Thoracic Vagal Efferent Nerve Stimulation Evokes Substance P-Induced Early Airway Bronchonstriction and Late Proinflammatory and Oxidative Injury in the Rat Respiratory Tract

2005 ◽  
Vol 12 (4) ◽  
pp. 671-681 ◽  
Author(s):  
Ping-Chia Li ◽  
Sheng-Chung Li ◽  
Yuan-Ju Lin ◽  
Jin-Tung Liang ◽  
Chiang-Ting Chien ◽  
...  
Keyword(s):  
Substance P ◽  
Respiratory Tract ◽  
Nerve Stimulation ◽  
Oxidative Injury ◽  
Efferent Nerve ◽  
Vagal Efferent Nerve

Regulation of central vascular blood flow in the turtle

1994 ◽  
Vol 267 (2) ◽  
pp. R569-R578 ◽  
Author(s):  
S. G. Comeau ◽  
J. W. Hicks
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Nerve Stimulation ◽  
Lung Ventilation ◽  
Efferent Nerve ◽  
Cardiovascular Changes ◽  
Afferent Nerves ◽  
Adrenergic Control ◽  
Vagal Afferent ◽  
Vagal Efferent Nerve

The purpose of this study was to determine the effects of vagal nerve stimulation on the pulmonary and systemic circulations in the turtle Pseudemys scripta. The heart rate (HR), systemic vascular resistance (Rsys), pulmonary vascular resistance (Rpul), total pulmonary blood flow (Qpul), and total systemic blood flow (Qsys) were measured during electrical stimulation of the vagal efferent and the vagal afferent nerves. Vagal efferent nerve stimulation resulted in a bradycardia, increased Rsys and Rpul, and a 60% reduction in the Qpul and Qsys. These cardiovascular changes were eliminated after an intravenous injection of atropine. In contrast, vagal afferent nerve stimulation resulted in a tachycardia, a twofold increase in Rsys, a reduction in Rpul, and an 85% increase in Qpul. These changes were eliminated after pretreating the animals with bretylium tosylate (10 mg/kg). An intravenous infusion of epinephrine (0.1 micrograms/kg) produced cardiovascular changes similar to vagal afferent stimulation. The cardiovascular changes resulting from afferent and efferent nerve stimulation were similar to the cardiovascular adjustments often associated with intermittent lung ventilation in reptiles. The results of our study suggest that such cardiovascular changes are under cholinergic and adrenergic control.

Mechanism underlying the response to vasodilator nerve stimulation in isolated dog and monkey cerebral arteries

1990 ◽  
Vol 259 (5) ◽  
pp. H1511-H1517 ◽  
Author(s):  
N. Toda ◽  
T. Okamura
Keyword(s):  
Nitric Oxide ◽  
Electrical Stimulation ◽  
Coronary Artery ◽  
Substance P ◽  
Nerve Stimulation ◽  
Cerebral Arteries ◽  
Inhibitory Effect ◽  
Synthesis Inhibitor ◽  
Transmural Stimulation ◽  
Stimulation Of

Relaxant responses to transmural electrical stimulation and nicotine of cerebral artery strips obtained from dogs and Japanese monkeys were abolished by tetrodotoxin and hexamethonium, respectively, and suppressed by treatment with NG-monomethyl-L-arginine (L-NMMA), a nitric oxide (NO) synthesis inhibitor. The inhibitory effect was prevented and reversed by L-arginine but not by D-arginine. The relaxations suppressed by L-NMMA were not increased by exogenously applied NO. Endothelium denudation did not alter the response to transmural stimulation and nicotine or the inhibitory effect of L-NMMA. D-NMMA did not inhibit the response to vasodilator nerve stimulation. Dog coronary artery relaxations caused by transmural stimulation were not inhibited by L-NMMA but reversed to contractions by propranolol. Relaxations caused by substance P of dog cerebral arteries treated with indomethacin were dependent on endothelium and inhibited by L-NMMA, whereas those by NO and nitroglycerin, endothelium-independent relaxations, were unaffected. It is concluded that chemical and electrical stimulation of vasodilator nerves relaxes dog and monkey cerebral arteries, possibly by a mediation of NO rather than a stimulating action of NO on the release of vasodilator transmitter. Endothelium-dependent relaxations by substance P of dog cerebral arteries appear to be mediated by NO.

Airway neutral endopeptidase-like enzyme modulates tachykinin-induced bronchoconstriction in vivo

1988 ◽  
Vol 65 (6) ◽  
pp. 2585-2591 ◽  
Author(s):  
D. J. Dusser ◽  
E. Umeno ◽  
P. D. Graf ◽  
T. Djokic ◽  
D. B. Borson ◽  
...  
Keyword(s):  
Substance P ◽  
Guinea Pig ◽  
Vagus Nerve ◽  
Nerve Stimulation ◽  
Guinea Pigs ◽  
Vagus Nerve Stimulation ◽  
Neutral Endopeptidase ◽  
Base Line ◽  
Pulmonary Resistance

To determine whether neutral endopeptidase (NEP), also called enkephalinase (EC 3.4.24.11), modulates the effects of exogenous and endogenous tachykinins in vivo, we studied the effects of aerosolized phosphoramidon, a specific NEP inhibitor, on the responses to aerosolized substance P (SP) and on the atropine-resistant response to vagus nerve stimulation (10 V, 5 ms for 20 s) in guinea pigs. SP alone (10(-7) to 10(-4) M; each concentration, 7 breaths) caused no change in total pulmonary resistance (RL, P greater than 0.5). Phosphoramidon (10(-4) M, 90 breaths) caused no change either in base-line RL (P greater than 0.5) or in the response to aerosolized acetylcholine (P greater than 0.5). However, in the presence of phosphoramidon, SP (7 breaths) produced a concentration-dependent increase in RL at concentrations greater than or equal to 10(-5) M (P less than 0.001). Phosphoramidon (10(-7) to 10(-4) M; each concentration, 90 breaths) induced a concentration-dependent potentiation of SP-induced bronchoconstriction (10(-4) M, 7 breaths; P less than 0.01). Vagus nerve stimulation (0.5-3 Hz), in the presence of atropine, induced a frequency-dependent increase in RL (P less than 0.001). Phosphoramidon potentiated the atropine-resistant responses to vagus nerve stimulation (P less than 0.001) at frequencies greater than 0.5 Hz. The tachykinin antagonist [D-Arg1,D-Pro2,D-Trp7,9,Leu11]-substance P abolished the effects of phosphoramidon on the atropine-resistant response to vagus nerve stimulation (2 Hz, P less than 0.005). NEP-like activity in tracheal homogenates of guinea pig was inhibited by phosphoramidon with a concentration producing 50% inhibition of 5.3 +/- 0.8 nM.(ABSTRACT TRUNCATED AT 250 WORDS)

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