Stimulus Response Curves of Single Carotid Body Chemoreceptor Afferent Fibres

Nature ◽  
1967 ◽  
Vol 215 (5101) ◽  
pp. 654-655 ◽  
Author(s):  
T. J. BISCOE ◽  
S. R. SAMPSON ◽  
M. J. PURVES
Keyword(s):  
Carotid Body ◽  
Response Curves ◽  
Stimulus Response

Dopamine and ventilatory effects of hypoxia and almitrine in chronically hypoxic rats

1989 ◽  
Vol 67 (1) ◽  
pp. 186-192 ◽  
Author(s):  
R. A. Wach ◽  
D. Bee ◽  
G. R. Barer
Keyword(s):  
Carotid Body ◽  
Ventilatory Response ◽  
Response Curves ◽  
Enhancing Effect ◽  
Stimulus Response ◽  
Ventilatory Responses ◽  
Carotid Bodies ◽  
Ventilatory Effects ◽  
Ventilatory Response To Hypoxia

We hypothesized that the temporary blunted ventilatory response to hypoxia seen in chronically hypoxic rats could be related to the increased amount of dopamine found in their carotid bodies. Rats, kept 2–3 wk in 10% O2, showed reduced nonisocapnic ventilatory responses to 21–12% inspiratory O2 fraction compared with control rats. Stimulus-response curves to almitrine, which simulates the action of hypoxia on the carotid body, were also depressed in chronically hypoxic rats. Responses to hypoxia and almitrine were significantly correlated in the two groups of rats. Dopamine depressed ventilation during normoxia, hypoxia, and almitrine stimulation in both groups, an action abolished by the dopamine-2 antagonist domperidone. Domperidone slightly increased responses to hypoxia and almitrine in control rats but had a greater enhancing effect in chronically hypoxic rats, such that there was no longer a difference between the responses of the two groups.

scholarly journals Mechanosensitive hyaluronan secretion: stimulus-response curves and role of transcription-translation-translocation in rabbit joints

2009 ◽  
Vol 94 (3) ◽  
pp. 350-361 ◽  
Author(s):  
A. K. T. Wann ◽  
K. R. Ingram ◽  
P. J. Coleman ◽  
N. McHale ◽  
J. R. Levick
Keyword(s):  
Response Curves ◽  
Stimulus Response

scholarly journals Analysis and Design of Stimulus Response Curves of E. coli

Metabolites ◽  
2012 ◽  
Vol 2 (4) ◽  
pp. 844-871
Author(s):  
Andreas Kremling ◽  
Anna Goehler ◽  
Knut Jahreis ◽  
Markus Nees ◽  
Benedikt Auerbach ◽  
...  
Keyword(s):  
Response Curves ◽  
Analysis And Design ◽  
E Coli ◽  
Stimulus Response

Inhibition of nitric oxide synthesis attenuates thermally induced asthma

2001 ◽  
Vol 91 (2) ◽  
pp. 703-708 ◽  
Author(s):  
C. Kotaru ◽  
M. Skowronski ◽  
A. Coreno ◽  
E. R. McFadden
Keyword(s):  
Nitric Oxide ◽  
Minute Ventilation ◽  
Isotonic Saline ◽  
Forced Expiratory Volume ◽  
Response Curves ◽  
Thermally Induced ◽  
Stimulus Response ◽  
Fractional Concentration ◽  
Exhaled Air ◽  
The Right

To determine whether the inhibition of nitric oxide (NO) synthesis attenuates thermally induced obstruction, we had 10 asthmatic volunteers perform isocapnic hyperventilation with frigid air after inhaling 1 mg of N G-monomethyl-l-arginine (l-NMMA) or isotonic saline in a blinded fashion. The challenges were identical in all respects, and there were no differences in baseline lung function [1-s forced expiratory volume (FEV1); saline 2.8 ± 0.3 liters, l-NMMA 2.9 ± 0.3 liters; P = 0.41] or prechallenge fractional concentration of nitric oxide in the exhaled air (FeNO) [saline 23 ± 6 parts/billion (ppb),l-NMMA 18 ± 4 ppb; P = 0.51]. Neither treatment had any impact on the FEV1, pulse, or blood pressure. After l-NMMA, FeNO fell significantly ( P < 0.0001), the stimulus-response curves shifted to the right, and the minute ventilation required to reduce the FEV1 20% rose 53.5% over control ( P = 0.02). The results of this study demonstrate that NO generated from the airways of asthmatic individuals may play an important role in the pathogenesis of thermally induced asthma.

Tachykinins mediate bronchoconstriction elicited by isocapnic hyperpnea in guinea pigs

1989 ◽  
Vol 66 (3) ◽  
pp. 1108-1112 ◽  
Author(s):  
D. W. Ray ◽  
C. Hernandez ◽  
A. R. Leff ◽  
J. M. Drazen ◽  
J. Solway
Keyword(s):  
Tidal Volume ◽  
Guinea Pigs ◽  
Minute Ventilation ◽  
Response Curves ◽  
Mechanically Ventilated ◽  
Stimulus Response ◽  
Respiratory System Resistance ◽  
Water Saturated ◽  
And Control ◽  
Isocapnic Hyperpnea

We tested the hypothesis that tachykinins mediate hyperpnea-induced bronchoconstriction (HIB) in 28 guinea pigs. Stimulus-response curves to increasing minute ventilation with dry gas were generated in animals depleted of tachykinins by capsaicin pretreatment and in animals pretreated with phosphoramidon, a neutral metalloendopeptidase inhibitor. Sixteen anesthetized guinea pigs received capsaicin (50 mg/kg sc) after aminophylline (10 mg/kg ip) and terbutaline (0.1 mg/kg sc). An additional 12 animals received saline (1 ml sc) instead of capsaicin. One week later, all animals were anesthetized, given propranolol (1 mg/kg iv), and mechanically ventilated (6 ml/kg, 60 breaths/min, 50% O2 in air fully water saturated). Phosphoramidon (0.5 mg iv) was administered to five of the noncapsaicin-treated guinea pigs. Eucapnic dry gas (95% O2–5% CO2) hyperpnea “challenges” were performed by increasing the tidal volume (2–6 ml) and frequency (150 breaths/min) for 5 min. Capsaicin-pretreated animals showed marked attenuation in HIB, with a rightward shift of the stimulus-response curve compared with controls; the estimated tidal volume required to elicit a twofold increase in respiratory system resistance (ES200) was 5.0 ml for capsaicin-pretreated animals vs. 3.7 ml for controls (P less than 0.03). Phosphoramidon-treated animals were more reactive to dry gas hyperpnea compared with control (ES200 = 2.6 ml; P less than 0.0001). Methacholine dose-response curves (10(-11) to 10(-7) mol iv) obtained at the conclusion of the experiments were similar among capsaicin, phosphoramidon, and control groups. These findings implicate tachykinin release as an important mechanism of HIB in guinea pigs.

Chronic intermittent hypoxia alters NMDA and AMPA-evoked currents in NTS neurons receiving carotid body chemoreceptor inputs

2007 ◽  
Vol 292 (6) ◽  
pp. R2259-R2265 ◽  
Author(s):  
Patricia M. de Paula ◽  
Gleb Tolstykh ◽  
Steve Mifflin
Keyword(s):  
Sleep Apnea ◽  
Nmda Receptors ◽  
Dose Response ◽  
Carotid Body ◽  
Intermittent Hypoxia ◽  
Receptor Activation ◽  
Response Curves ◽  
Ampa And Nmda Receptors ◽  
Afferent Inputs ◽  
Dose Response Curves

Chronic exposure to intermittent hypoxia (CIH) has been used in animals to mimic the arterial hypoxemia that accompanies sleep apnea. Humans with sleep apnea and animals exposed to CIH have elevated blood pressures and augmented sympathetic nervous system responses to acute exposures to hypoxia. To test the hypothesis that exposure to CIH alters neurons within the nucleus of the solitary tract (NTS) that integrate arterial chemoreceptor afferent inputs, we measured whole cell currents induced by activation of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) and N-methyl-d-aspartate (NMDA) receptors in enzymatically dispersed NTS neurons from normoxic (NORM) and CIH-exposed rats (alternating cycles of 3 min at 10% O2 followed by 3 min at 21% O2 between 8 AM and 4 PM for 7 days). To identify NTS neurons receiving carotid body afferent inputs the anterograde tracer 4- (4-(dihexadecylamino)styryl- N-methylpyridinum iodide (DiA) was placed onto the carotid body 1 wk before exposure to CIH. AMPA dose-response curves had similar EC50 but maximal responses increased in neurons isolated from DiA-labeled CIH (20.1 ± 0.8 μM, n = 9) compared with NORM (6.0 ± 0.3 μM, n = 8) rats. NMDA dose-response curves also had similar EC50 but maximal responses decreased in CIH (8.4 ± 0.4 μM, n = 8) compared with NORM (19.4 ± 0.6 μM, n = 9) rats. These results suggest reciprocal changes in the number and/or conductance characteristics of AMPA and NMDA receptors. Enhanced responses to AMPA receptor activation could contribute to enhanced chemoreflex responses observed in animals exposed to CIH and humans with sleep apnea.

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