Ultrastructural and fluorescence histochemical studies on the innervation of the tracheo bronchial muscle of normal cats and cats treated with 6-hydroxydopamine

Silva, Douglas G.; Ross, Gordon

doi:10.1016/s0022-5320(74)90013-6

Cited by 44 publications

(10 citation statements)

References 17 publications

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“…Autoradiographic studies have demonstrated tifat sulphate is mainly incorporated into submucosal glands and tritiated glucose is taken up predominantly by epithelial cells (Gallagher, Hall, Jeffery, Phipps & Richardson, 1978). Nerve fibres, believed on ultrastructural grounds to be cholinergic, have been observed adjacent to the mucous and serous cells of the cat tracheal submucosal glands (Silva & Ross, 1974;Murlas, Nadel & Basbaum, 1980), while epithelial secretary cells such as goblet cells are not thought to be innervated (Florey et al 1932). The radiolabelling pattern (rich in 35S, poor in 3H) of secretions collected in response to vagal stimulation can be explained if they originate mainly from the submucosal glands.…”

Section: Discussionmentioning

confidence: 99%

Evidence for non‐cholinergic, non‐adrenergic nervous control of mucus secretion into the cat trachea.

Peatfield¹,

Richardson²

1983

The Journal of Physiology

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SUMMARY1. We have investigated the effects of electrical stimulation of the vagus nerves on the output of mucus glycoproteins (mucins), radiolabelled with 3H and 35S, into the trachea of anaesthetized cats.2. In five control experiments, stimulation of the vagus nerves on four successive occasions, separated by 1 h, caused significant rises in the output of radiolabelled mucins. In these experiments repetition of stimulation did not appear to lessen the response.3. In a parallel series of five experiments the vagus nerves were again stimulated on four occasions, but atropine was administered in increasing doses between the stimuli. Large responses, not significantly less than those seen in the corresponding control stimulations, were seen even in the presence of the highest dose of atropine. In this series of experiments, however, the effect of the last vagal stimulation (with the highest dose of atropine) was significantly less then the first (no atropine).4. Administration of phentolamine and l-propranolol in addition to atropine failed to reduce the response to vagal stimulation significantly.5. We conclude that, while cholinergic nerves can probably explain part of the increase in mucin output which occurs with vagus nerve stimulation, there is a large response mediated by a non-cholinergic, non-adrenergic neurotransmitter. Possible neurotransmitters and the relationship of these findings to those of earlier studies are discussed.

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Section: Discussionmentioning

confidence: 99%

Evidence for non‐cholinergic, non‐adrenergic nervous control of mucus secretion into the cat trachea.

Peatfield¹,

Richardson²

1983

The Journal of Physiology

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“…Bronchioles of rabbits, sheep, pigs, goats, and bulls are reported to have no adrenergic innervation (Mann, 1971). However, there is no general agreement about sympathetic innervation of the bronchiolar smooth muscle of the cat (Silva and Ross, 1974). Cat bronchioles have been reported to contain /?-2 receptors (Lulich et al, 1976).…”

Section: Discussionmentioning

confidence: 99%

Evidence for lack of innervation of beta-2 adrenoceptors in the blood vessels of the gracilis muscle of the dog.

Russell¹,

Moran²

1980

Circulation Research

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Cardiac /S-l adrenoceptors respond to sympathetic nerve stimulation (SNS), but it is not clear that SNS evokes fi-2 adrenoceptor-mediated vasodilation. Sensitivity of B adrenoceptors to catecholamines and to SNS was evaluated in dogs. Norepinephrine (NE) and epinephrine (E) were equipotent vasoconstrictors (femoral artery blood flow or gracilis autoperfusion pressure) before aadrenoceptor blockade with dibozane (DIB). After DIB, NE was 1/100 as potent a vasodilator as E, which was equipotent with isoproterenol (ISO). SNS evoked gracilis muscle vasoconstriction before DIB and vasodilation after. Dilation induced by SNS or acetylcholine (ACH) after DIB was blocked by atropine (AT), but that caused by NE was not. Dilation evoked by NE, E, or I after DIB and AT was blocked by propranolol (PROP). Vasoconstrictor responses to NE, E, or SNS in dogs without DIB were not augmented by PROP at a dose that blocked the dilator effect of ISO. NE and E were equipotent and both 1/10 as potent as ISO as positive inotropic and chronotropic agents. Cardiac responses to NE, E, ISO, and SNS were antagonized by PROP. Subclassification of adrenoceptors that subserve cardiac stimulation as fi-1 and that subserve vasodilation as fi-2 was substantiated. Cardiac fi-1 adrenoceptors responded to SNS and to circulating E and NE. Vascular fi-2 adrenoceptors responded to circulating E, to ISO, and to high doses of NE, but not to SNS. fi-2 Adrenoceptors in blood vessels appear not to be innervated and may function as hormone receptors sensitive primarily to E released from the adrenal medulla, rather than to NE released from adrenergic nerves.

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“…The previous reports have often included strong statements on the density or otherwise of the innervation (e.g. Silva & Ross, 1974) but none have contained quantitative estimates of the density. The previously published micrographs have concentrated on the nerves, and few have included large regions of muscle in order to place the nerves in perspective.…”

Section: Tracheal Muscle and Nervesmentioning

confidence: 99%

A study of excitatory neuromuscular transmission in the bovine trachea

Cameron¹,

Kirkpatrick²

1977

The Journal of Physiology

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1. The excitatory innervation of bovine tracheal smooth muscle has been studied with the sucrose‐gap apparatus. 2. Single 2 ms electrical stimuli applied to the whole tissue excited intrinsic nerves, and produced a small transient depolarization of the smooth muscle, the excitatory junction potential (e.j.p.). The e.j.p. caused a twitch‐type contraction; twitches and e.j.p.s summated during repetitive stimulation but facilitation was not observed, and action potentials were never elicited. 3. The effects of electrical stimulation could be abolished by atropine (5 × 10−7 mol/l) and augmented by neostigmine (4 × 10−6 mol/l), and were mimicked by exogenous acetylcholine (1·0 μg/ml). 4. With the electron microscope, the density of innervation was found to be low (one axon per ninety smooth muscle cells). Axons were found in small groups in the clefts between bundles of cells, but no axons penetrated within the muscle bundles. Naked axon varicosities containing agranular vesicles were seen, but no axon approached within 200 nm of a smooth muscle cell. 5. It is difficult to reconcile the sparsity of innervation with the dependence of the tissue on nerve excitation to initiate activity.

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Ultrastructural and fluorescence histochemical studies on the innervation of the tracheo bronchial muscle of normal cats and cats treated with 6-hydroxydopamine

Cited by 44 publications

References 17 publications

Evidence for non‐cholinergic, non‐adrenergic nervous control of mucus secretion into the cat trachea.

Evidence for non‐cholinergic, non‐adrenergic nervous control of mucus secretion into the cat trachea.

Evidence for lack of innervation of beta-2 adrenoceptors in the blood vessels of the gracilis muscle of the dog.

A study of excitatory neuromuscular transmission in the bovine trachea

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