Multiple Receptors and Binding Sites for Tachykinins

Iversen, L. L.; Foster, Alan C.; Watling, Keith J.; McKnight, A.T.; Williams, Brian J.; Lee, C. M.

doi:10.1007/978-1-4612-4672-5_14

Cited by 24 publications

(28 citation statements)

References 14 publications

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“…tP < 0.05 or ttP < 0.01 compared to the lowest dose of either mediator in animals pretreated with inhaled saline (0.9%; 60 breaths). NK2 receptor is present in higher concentration in airway smooth muscle, causing contraction when activated (Iversen, 1985). Our data, showing that NKA is relatively more potent in causing an increase in RL than airway microvascular leakage, compared to inhaled SP, provides further evidence that such receptors may be important in the in vivo situation in guinea-pig.…”

Section: Discussionsupporting

confidence: 54%

“…It has been suggested that NKA and SP cause their effects by activating two distinct receptors, called neurokinin, (NK1) and neurokinin2 (NK2) receptors (Iversen, 1985). SP is believed to be more potent in stimulating NK1 receptors, and NKA more potent in stimulating NK2 receptors (Iversen, 1985).…”

Section: Discussionmentioning

confidence: 99%

“…SP is believed to be more potent in stimulating NK1 receptors, and NKA more potent in stimulating NK2 receptors (Iversen, 1985). A third receptor subtype, neurokinin3 receptor (NK3), is more specific for neurokinin B (NKB), but this peptide has not been found to be present in the airways of guinea pig (Hua et al, 1985).…”

Section: Discussionmentioning

confidence: 99%

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Differential effects of phosphoramidon on neurokinin A‐ and substance P‐induced airflow obstruction and airway microvascular leakage in guinea‐pig

Lötvall

Elwood

Tokuyama

et al. 1991

British J Pharmacology

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1 The effects of the inhaled neuropeptides, neurokinin A (NKA) and substance P (SP) on lung resistance (RL) and airway microvascular permeability were studied in anaesthetized guinea-pigs.2 Single doses of inhaled NKA (3 x 10-, 1 x 10-, 3 x 10-4M; 45 breaths) and SP (1 x 10-4, 3 x 10-4, 1 X 10-3; 45 breaths) caused a dose-dependent increase in both RL and airway microvascular leakage, assessed as extravasation of the albumin marker, Evans blue dye.3 NKA at 1 x 10-4 and 3 x 10-4M resulted in a significantly higher increase in RL than SP at the same doses.4 Inhaled SP (3 x 10-4M; 45 breaths) caused significantly higher Evans blue dye extravasation in main bronchi and proximal intrapulmonary airways compared to the same dose of NKA. 5 Pretreatment with the specific inhibitor of neural endopeptidase (NEP24.11), phosphoramidon, caused an approximately 100 fold leftward shift of the RL responses to inhaled NKA and SP. 6 Phosphoramidon significantly potentiated both NKA-and SP-induced airway microvascular leakage at proximal intrapulmonary airways, but not at any other airway level. 7 Inhibition of NEP24.11 potentiate both the SP-or NKA-induced airflow obstruction to a larger extent than the induced airway microvascular leakage, suggesting that NEP24.11 is more important in the modulation of the airflow obstruction observed after these mediators.

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Section: Discussionsupporting

confidence: 54%

Section: Discussionmentioning

confidence: 99%

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Differential effects of phosphoramidon on neurokinin A‐ and substance P‐induced airflow obstruction and airway microvascular leakage in guinea‐pig

Lötvall

Elwood

Tokuyama

et al. 1991

British J Pharmacology

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“…Studies using a series of mammalian tachykinins have suggested the presence of distinct receptor subtypes (Iversen, 1985). Substance P(SP), an 11-amino acid peptide, contracts human airway smooth muscle in vitro (Karlsson & Persson, 1986) and when given intravenously to human subjects increases HR and SkT whilst causing diastolic BP to fall.…”

Section: Introduction Methodsmentioning

confidence: 99%

Comparison of neurokinin A and substance P on cardiovascular and airway function in man.

Evans

Dixon

Clarke

et al. 1988

Brit J Clinical Pharma

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The airway and cardiovascular effects of intravenous neurokinin A (NKA) and substance P (SP) were compared in six normal subjects. Both SP and NKA increased skin temperature (SkT) and heart rate (HR), but SP was more potent than NKA by factors of 6 and 20 respectively. No change in systolic blood pressure (BP) occurred with either peptide, but diastolic BP fell significantly with SP infusion. SP caused bronchodilation and NKA bronchoconstriction. NKA and SP have differing physiological roles and may activate different receptor populations.

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“…A variety of evidence now supports the existence of multiple receptors for tachykinin peptides in different tissues (see reviews by Watson, 1984a;Iversen, 1985; Table 1). At the SP-P receptor type, exemplified by the receptor present in guinea-pig ileum longitudinal smooth muscle, substance P is active in nanomolar concentrations and is approximately equipotent with eledoisin, kassinin and physaelamin (Lee et al, 1982).…”

Section: Introductionmentioning

confidence: 99%

Effects of tachykinins on inositol phospholipid hydrolysis in slices of hamster urinary bladder

Bristow

Curtis

Suman‐Chauhan

et al. 1987

British J Pharmacology

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1Tachykinin-stimulated inositol phospholipid hydrolysis was examined in slices of hamster urinary bladder.2 In the presence of lithium, to inhibit inositol monophosphatase activity, substance P, eledoisin and related tachykinins induced large, dose-dependent increases in [3H]-inositol monophosphate accumulation. 3 The responses to substance P and eledoisin were not antagonized by the cholinoceptor antagonist, atropine. 4 The rank order of potency for various tachykinins was kassinin> neurokinin A> neurokinin B > eledoisin > physaelamin > substance P > substance P methyl ester. 5 The synthetic analogue [p-Glu6, D-Pro9] SP (6-11) was considerably more potent than its L-prolyl stereoisomer at stimulating inositol phospholipid hydrolysis. 6 These results suggest that in the hamster urinary bladder, tachykinin-induced inositol phospholipid breakdown is mediated via tachykinin receptors of the SP-E type, as opposed to the SP-P type.

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Multiple Receptors and Binding Sites for Tachykinins

Cited by 24 publications

References 14 publications

Differential effects of phosphoramidon on neurokinin A‐ and substance P‐induced airflow obstruction and airway microvascular leakage in guinea‐pig

Differential effects of phosphoramidon on neurokinin A‐ and substance P‐induced airflow obstruction and airway microvascular leakage in guinea‐pig

Comparison of neurokinin A and substance P on cardiovascular and airway function in man.

Effects of tachykinins on inositol phospholipid hydrolysis in slices of hamster urinary bladder

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