Effect of substance P and eledoisin on K+ efflux, amylase release and cyclic nucleotide levels in slices of rat parotid gland

Rudich, Lynn; Butcher, Fred R.

doi:10.1016/0304-4165(76)90317-2

Cited by 82 publications

(35 citation statements)

References 18 publications

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“…In some secretory tissues CGRP has been shown to have a vasodilatory effect with increasing vascular permeability (Lundberg et al 1988). SP promotes secretomotor and vasodilatory effects (Rudich & Butcher, 1976) and protein secretion (Singh et al 1994). Demonstration of both neuropeptides was found to play a role both in the glandular tissue and the blood vessels of the cavernous body in the efferent tear ducts.…”

Section: mentioning

confidence: 97%

Innervation of the cavernous body of the human efferent tear ducts and function in tear outflow mechanism

et al. 2000

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The lacrimal sac and nasolacrimal duct are surrounded by a wide cavernous system of veins and arteries comparable to a cavernous body. The present study aimed to demonstrate the ultrastructure of the nervous tissue and the localisation of neuropeptides involved in the innervation of the cavernous body, a topic not previously investigated. Different S-100 protein antisera, neuronal markers (neuron-specific enolase, anti-200 kDa neurofilament), neuropeptides (substance P, neuropeptide Y, calcitonin gene-related peptide, vasoactive intestinal polypeptide) and the neuronal enzyme tyrosine hydroxylase were used to demonstrate the distribution pattern of the nervous tissue. The ultrastructure of the innervating nerve fibres was also examined by means of standard transmission electron microscopy.The cavernous body contained specialised arteries and veins known as barrier arteries, capacitance veins, and throttle veins. Perivascularly, the tissue was rich in myelinated and unmyelinated nerve fibres in a plexus-like network. Small seromucous glands found in the region of the fundus of the lacrimal sac were contacted by nerve fibres forming a plexus around their alveoli. Many nerve fibres were positive for S-100 protein (S 100), neuron-specific enolase (NSE), anti-200 kDa neurofilament (RT 97), calcitonin gene-related peptide (CGRP), substance P (SP), tyrosine hydroxylase (TH), and neuropeptide Y (NPY). Vasoactive intestinal polypeptide (VIP) immunoreactivity was only demonstrated adjacent to the seromucous glands.Both the density of nerve fibres as well as the presence of various neuropeptides emphasises the neural control of the cavernous body of the human efferent tear ducts. By means of this innervation, the specialised blood vessels permit regulation of blood flow by opening and closing the lumen of the lacrimal passage as effected by the engorgement and subsidence of the cavernous body, at the same time regulating tear outflow. Related functions such as a role in the occurrence of epiphora related to emotional responses are relevant. Moreover, malfunction in the innervation of the cavernous body may lead to disturbances in the tear outflow cycle, ocular congestion or total occlusion of the lacrimal passages.

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Section: mentioning

confidence: 97%

Innervation of the cavernous body of the human efferent tear ducts and function in tear outflow mechanism

et al. 2000

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“…Butcher (1975) Leslie, Putney & Sherman, 1976). Substance P has been shown to have no effect on cyclic nucleotide levels in the parotid gland (Rudich & Butcher, 1976). The results described here show that noradrenaline-stimulated amylase release is inhibited less than substance P or carbachol-stimulated amylase release by the absence of Ca2+, and this is possibly explained by the /3-receptor-mediated component in the noradrenaline response.…”

Section: Discussionmentioning

confidence: 51%

“…Moreover, in vitro studies show several substance P effects on salivary gland preparations (Rudich & Butcher, 1976;Friedman & Selinger, 1978;Jones & Michell, 1978;Gallacher & Petersen, 1980), and point to the existence of separate a-adrenoceptor, substance P and muscarinic receptors acting via a common ion 0007-1188/81/060517-007 $01.00 channel mechanism (Putney, 1977;Gallacher & Petersen, 1980). In peripheral tissue bioassays, the potency rank order of synthetic C-terminal fragments of substance P (Bury & Mashford, 1976;Blumberg & Teichberg, 1979) or of tachykinins (naturally-occurring substance P-like peptides; Erspamer, Erspamer & Piccinelli, 1980), has been used as a tool to study the substance P receptor.…”

Section: Introductionmentioning

confidence: 99%

The EFFECTS OF SUBSTANCE P AND RELATED PEPTIDES ON Α‐AMYLASE RELEASE FROM RAT PAROTID GLAND SLICES

Brown

Hanley

1981

British J Pharmacology

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1 The effects of substance P and related peptides on amylase release from rat parotid gland slices have been investigated. 2 Supramaximal concentrations (1 F.M) of substance P caused enhancement of amylase release over the basal level within 1 min; this lasted for at least 40 min at 30°C. 3 Substance P-stimulated amylase release was partially dependent on extracellular calcium and could be inhibited by 50% upon removal of extracellular calcium.4 Substance P stimulated amylase release in a dose-dependent manner with an ED50 of 18 nm. 5 All C-terminal fragments of substance P were less potent than substance P in stimulating amylase release. The C-terminal hexapeptide of substance P was the minimum structure for potent activity in this system, having 1/3 to 1/8 the potency of substance P. There was a dramatic drop in potency for the C-terminal pentapeptide of substance P or substance P free acid. Physalaemin was more potent than substance P (ED50 = 7 nM), eledoisin was about equipotent with substance P (ED5o = 17 nM), and kassinin less potent than substance P (ED50 = 150 nM).6 The structure-activity profile observed is very similar to that for stimulation of salivation in vivo, indicating that the same receptors are involved in mediating these responses. 7 All the fragments of substance P tested were capable of eliciting a full amylase release response. This indicates that the apparent partial agonist action of the C-terminal nonapeptide fragment on in vivo salivation is not explicable at the receptor level.

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“…Stimuli mediated through P-adrenoceptors induce parotid glands, adrenoceptor and cholinoceptor agonsecretion from the salivary glands by elevating the ists (Butcher et al, 1975;Leslie et al, 1976) and intracellular cyclic AMP level, while stimuli mediated substance P or a closely related peptide (Rudich & through muscarinic cholinoceptors and substance P Butcher, 1976;Gallacher, 1983) stimulate amylase receptors also induce the secretion by eliciting Ca2+ secretion, although P-adrenoceptor agonist is the most influx into acinar cells (Butcher & Putney, 1980). In rat effective.…”

Section: Introductionmentioning

confidence: 99%

Dopamine‐induced amylase secretion from rat parotid salivary gland in vitro: an effect mediated via noradrenergic and cholinergic nerves.

Hata

Ishida

Kondo

1986

British J Pharmacology

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1 The effect of dopamine on amylase secretion by rat parotid tissue was examined in vitro.2 Dopamine induced marked amylase secretion from the tissue in a dose-dependent manner. Its EC50 value was about 4 gM and the maximal response was obtained at a concentration of 100 AM.3 The dopamine-induced secretion was inhibited by the dopamine-antagonists haloperidol, (+)-butaclamol and spiroperidol. 4 Atropine reduced the dopamine-induced secretion significantly, and physostigmine enhanced the secretion. 5 Parasympathectomy of the gland resulted in a significant decrease in the dopamine-induced secretion, but did not reduce the secretion induced by dopamine with atropine. 6 Dopamine-induced ACh release from parasympathetic nerve terminals in the tissue was studied in tissue preparations that had been loaded with [3H]-choline. Dopamine elicited Ca2+-sensitive tritium release, and dopamine antagonists or parasympathectomy prevented this release. 7 Sympathectomy or reserpine treatment of rats resulted in significant decrease in the dopamineinduced secretion, but increase in noradrenaline (NA)-or isoprenaline-induced secretion. 8 Dopamine-induced NA release was studied by preloading the parotid tissue with [3H]-NA. Dopamine induced Ca2"-sensitive tritium release, and dopamine antagonists or sympathectomy prevented the release. 9 Several lines of circumstantial evidence strongly suggested that dopamine has a specific site for action in the parotid tissue that is independent of NA receptors. 10 In sympathectomized or reserpine-treated glands, atropine completely inhibited the dopamineinduced amylase secretion, suggesting that dopamine did not have a direct effect on postsynapses. 11 These findings indicate that dopamine induces amylase secretion in two indirect ways mediated through ACh and NA released from parasympathetic and sympathetic nerve terminals, respectively.

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Effect of substance P and eledoisin on K+ efflux, amylase release and cyclic nucleotide levels in slices of rat parotid gland

Cited by 82 publications

References 18 publications

Innervation of the cavernous body of the human efferent tear ducts and function in tear outflow mechanism

Innervation of the cavernous body of the human efferent tear ducts and function in tear outflow mechanism

The EFFECTS OF SUBSTANCE P AND RELATED PEPTIDES ON Α‐AMYLASE RELEASE FROM RAT PAROTID GLAND SLICES

Dopamine‐induced amylase secretion from rat parotid salivary gland in vitro: an effect mediated via noradrenergic and cholinergic nerves.

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