In vivo autoradiographic demonstration of β-adrenergic binding sites in adult rat type II alveolar epithelial cells

Smith, Dale M.; Sidhu, Navjeet K.

doi:10.1016/0024-3205(84)90484-3

Cited by 8 publications

(2 citation statements)

References 23 publications

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“…The presence oftwo pools oftissue surfactant Previously we proposed that the alveolar compartment is supplied by two pools of tissue surfactant (Nicholas et al, 1982a;Nicholas & Barr, 1983;Power et al, 1986;1987). The first is relatively small, turns over rapidly and is under the control of the sympathetic nervous system.…”

Section: Control Ofsurfactant In Hyperpnoeic Ratsmentioning

confidence: 99%

“…Specifically, P-©) The Macmillan Press Ltd 1988 adrenoceptor agonists are consistently shown to increase surfactant release in the foetal lung (Enhorning et al, 1977), in adult lung slices (Gilfillan et al, 1983) and in the isolated perfused lung (Nicholas & Barr, 1981;Brown & Longmore 1981;Massaro et al, 1982). Furthermore, these drugs release surfactant from isolated alveolar type II cells (Dobbs & Mason, 1979;Mettler et al, 1981) and P-adrenoceptors have been identified in these cells (Smith & Sidhu, 1984). There is much less concensus over the ability of drugs acting on muscarinic cholinoceptors to induce release.…”

Section: Introductionmentioning

confidence: 99%

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Control of alveolar surfactant in rats at rest and during prolonged hyperpnoea: pharmacological evidence for two tissue pools of surfactant

Barr

Nicholas

Power

1988

British J Pharmacology

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Propranolol, atropine and indomethacin (i.p.) affect neither the amount (PLalv), nor the specific activity (PLalvsp.act.) of alveolar surfactant‐type phospholipids lavaged from the lungs of unanaesthetized rats, either at rest or made hyperpnoeic for 24 h with 5%CO2/13%O2/82%N2. Whereas salbutamol (280 μg kg−1 body weight, i.p.) consistently increased PLalv and PLalvsp.act., pilocarpine (1.5, 3, 10 and 50 mg kg−1, i.p.) and labetalol (1 and 5 mg kg−1, i.p.) had no effect. The dose of pilocarpine reported by others to release surfactant (150 mg kg−1) induced marked salivation, diarrhoea, chromodacryorrhoea and a three‐fold increase in tidal volume. In the isolated perfused lung of the rat, salbutamol (1.5 μm) consistently increased PLalvsp.act, whereas pilocarpine (0.1 and 1 μM) had no effect on these variables. In the isolated perfused lung, the maximum amount of surfactant that could be released by salbutamol (0.5 mM) was smaller than that which could be released in response to an increase in tidal volume (peak inflation pressure 28 cmH2O). When the concentration of salbutamol in the isolated perfused lung was adjusted to produce the same increase in PLalv as did a single simulated deep breath, the PLalvsp.act was significantly increased by salbutamol, but not by the simulated deep breath. We conclude, that neither the autonomic nervous system nor the prostaglandin system is essential for the release of surfactant at rest or during hyperpnoea. Furthermore, we suggest that two pools of surfactant, with different release mechanisms, exist in lung tissue.

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Section: Control Ofsurfactant In Hyperpnoeic Ratsmentioning

confidence: 99%