The Role of Cyclic Nucleotides and Related Compounds in Nerve‐mediated Vasodilatation in the Cat Submandibular Gland

Jones, Christopher J.; Mann, Giovanni E.; Smaje, L. H.

doi:10.1111/j.1476-5381.1980.tb14563.x

Cited by 12 publications

(3 citation statements)

References 29 publications

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“…The vascular escape seen after NA infusions or sympathetic nerve stimulation in normal animals coincides in time with a-receptor mediated release of vasodilatory metabolites, such as adenosine, from effector cells (Fredholm 1976, Fredholm & Hedqvist 1978. Purine compounds including adenosine have also been shown to cause vasodilation in the cat submandibular gland (Jones et al 1980). It has also been reported that /?-adrenoceptor blockade reduces the rapid vasodilation seen after sympathetic nerve stimulation (Bhoola et al 1965).…”

Section: Discussionmentioning

confidence: 99%

Pancreatic polypeptide family (APP, BPP, NPY and PYY) in relation to sympathetic vasoconstriction resistant to α‐adrenoceptor blockade

Lundberg

Tatemoto

1982

Acta Physiologica Scandinavica

527

119

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Electrical stimulation of the cat cervical sympathetic trunk caused submandibular salivary secretion and vasoconstriction simultaneously with a contraction of the nictitating membrane. Following a-and /I-adrenoceptor blockade by phentolamine or phenoxybenzamine combined with propranolol, the salivary response and the nictitating membrane contraction upon sympathetic stimulation were almost abolished. A considerable vasoconstrictor response (up to 40% of control) however still remained in the submandibular gland. This yasoconstriction, which persisted after a-adrenoceptor blockade, was rather slow in onset and had a long duration without any poststimulatory hyperemia. Local intra-arterial infusions of noradrenaline caused submandibular vasoconstriction, salivary secretion and nictitating membrane contraction. The blood flow response to exogenous noradrenaline did, however, not mimic the effects of sympathetic nerve stimulation with regard to vascular escape. Whereas the vascular escape after nerve stimulation was followed by a prolonged vasoconstriction with a gradual decline, the escape after noradrenaline infusions was accompanied by a normalization of blood flow. Local intra-arterial infusions of pancreatic polypeptide (PP)-related peptides caused a slowly developing vasoconstriction with a long duration in the submandibular gland, but no salivary secretion or contraction of the nictitating membrane. The relative molar potencies as vasoconstrictory agents were about PYY: 1, neuropeptide Y (NPY):5, avian and bovine pancreatic polypeptid 100. The vasoconstrictor effects of PP-related peptides were resistant to a-adrenoceptor blockade and present also in sympathectomized animals, suggesting a direct action on vascular smooth muscle. Combined local infusions of noradrenaline and NPY caused a vascular response in the submandibular salivary gland which was similar to that seen upon sympathetic nerve stimulation. PYY and NPY caused increase in systemic arterial blood pressure upon systemic administration which indicates general vasoconstrictor actions. This effect was accompanied by a transient bradycardia which was due to inhibition of sympathetic tone, since it was absent in animals treated with propranolol.In conclusion, the present findings illustrate the differential sensitivity to a-adrenoceptor antagonists of the submandibular vasoconstriction and salivation as well as smooth muscle contraction of the nictitating membrane induced by sympathetic nerve stimulation. This remaining vasoconstriction may be explained by release of a nonadrenergic, PP-related transmitter such as NPY which may be present together with noradrenaline in the vascular nerves. Release of an additional vasoconstrictory factor may also account for the finding that infusions of noradrenaline do not mimic the vascular effects of sympathetic nerve stimulation in vivo.

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Section: Discussionmentioning

confidence: 99%

Pancreatic polypeptide family (APP, BPP, NPY and PYY) in relation to sympathetic vasoconstriction resistant to α‐adrenoceptor blockade

Lundberg

Tatemoto

1982

Acta Physiologica Scandinavica

527

119

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“…In experiments designed to test the sodium-dependency of amino acid transport the NaCl and NaHCO3 in the perfusate were removed and replaced by equimolar quantities of buffered Trizma HCl (Sigma). In these experiments 1 mM-adenosine (Sigma) was added to both sodium-free and control perfusates to maintain maximal vasodilatation in the preparation (Jones, Mann & Smaje, 1980). All perfusates were maintained at 37 'C and gassed with 95% 02-5% C02 to a pH of 7 3-7 4.…”

Section: Perfusatesmentioning

confidence: 99%

Transport specificity for neutral and basic amino acids at maternal and fetal interfaces of the guinea‐pig placenta

Eaton

Mann

Yudilevich

1982

The Journal of Physiology

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SUMMARY1. The unidirectional influx of amino acids into the guinea-pig syncytiotrophoblast was measured using a single circulation paired-tracer dilution technique which allows separate characterization of both fetal and maternal interfaces. An in situ preparation perfused through the fetal circulation was used to examine the fetal side, while an isolated preparation perfused through both the fetal and maternal circulations was used to study both interfaces simultaneously.2. On the fetal side the maximal uptake (Umax) determined at tracer concentrations was high for the short-chain neutral amino acid alanine (76%) and the long-chain neutrals, leucine (75%), phenylalanine (90 %) and tyrosine (82 %) and for the basic amino acid lysine (65 %). In contrast, Umax was negligible for a-methylaminoisobutyric acid and taurine, a fl-amino acid.3. The uptake of alanine and phenylalanine on the fetal side was inhibited by both short-chain (alanine, serine, cysteine) and long-chain (phenylalanine, methionine, leucine) neutral amino acids. D-alanine had no effect on L-alanine uptake whereas D-phenylalanine significantly inhibited that of L-phenylalanine. Diaminobutyric acid, lysine and arginine were effective inhibitors of alanine uptake but had no effect on phenylalanine uptake.4. On the maternal side uptake of alanine, phenylalanine and lysine was measured. Over a wide range of concentrations self-inhibition of alanine influx was similar to the cross-inhibition observed with phenylalanine. In contrast, the influx ofphenylalanine, which was strongly self-inhibited, was only partially cross-inhibited by alanine.5. Influx of alanine and phenylalanine was measured at various perfusate concentrations and was found to be saturable on both maternal and fetal sides. The data were fitted to a single hyperbola and, on the maternal side, the Km for alanine (10.3 + 2.7 mM, mean + S.E., n = 3) was three-fold higher than the value measured for phenylalanine (3-1 + 0-8 mM). On the fetal side the Km values for alanine (8-4 + 1-4 mM, n = 4) and phenylalanine (11-9+ 1-9 mm, n = 3) were similar.6. The uptake of alanine, phenylalanine and lysine appeared to be highly sodiumdependent accounting for 40-70 % ofthe total influx. However, the inhibited fractions were found to be different on the two sides of the placenta.7. The results ofuptake, cross-inhibition and Na+-dependency experiments suggest B. M. EATON, G. E. MANN AND D. L. YUDILEVICH the presence of an alanine-serine-cysteine (ASC) type system and a leucine (L) type system with markedly overlapping specificities at both the fetal and maternal interfaces. Separate kinetic characterization of a two carrier system was not possible under the conditions of these experiments. However, kinetic parameters for the over-all transport of alanine and phenylalanine were measured.

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“…Desensitisation of muscarinic receptors by ATP and 3 0 -O-(4-benzoyl)benzoyl ATP (Bz-ATP) acting on P2X 7 receptors in rat parotid acinar cells has been reported (Fukushi 1999). Intra-arterial administration of various nucleotides, including ATP and ADP to the cat submandibular salivary gland led to increase in blood flow, possible mimicking neurally released ATP as a cotransmitter in parasympathetic and/or sympathetic nerves (Jones et al 1980). Reviews of the distribution and function of P2 nucleotide receptors in salivary glands are available (Novak 2003;Turner et al 1999).…”

Section: Exocrine Glandsmentioning

confidence: 96%

Peripheral Nervous System

Burnstock¹,

Verkhratsky

2012

Purinergic Signalling and the Nervous System

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The Role of Cyclic Nucleotides and Related Compounds in Nerve‐mediated Vasodilatation in the Cat Submandibular Gland

Cited by 12 publications

References 29 publications

Pancreatic polypeptide family (APP, BPP, NPY and PYY) in relation to sympathetic vasoconstriction resistant to α‐adrenoceptor blockade

Pancreatic polypeptide family (APP, BPP, NPY and PYY) in relation to sympathetic vasoconstriction resistant to α‐adrenoceptor blockade

Transport specificity for neutral and basic amino acids at maternal and fetal interfaces of the guinea‐pig placenta

Peripheral Nervous System

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