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The authors studied changes in beta- and alpha 1-adrenoceptors (beta-AC, alpha 1-AC) as well as in m-cholinoceptors in tuberculosis, pneumonia and cancer. Specimens of the lung parenchyma were obtained at thoracic surgery from 43 patients. Relevant ligands binding to the receptors was evaluated by incubation of the membrane proteins with radioligands varying in concentrations. Irrespective of the inflammation variant, beta-AC and alpha 1-AC levels were found decreased this being an correlation with the scope of fibrous and destructive involvement. The degree of the process chronicity and advance was judged from a decline in the binding parameters for beta-AC and alpha 1 AC. A dramatic fall in alpha 1 AC occurred in tuberculosis. This may be related to microcirculatory failure and vascular deformity. The levels of m-cholinoceptors underwent insignificant changes in pulmonary inflammation, whereas lung cancer displayed their sharp rise.

Adrenergic receptors were studied in human lung parenchyma obtained from 10 patients with tuberculoma after segmental resection within the limits of surrounding normal tissues (controls) as well as from 10 patients with destructive pulmonary tuberculosis. Binding of alpha-adrenergic radioligand 3H-prazosin was saturable with high rate of affinity in lung parenchymal membranes of both normal tissues and tissues impaired with tuberculosis. The Scatchard analysis indicated that the affinity of 3H-prazosin binding was not altered in patients with tuberculosis, while amount of the ligand binding sites was significantly decreased as compared with control preparations (KD = 0.5 +/- 0.9 nM, Bmax = 273.5 +/- 59.9 fmol/mg in controls; KD = 0.5 +/- 0.07 nM, Bmax = 51.7 +/- 7.5 fmol/mg in tuberculous lung parenchyma). beta-Adrenergic and muscarinic acetylcholinergic receptors were studied in lung parenchyma of patients with tuberculosis. Binding parameters of beta-adrenergic ligand 3H-dihydroalprenolol and muscarinic antagonist 3H-quinuclidinyl benzylate were similar to those of control values. Amount of 3H-dihydroalprenolol binding sites was not markedly altered while content of 3H-prazosin binding sites was considerably decreased in lung parenchyma of patients with tuberculosis as compared with normal state. The data obtained suggest that population of alpha-adrenergic receptors was decreased in human lung parenchyma under conditions of destructive tuberculosis.

beta-Adrenergic and muscarinic cholinergic receptors have been investigated in human lung parenchyma during cancer and chronic pneumonia as compared with normal tissue, obtained after segmental resection of tuberculoma from surrounding normal tissues. Binding of beta-adrenergic radioligand 3H-dihydroalprenolol (3H-DHA) and muscarinic antagonist 3H-quinuclidinyl benzylate (3H-QNB) was saturating with high rate of affinity in lung parenchyma membranes of both controls and patients with cancer and chronic pneumonia. Amount of binding sites of 3H-QNB was significantly increased in cancer (Bmax = 377.5 +/- 65.5 fmole/mg) and did not change in chronic pneumonia (Bmax = 97.7 +/- 14.7 fmole/mg) as compared with normal tissues (Bmax = 108.9 +/- 12.1 fmole/mg); a number of binding sites of 3H-DHA was significantly decreased both in lung parenchyma under conditions of cancer (Bmax = 84.1 +/- 14.5 fmole/mg) and chronic pneumonia (Bmax = 113.8 +/- 10.3 fmole/mg) as compared with normal tissue (Bmax = 456.7 +/- 73.7 fmole/mg). The affinity of 3H-DHA and 3H-QNB binding was practically unaltered. The results obtained suggest the important role of beta-adrenergic receptors in formation of lung cancer in the patients with pneumonia.