in this pathway is cAMP-dependent protein phosphorylation.


1987 ◽  
Vol 64 (2) ◽  
pp. 433-443 ◽  
Author(s):  
Terry D. Etherton ◽  
James P. Wiggins ◽  
Christina M. Evock ◽  
Chung S. Chung ◽  
John F. Rebhun ◽  
...  

1962 ◽  
Vol 41 (2) ◽  
pp. 268-273 ◽  
Author(s):  
Ralph I. Dorfman

ABSTRACT The stimulating action of testosterone on the chick's comb can be inhibited by the subcutaneous injection of 0.1 mg of norethisterone or Ro 2-7239 (2-acetyl-7-oxo-1,2,3,4,4a,4b,5,6,7,9,10,10a-dodecahydrophenanthrene), 0.5 mg of cortisol or progesterone, and by 4.5 mg of Mer-25 (1-(p-2-diethylaminoethoxyphenyl)-1-phenyl-2-p-methoxyphenyl ethanol). No dose response relationship could be established. Norethisterone was the most active anti-androgen by this test.


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