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PubMed1972

The importance of timing on the respiratory effects of intermittent carotid body chemoreceptor stimulation.

1. The respiratory response, measured directly as tidal volume or indirectly by using integrated peak phrenic activity, to brief intermittent chemical stimulation or depression of the carotid body was determined in anaesthetized cats. Recordings of carotid sinus nerve impulses allowed precise timing of the stimulus.2. Stimulation of the carotid body had a rapid effect on air flow, tidal volume and phrenic discharge rate only if given during inspiration. Increases in tidal volume and peak phrenic discharge occurred only if stimulation was applied during the last half of inspiration. Stimulation during expiration had no effect on the form or magnitude of subsequent breaths.3. Depression of the carotid body by NH(4)OH led to decreased tidal volume and phrenic discharge if it occurred during inspiration but had no effect if it occurred during expiration.4. Stimuli in expiration led to a prolongation of expiration. Stimuli in late inspiration caused prolongation of both inspiration and expiration.5. All of the effects noted were eliminated by bilateral carotid body denervation.6. The findings are similar to those following electrical stimulation of the carotid sinus nerve and are attributable to modulation of carotid body signals by the central respiratory neurones.

Action Potentials↗
PubMed1973

Chemoreceptor properties of glomus tissue found in the carotid region of the cat.

1. ;Miniglomera' appearing as small masses of tissue with ample vascularization were found around the common carotid artery of the cat. Physiological, gross anatomical and electron microscopic studies were conducted on these tissues.2. The chemosensory function of each ;miniglomus' was evident from the behaviour of the afferent nerve fibres supplying the tissue: afferent responses became more active during asphyxia, when the blood flow through the tissue was reduced or blocked and when cyanide or ACh were applied. The afferent impulses became more infrequent during hyperventilation.3. Sensory frequency response curves constructed against percentage of inhaled O(2) showed that the impulses of single units increased in frequency with lowering of O(2) content of the inhaled gas.4. These miniglomera are innervated by afferent fibres emerging from the nodose ganglion; sometimes these fibres are contained in the aortic or common carotid baroreceptor nerves, but sometimes they emerge as independent nerves. None of the miniglomera are supplied by branches of the sinus nerve.5. The fine structure of the miniglomus is similar to that of the carotid body. The tissue contains two types of cells: glomus cells which contain dense cored granules, and sustentacular cells whose fine processes enclose the former. Membrane densifications occur where glomus cells lie adjacent to one another or where they are contacted by nerve terminals. Nerve fibres are common in the miniglomus but they contact glomus cells less frequently than in the carotid body.

Acetylcholine↗
PubMed1974

The role of arterial chemoreceptors in the breath-by-breath augmentation of inspiratory effort in rabbits during airway occlusion or elastic loading.

1. The breath-by-breath augmentation of inspiratory effort in the five breaths following airway occlusion or elastic loading was assessed in anaesthetized rabbits from changes of airway pressure, diaphragm e.m.g. and lung volume.2. When the airway was occluded in animals breathing air, arterial O(2) tension fell by 20 mmHg and CO(2) tension rose by 7 mmHg within the time of the first five loaded breaths.3. Inhalation of 100% O(2) or carotid denervation markedly reduced the breath-by-breath progression but had little or no effect on the responses at the first loaded breath.4. These results indicate that the breath-by-breath augmentation of inspiratory effort following addition of a load is mainly due to asphyxial stimulation of the carotid bodies, rather than to the gradual emergence of a powerful load-compensating reflex originating in the chest-wall, as postulated by some workers.5. The small residual progression seen in animals breathing 100% O(2) or following carotid denervation was not eliminated (a) by combining these procedures or (b) by addition of gas to the lungs to prevent the progressive lung deflation which occurred during airway occlusion.6. Bilateral vagotomy, when combined with carotid denervation, abolished the residual breath-by-breath progression of inspiratory effort.

Airway Obstruction↗
PubMed1992

Mitochondrial function in type I cells isolated from rabbit arterial chemoreceptors.

1. In this, and the accompanying paper (Duchen & Biscoe, 1992), we test the hypothesis that the oxygen sensitivity of mitochondrial electron transport forms a basis for transduction in the carotid body, the primary peripheral arterial oxygen sensor. We here describe for isolated type I cells the changes in autofluorescence of mitochondrial NAD(P)H that accompany changes in PO2. 2. NAD(P)H autofluorescence (excitation, 340-360 nm; emission peak, 450 nm) increased with anoxia, reflecting a rise in the NAD(P)H/NAD(P) ratio. Graded increases in autofluorescence were seen in response to graded decreases in PO2, suggesting that mitochondrial function is progressively altered below a PO2 of about 60 mmHg. 3. A mitochondrial origin for the NAD(P)H autofluorescence was suggested by the mutual exclusion of the responses to anoxia and cyanide. 4. Oxidized flavoproteins fluoresce when excited at 450 nm with an emission peak at 550 nm. The small signals obtained under these conditions increased with uncoupler and showed a graded decrease with falling PO2 reflecting a rise in the FADH/FAD ratio. 5. Hypoxia raises [Ca2+]i. The hypoxia-induced changes in mitochondrial function were not secondary to this rise. A brief K(+)-induced depolarization leads to a transient increase in [Ca2+]i. At the same time there is a rapid decrease in NAD(P)H autofluorescence followed by an increase that far outlasts the rise in [Ca2+]i. This delayed increase in autofluorescence was smaller than was the increase with anoxia, even though K(+)-induced depolarization raised [Ca2+]i more than does anoxia. In Ca(2+)-free solutions the depolarization-induced changes were abolished, while those associated with hypoxia were maintained. 6. The changes of autofluorescence with K(+)-induced depolarization appear to reflect (i) oxidation of NAD(P)H by stimulation of respiration following mitochondrial Ca2+ uptake and (ii) reduction of NAD(P) by the Ca(2+)-dependent activation of mitochondrial dehydrogenases. This activation could last several minutes following only 100 ms depolarization, while the changes accompanying hypoxia closely followed the time course of the change in PO2. 7. In similarly isolated rat or mouse chromaffin cells and mouse dorsal root ganglion neurons under identical conditions, no measurable change in autofluorescence or in [Ca2+]i was seen until the PO2 fell below about 5 mmHg. 8. Carbonyl cyanide p-trifluoromethoxy-phenylhydrazone (FCCP) increases O2 consumption, oxidizing mitochondrial NADH and hence decreasing autofluorescence, (delta FFCCP). Blockade of electron transport by anoxia or CN- decreases O2 consumption, increasing mitochondrial NADH/NAD and autofluorescence (delta FCN). The fractional change in autofluorescence with FCCP, delta FFCCP/delta FFCCP+FCN), is thus a measure of resting O2 consumption.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

Mechanisms underlying chemoreceptor inhibition induced by atrial natriuretic peptide in rabbit carotid body.

1. Previous studies in our laboratory revealed the presence of atrial natriuretic peptide (ANP) in preneural chemosensory type I cells of the cat carotid body, and demonstrated that submicromolar concentrations of the peptide inhibited carotid sinus nerve (CSN) activity evoked by hypoxia. In the present study, we have evaluated the role of the cyclic nucleotide second messenger, cyclic GMP (cGMP), and the involvement of type I cells in rabbit chemosensory inhibition. 2. Submicromolar concentrations of the potent ANP analogue, APIII, greatly elevated both the content and release of cGMP from the carotid body. Denervation experiments confirmed earlier immunocytochemical studies which suggested that APIII-induced cGMP production occurs almost exclusively in type I cells; these experiments also indicate that both the sympathetic and sensory innervation to the carotid body exert a trophic influence on the metabolism of this second messenger. 3. Submicromolar concentrations of APIII inhibited the CSN activity evoked by hypoxia (79.8 +/- 3.2% (mean +/- S.E.M.) inhibition with 100 nM APIII) and nicotine (74.5 +/- 3.6% inhibition with 100 nM APIII), but did not affect basal CSN activity established in 100% O2-equilibrated superfusion solutions. 4. The biologically inactive analogue of ANP, C-ANP, failed to produce CSN inhibition; however, the inhibitory effects of APIII were mimicked by cell-permeant analogues of cGMP (dibutyryl-cGMP and 8-bromo-cGMP, 2 mM), which likewise did not alter basal CSN activity. Because we found that unmodified cGMP was an ineffective inhibitor of CSN activity, our data suggest that APIII inhibition is mediated intracellularly by cGMP produced within the type I cells. 5. APIII does not inhibit the CSN activity produced by 20 mM K+ (in zero Ca2+ media), which very probably results from direct depolarization of the sensory nerve terminals. 6. Catecholamine release from the carotid body evoked by hypoxia is likewise not altered by APIII (100 nM). 7. The data are consistent with the notion that APIII and analogues of cGMP alter the release of excitatory and/or inhibitory transmitters from chemosensory type I cells in the carotid body.

Animals↗