Supersensitivity of Salivary Glands of Rabbits.

Nordenfelt, I.; Ohlin, Per

doi:10.1111/j.1748-1716.1957.tb01506.x

Cited by 44 publications

(17 citation statements)

References 5 publications

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“…Virtually nothing is known about the rabbit submandibular salivation except that, like other spontaneously secreting glands, it is entirely unaffected by atropine in doses which readily block the salivation induced by stimulation of the chorda tympani nerve (Nordenfelt & Ohlin, 1957).…”

Section: Introductionmentioning

confidence: 99%

Spontaneous salivation in the rabbit submandibular gland

Smaje¹

1973

The Journal of Physiology

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summABY 1. Salivation has been studied in the submandibular gland of the rabbit. A very slow spontaneous salivation took place when all possibility of nerve influence had been excluded. Salivation was not due to ultrafiltration.2. The 'spontaneous' saliva had a mean K concentration of 148 mM and Na concentration of 46 mm. With increasing salivation rate produced by parasympathetic nerve stimulation, K concentration fell to a plateau level of about 30 mm whilst Na concentration fell rapidly to reach the low value of 3 mM, then began to rise again at the higher flow rates.3. Ligation of the submandibular duct produced a reversal of the ion concentrations in spontaneous saliva. By 4 days K concentration was lower and that of Na higher than control values until by 2 weeks the effect was maximal with mean concentrations of 25 mm for K and 153 mm for Na.4. Ouabain increased the spontaneous salivation rate and ethacrynic acid slowed or prevented it altogether. On the basis of the known sites of action of these drugs it is postulated that two pumps are involved in the regulation of spontaneous salivation. There appears to be basal activity of an acinar mechanism pumping NaCl into the lumen, taking water with it. This pump is activated directly or indirectly by the intracellular Na concentration which itself is controlled by an Na-K exchange pump.5. Excitation of the sympathetic trunk produced a small, though definite, increase in salivation rate. There was evidence that myoepithelial cells might also be involved in the sympathetic response and that they were activated by a receptor stimulation. Salivation evoked by sympathetic nerve stimulation would seem to be a response to , receptor stimulation, but the possibility that activation of both ar and ft receptors was required could not be excluded entirely.

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Section: Introductionmentioning

confidence: 99%

Spontaneous salivation in the rabbit submandibular gland

Smaje¹

1973

The Journal of Physiology

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“…This represents a substantial increase in salivary flow since the 'spontaneous' flow which is present in the normally innervated gland is in the order of a single drop every hour as determined by Nordenfelt & Ohlin (1957). Furthermore, unlike the 'paralytic' flow in cats which showed a tendency to decline and sometimes disappear entirely after several hours (see Emmelin, 1952), the 'paralytic' flow in rabbits, although showing a small reduction in experiments lasting 5-6 h, did not disappear.…”

Section: Discussionmentioning

confidence: 88%

‘Paralytic’ Secretion After Parasympathectomy of Rabbit Submandibular Glands Includes a Cholinergic Component

Garrett

Kyriacou

1988

Exp Physiol

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SUMMARYChronic parasympathetic decentralization of submandibular glands in rabbits has been studied after 3 weeks, in acute experiments under urethane anaesthesia. A 'paralytic' secretion occurred from the supersensitive denervated glands and it was not attributable to an increase in the 'spontaneous' flow, that is present in normal glands. The 'paralytic' secretion was completely inhibited by atropine, after which a 'spontaneous' flow, that was similar to the contralateral glands, persisted. The a-adrenergic blocker dihydroergotamine, when given before atropine, reduced the 'paralytic' secretion by 50-75% but when this drug was given after atropine it had no additional effect. The fl-adrenergic blocker propanolol did not cause a reduction in the 'paralytic' secretion. Superior cervical ganglionectomy, in contrast, did not give rise to a significant 'paralytic' flow. The results suggest that acetylcholine, released spontaneously from terminals of postganglionic parasympathetic nerves, plays an essential part in the 'paralytic' secretion that occurs from rabbit submandibular glands after preganglionic denervation. Circulating catecholamines make a secondary contribution, acting synergistically with the acetylcholine on the supersensitive secretory cells.

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“…One possibility is that the facial nerve contributes to the innervation of the gland as is the case in dogs [Ekstr6m and Holmberg, 1972], another is that nerves travel along the blood vessels to the gland as is the case both in dogs [Holmberg, 1971] and in cats [EkstrOm and Emmelin, 1974]. In experiments by Nordenfelt and Ohlin [1957] the facial, lingual and chorda tympani nerves in rabbits were stimulated electrically; in one animal a small secretion from the parotid gland was obtained when the facial nerve was excited.…”

Section: Disc-ussionmentioning

confidence: 99%

Uncharted Cholinergic Nerves in the Rabbit Parotid Gland

Alm

Ekström

1976

Exp Physiol

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Cholinergic nerves are shown to be left in the rabbit parotid gland after avulsion of the auriculo-temporal nerve: a cholinesterase inhibitor injected through the duct caused secretion, thereby revealing leakage of acetylcholine from cholinergic nerve endings, and acetylcholinesterase positive nerves were found histochemically. The incomplete cholinergic denervation offers an explanation to the fact that some choline acetyltransferase activity remains in the 'denervated' glands.In the rabbit parotid glands a rapid and profound fall in the activity of the acetylcholine synthesizing enzyme, choline acetyltransferase, was found by Nordenfelt [1964] to follow a parasympathetic denervation, caused by section of the auriculo-temporal nerve. This finding probably indicates a neuronal localization for the enzyme. However, some enzyme activity usually remained suggesting either the presence of unsevered cholinergic neurones or other sources for the enzyme in the gland. In such denervated parotid glands of other species, i.e. cats [Nordenfelt, 1963; Ekstrom and Emmelin, 1974], dogs [Ekstrom and Holmberg, 1972] and rats [Ekstrom, 1974] a low choline acetyltransferase activity may be demonstrated also. In cats and dogs the residual enzyme activity seems to be accounted for, since several investigations, both physiological and histochemical, show that the denervation is incomplete leaving some cholinergic nerve fibres intact [Emmelin and Str6mblad, 1958;Emmelin and Holmberg, 1967;Garrett, 1966;Garrett and Holmberg, 1972;Holmberg, 1972; Ekstrom and Emmelin, 1974]. Accordingly, by including not only section of the auriculo-temporal nerve in the denervation procedure, but division of nerve strands on the internal maxillary artery [Holmberg, 1971] and the facial nerve the choline acetyltransferase activity of the parotid gland of dogs in most cases reached values below the limit of detection [Ekstrom and Holmberg, 1972].The present experiments investigate whether in rabbits also there are some cholinergic neurones left following avulsion of the auriculo-temporal nerve. This was done by the use of a cholinesterase inhibitor injected through the duct into the gland; such a substance is known to cause secretion of saliva by preserving acetylcholine leaking from the nerve endings [Emmelin and Stromblad, 1958]. Further, nerves stained for acetylcholinesterase were looked for. METHODSSixteen rabbits of both sexes weighing 1-9-3-2 kg were used. Under ether and pentobarbitone (35 mg/kg i.p.) anaesthesia the following experimental procedures were 127

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Supersensitivity of Salivary Glands of Rabbits.

Cited by 44 publications

References 5 publications

Spontaneous salivation in the rabbit submandibular gland

Spontaneous salivation in the rabbit submandibular gland

‘Paralytic’ Secretion After Parasympathectomy of Rabbit Submandibular Glands Includes a Cholinergic Component

Uncharted Cholinergic Nerves in the Rabbit Parotid Gland

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