Abstract
1 Effects of nitroglycerine (NG) on the membrane and contractile properties of the smooth muscle cell of the isolated coronary artery of the pig were observed.
2 NG, up to a concentration of 10-5 M, modified neither the membrane potential nor the membrane resistance. Increased concentrations of NG (> 2.8 × 10-5 M) hyperpolarized the membrane, reduced the membrane resistance and enhanced the rectifying property of the membrane measured by depolarization pulses. These phenomena observed with a high concentration of NG are the result of an increase in the K-conductance of the membrane.
3 NG (2.8 × 10-5 M) did not modify the membrane potential displaced by various concentrations of excess [K]o. In low [K]o, NG (2.8 × 10-5 M) hyperpolarized the membrane to a greater extent than that observed in Krebs solution. The effects of NG (10-6 to 2.8 × 10-5 M) on the membrane potential were not modified by simultaneous application of 2 × 10-6 M acetylcholine (ACh).
4 NG (2.8 × 10-6 M) consistently raised the mechanical threshold required for tension development and suppressed the amplitude of the contraction evoked by excess [K]o, ACh or electrical depolarization of the membrane. The dose-response curve shifted to the right in the presence of NG noncompetitively in all the conditions employed to develop the tension.
5 When the tissue was immersed in Ca-free (EGTA) solution, ACh (5 × 10-6 M) evoked a contraction even after the tissue had lost the ability to contract to repetitive applications of 118 mM [K]o in Ca-free (EGTA) solution. However, the tissue finally failed to contract to repetitively applied ACh. At this stage, 2.5 mM [Ca]o evoked a small contraction, after which the response was briefly restored to 5 × 10-6 M ACh. This transient response to ACh was reduced by NG (5.6 × 10-6 M) when NG was added either simultaneously with ACh or with the previous Ca application. However, the inhibition was greater in the former than the latter case.
6 Cysteine (1 to 2 mM), without modifying the membrane potential or membrane resistance, partly restored the contraction evoked by excess [K]o or ACh which had been reduced by NG.
7 The mechanism of action of NG on the smooth muscle cell of the coronary artery of the pig is postulated to be due to a nonselective suppression of the Ca-mobilization from the store site with no noticeable change in the membrane properties.
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Selected References
These references are in PubMed. This may not be the complete list of references from this article.
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