The physiological and pharmacological properties of ciliary muscle isolated from fresh human eyes were investigated. The muscle exhibited no spontaneous activity. Concentration-dependent contractions in response to carbachol were competitively antagonized by atropine (pA2 = 8.95). The muscle, precontracted by carbachol (2.7 X 10(-4)M), responded to the application of isoprenaline by concentration-dependent relaxation blocked by propranolol (3.5 X 10(-9)M to 3.5 X 10(-8)M; pA2 = 9.15). Angiotensin-evoked contractions were antagonized by 8-Ala-angiotensin II (4.5 X 10(-8)M) in a competitive manner, but were not inhibited by phentolamine or propranolol. Contractions generated by electrical stimulation of the muscle (30 ms, 20 Hz, 60 pulses) were antagonized by atropine (10(-7) M) and tetrodotoxin (6.3 X 10(-7) M). Phentolamine and propranolol did not influence these responses. An increase of the external potassium concentration ([K+]o) from 5.4 to 158.8 mM produced a mechanical response, antagonized by atropine, but not influenced by tetrodotoxin, phentolamine or propranolol. The human ciliary muscle appears to carry muscarinic and angiotensin receptors and beta 2-adrenoceptors. The estimate of Katropine for muscarinic receptors mediating carbachol-induced contractions agrees with estimates of Katropine reported for human and rabbit iris.
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Lograno et al. (1986) studied this question.
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