ROLE OF EXTRACELLULAR CALCIUM IN THE EFFECTS OF SUBSTANCE P AND NEUROKININ A ON GUINEA PIG TRACHEA AND HUMAN BRONCHUS

1988 ◽  
Vol 2 (1) ◽  
pp. 47-55 ◽  
Author(s):  
R. MATRAN ◽  
E. NALINE ◽  
C. ADVENIER ◽  
A. LOCKHART ◽  
J.F. TRICOT ◽  
...  
Keyword(s):  
Substance P ◽  
Guinea Pig ◽  
Extracellular Calcium ◽  
Neurokinin A ◽  
Human Bronchus

Tachykinin recovery during postmortem bronchoconstriction in guinea pig lungs

1991 ◽  
Vol 70 (3) ◽  
pp. 1215-1219 ◽  
Author(s):  
M. A. Martins ◽  
S. A. Shore ◽  
J. M. Drazen
Keyword(s):  
Substance P ◽  
Guinea Pig ◽  
Neutral Endopeptidase ◽  
Neurokinin A ◽  
Opening Pressure ◽  
Airway Opening ◽  
Isolated Lungs ◽  
Peak Value

We examined the role of substance P (SP) and neurokinin A (NKA) in the postmortem bronchoconstriction in guinea pig lungs using isolated lungs superfused via the trachea. Airway opening pressure (Pao) during superfusion was monitored and the superfusate collected for analysis of SP- and NKA-like immunoreactivities (SP-LI and NKA-LI, respectively). Peak Pao (39.0 +/- 3.9 cmH2O) was reached 10 min after starting superfusion; Pao decreased slowly thereafter, reaching only 9.9 +/- 2.2% of the peak value 2 h after starting superfusion (P less than 0.005); 12.6 +/- 2.6 and 34.0 +/- 9.7 fmol of SP-LI and NKA-LI, respectively, were found in the fraction corresponding to 10-20 min of superfusion. Recovered immunoreactivities decreased to 5.2 +/- 0.3 and 9.3 +/- 1.8 fmol of SP-LI and NKA-LI, respectively, in the fraction corresponding to 110-120 min of superfusion (P less than 0.05). Inhibition of neutral endopeptidase with thiorphan resulted in significantly greater increases in Pao (P less than 0.005) and augmentation of the recovery of SP-LI and NKA-LI (P less than 0.05 and P less than 0.001, respectively). Capsaicin treatment of animals 7-10 days before the removal of their lungs abolished the increase in Pao during superfusion and resulted in a significant decrease in the amount of SP-LI and NKA-LI recovered. Our data confirm that tachykinin release occurs during postmortem bronchoconstriction in guinea pig lungs and, furthermore, that tachykinin degradation by NEP modulates the intensity of this response.

Neurokinin A but not neurokinin B and substance P induces codeine-resistant coughs in awake guinea-pig

1992 ◽  
Vol 37 ◽  
pp. S154
Author(s):  
K. Takahama ◽  
J. Fuchikami ◽  
Y. Isohama ◽  
H. Kai ◽  
T. Miyata
Keyword(s):  
Substance P ◽  
Guinea Pig ◽  
Neurokinin A ◽  
Neurokinin B

Substance P-induced histamine release in tracheally perfused guinea pig lungs

1995 ◽  
Vol 78 (4) ◽  
pp. 1234-1241 ◽  
Author(s):  
C. M. Lilly ◽  
A. E. Hall ◽  
I. W. Rodger ◽  
L. Kobzik ◽  
K. J. Haley ◽  
...  
Keyword(s):  
Mast Cells ◽  
Substance P ◽  
Guinea Pig ◽  
Histamine Release ◽  
Receptor Activation ◽  
Neurokinin A ◽  
Histamine Liberation ◽  
Nk1 Antagonist ◽  
Nk2 Receptor ◽  
Receptor Agonists And Antagonists

The capacity of substance P (SP) and endogenously released tachykinins to liberate histamine was examined in isolated tracheally perfused guinea pig lungs. Increasing doses of tracheally injected SP were associated with the recovery of increasing amounts of histamine from lung effluent. The mechanism of SP-induced histamine liberation was explored in studies with neurokinin-(NK) receptor agonists and antagonists. Tracheal injection of either the NK1 agonist [Sar9,Met(O2)11]SP or the NK2 agonist [beta-Ala8]-neurokinin A-(4–10) was associated with a significant increase in histamine recovery from lung effluent. In addition, both the NK1 antagonist CP-99994 and the NK2 antagonist SR-48968 significantly inhibited SP-induced histamine release. These findings support the hypothesis that SP can liberate histamine from guinea pigs lungs by a mechanism that depends predominantly on NK1- and NK2-receptor activation. The liberation of endogenous tachykinins by acute tracheal injection of capsaicin was also associated with augmented histamine recovery, which was inhibited by combined NK1- and NK2-receptor blockade. Tracheal injection of SP was associated with an increase in the percentage of airway mast cells exhibiting histological evidence of degranulation. This study demonstrates that exogenous SP, as well as endogenous tachykinins released from capsaicin-sensitive neurons, can liberate histamine, most likely from airway mast cells, by a mechanism that depends predominantly on the activation of NK1 and NK2 receptors.

Substance P-inducing massive postmortem bronchoconstriction in guinea pig lungs

1987 ◽  
Vol 62 (2) ◽  
pp. 746-751 ◽  
Author(s):  
Y. L. Lai ◽  
A. F. Cornett
Keyword(s):  
Substance P ◽  
Guinea Pig ◽  
Sensory Nerve ◽  
Transpulmonary Pressure ◽  
Blocking Agent ◽  
Base Line ◽  
Time Period ◽  
Exogenous Substance ◽  
Inflation Volume

To further examine the role that substance P plays in initiating the observed massive postmortem bronchoconstriction in guinea pig lungs and to explore the role of neural reflex in this airway spasm, six groups of animals were employed: control (n = 6), morphine (n = 6), substance P (n = 5), chronic capsaicin pretreatment + substance P (n = 5), tetrodotoxin (TTX) + acute capsaicin (n = 4), and chlorisondamine + acute capsaicin (n = 5). Pressure-volume curves were performed prior to and following the initiation of artificial pulmonary perfusion with 1% bovine serum albumin and 5% dextran in Tyrode's solution. A decrease in inflation volume (the lung volume between transpulmonary pressure of 0 and 30 cmH2O during inflation) was used as an index of bronchoconstriction. In control animals, inflation volume decreased to 20–30% of the base-line value at 15–30 min of perfusion, indicating massive bronchial constriction during this time period. Morphine (an agent inhibiting substance P release) significantly attenuated the spasm, whereas the presence of substance P in the perfusate markedly enhanced the constriction. Depletion of endogenous substance P by chronic capsaicin pretreatment did not affect exogenous substance P-induced spasm. Acute capsaicin-induced bronchoconstriction was significantly attenuated by TTX but was not affected by the ganglionic blocking agent, chlorisondamine. These data suggest that substance P initiates the massive postmortem bronchoconstriction in guinea pig lungs and that substance P is released by local stimulation of sensory nerve endings via axonal reflex.

Use of NK1 receptor antagonists in the exploration of physiological functions of substance P and neurokinin A

1995 ◽  
Vol 73 (7) ◽  
pp. 903-907 ◽  
Author(s):  
M. Qtsuka ◽  
K. Yoshioka ◽  
M. Yanagisawa ◽  
H. Suzuki ◽  
F.-Y. Zhao ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Electrical Stimulation ◽  
Substance P ◽  
Guinea Pig ◽  
Saphenous Nerve ◽  
Ventral Root ◽  
Neonatal Rat ◽  
Neurokinin A ◽  
Receptor Antagonists ◽  
Stimulation Of

Tachykinin NK1 receptor antagonists were used to explore the physiological functions of substance P (SP) and neurokinin A (NKA). Pharmacological profiles of three NK1 receptor antagonists, GR71251, GR82334, and RP 67580, were examined in the isolated spinal cord preparation of the neonatal rat. These tachykinin receptor antagonists exhibited considerable specificities and antagonized the actions of both SP and NKA to induce the depolarization of ventral roots. Electrical stimulation of the saphenous nerve with C-fiber strength evoked a depolarization lasting about 30 s of the ipsilateral L3 ventral root. This response, which is referred to as saphenous-nerve-evoked slow ventral root potential (VRP), was depressed by these NK1 receptor antagonists. In contrast, the saphenous-nerve-evoked slow VRP was potentiated by application of a mixture of peptidase inhibitors, including thiorphan, actinonin, and captopril in the presence of naloxone, but not after further addition of GR71251. Likewise, in the isolated coeliac ganglion of the guinea pig, electrical stimulation of the mesenteric nerves evoked in some ganglionic cells slow excitatory postsynaptic potentials (EPSPs), which were depressed by GR71251 and potentiated by peptidase inhibitors. These results further support the notion that SP and NKA serve as neurotransmitters producing slow EPSPs in the neonatal rat spinal cord and guinea pig prevertebral ganglia.Key words: substance P, neurokinin A, neurotransmitter, tachykinin antagonist, spinal cord.

Proteolytic Inactivation of Substance P and Neurokinin A in the Longitudinal Muscle Layer of Guinea Pig Small Intestine

2006 ◽  
Vol 47 (3) ◽  
pp. 856-864 ◽  
Author(s):  
R. Nau ◽  
G. Schäfer ◽  
C. F. Deacon ◽  
T. Cole ◽  
D. V. Agoston ◽  
...  
Keyword(s):  
Small Intestine ◽  
Substance P ◽  
Guinea Pig ◽  
Longitudinal Muscle ◽  
Muscle Layer ◽  
Neurokinin A ◽  
Longitudinal Muscle Layer
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