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PubMed1976

The relevance of peripheral baroreceptors and chemoreceptors to regulation of cerebral blood flow in the cat.

The contribution of neural vasomotor reflexes to the control of cerebral blood flow (CBF) was investigated in 30 cats lightly anesthetized with pentobarbital. CBF was measured both by kinetic analysis and by the intial slope technique of the washout curve of a bolus of 133Xe. Autoregulation (10 cats) and responsiveness to alteration in arterial PCO2 (PaCO2) (10 cats) and arterial PO2 (Pao2) (five cats) were assessed both before and after bilateral intracranial division of the 9th and 10th nerves. In an additional group (five cats), related changes in CBF to alteration of PaCO2 were recorded before and after unilateral section of the 7th and 8th nerves. Autoregulation was preserve after division of the 9th and 10th nerves and there was no significant change in the PaCO2 response curves. Section of the 7th and 8th cranial nerves did not produce conclusive results in the small number of cats studied. A conclusion that the facial nerves are not dominant in responses to hypercapnia seems justified, but a modulating role for these nerves is possible. These studies do not exclude a physiological role for these nerves in the autoregulation of CBF, but do indicate that the cerebral vascular bed apparently is capable of functioning normally after their division.

Animals↗
PubMed2001

O(2) modulates large-conductance Ca(2+)-dependent K(+) channels of rat chemoreceptor cells by a membrane-restricted and CO-sensitive mechanism.

Hypoxic inhibition of large-conductance Ca(2+)-dependent K(+) channels (maxiK) of rat carotid body type I cells is a well-established fact. However, the molecular mechanisms of such inhibition and the role of these channels in the process of hypoxic transduction remain unclear. We have examined the mechanisms of interaction of O(2) with maxiK channels exploring the effect of hypoxia on maxiK currents recorded with the whole-cell and the inside-out configuration of the patch-clamp technique. Hypoxia inhibits channel activity both in whole-cell and in excised membrane patches. This effect is strongly voltage- and Ca(2+)-dependent, being maximal at low [Ca(2+)] and low membrane potential. The analysis of single-channel kinetics reveals a gating scheme comprising three open and five closed states. Hypoxia inhibits channel activity increasing the time the channel spends in the longest closed states, an effect that could be explained by a decrease in the Ca(2+) sensitivity of those closed states. Reducing maxiK channels with dithiothreitol (DTT) increases channel open probability, whereas oxidizing the channels with 2,2'-dithiopyridine (DTDP) has the opposite effect. These results suggest that hypoxic inhibition is not related with a reduction of channel thiol groups. However, CO, a competitive inhibitor of O(2) binding to hemoproteins, fully reverts hypoxic inhibition, both at the whole-cell and the single-channel level. We conclude that O(2) interaction with maxiK channels does not require cytoplasmic mediators. Such interaction could be mediated by a membrane hemoprotein that, as an O(2) sensor, would modulate channel activity.

Animals↗
PubMed2000

Influence of chemoreceptor stimuli on genioglossal response to negative pressure in humans.

Genioglossal muscle (GG) activity is modulated by both chemoreceptive and mechanoreceptive reflexes that help stabilize airway patency. We assessed the effects of blood gas changes, within the range encountered during mild obstructive apnea-arousal cycles, on GG activity and the GG reflex to upper airway negative pressure. Eighteen healthy adults were studied while awake under 5 conditions: (1) baseline (PET(CO(2)) = 40 mm Hg, Sa(O(2)) = 99%); (2) hypercapnia (PET(CO(2)) = 45 mm Hg); (3) hypocapnia (PET(CO(2)) = 35 mm Hg, induced via hyperventilation with an iron lung ventilator); (4) hypoxia (Sa(O(2)) = 87%); and (5) hypercapnia plus hypoxia (PET(CO(2)) = 45 mm Hg, Sa(O(2)) = 87%). Measurements included airflow, choanal and epiglottic pressures (Pchoa and Pepi), upper airway resistance, phasic and tonic GG EMG, and the GG reflex to negative pressure (Pchoa = -12.5 cm H(2)O). Ventilation increased from a baseline of 10.7 up to 22.7 L. min(-1) under conditions of altered blood gases. Peak inspiratory phasic GG EMG increased from 6. 5 to 11.1% of maximal contraction but there were no significant changes in either tonic GG EMG (range, 4.3 to 5.8% of maximum) or magnitude of the GG reflex (range, 4.1 to 5.5% of maximum). Among conditions there was a high correlation between upper airway pressures and peak phasic GG EMG (Pchoa, r = 0.97, p < 0.01; Pepi, r = 0.87; p = 0.06). We conclude that in this range of blood gases: (1) the GG reflex to negative pressure is unchanged; (2) slow airway pressure changes throughout inspiration, generated either actively or passively, influence GG EMG activity; and (3) mechanoreceptive control of GG EMG can fully explain all changes in GG activity, suggesting that chemoreceptive inputs to GG are minimal, or are not simply summated with mechanoreceptor inputs.

Adult↗
PubMed1993

Comparison of peripheral chemoreceptor responses in monozygotic and dizygotic twin infants.

The peripheral chemoresponses of infant twin pairs were determined using a single-breath hyperoxic stimulus. A total of 43 twin pairs of comparable gestation and birth weight were studied during sleep at a mean (SD) age of 8 wk (1.4) while alternately breathing either air or 16% oxygen in nitrogen. Infants responded to a single breath of 100% oxygen by a reduction in ventilation; the mean (SEM) reduction in air was 273 ml/min (10.6) and in 16% oxygen 560 ml/min (18.4). Within-pair variances were compared in 14 monozygotic and 28 dizygotic pairs utilizing combined responses (air + 16% oxygen) computed for measurements made in behavioral quiet sleep and in 9 monozygotic and 20 dizygotic pairs for whom data were complete in polygraphically confirmed quiet sleep. The variance of responses within dizygotic twin pairs was greater than in monozygotic pairs when expressed in ml/min: F ratio 4.11 (p = 0.005) for all data and F ratio 7.67 (p = 0.003) in quiet sleep. Expressed in ml/min/kg the difference was less significant: F ratio 1.83 (p = 0.126) for all data and F ratio 3.46 (p = 0.039) in quiet sleep. Gender, birth weight, and birth order had no effect on these findings. This closer similarity of response in monozygotic twin pairs is explained by proposing a high degree of heritability for the response.

Chemoreceptor Cells↗
PubMed2002

Triple immunofluorescence staining with antibodies raised in the same species to study the complex innervation pattern of intrapulmonary chemoreceptors.

A general problem in immunocytochemistry is the development of a reliable multiple immunolabeling method when primary antibodies must be used that originate in the same species. We have developed a protocol for the immunodetection of three antigens in a single tissue preparation, using unconjugated primary antibodies raised in the same species. Immunocytochemical detection of neuronal nitric oxide synthase, calcitonin gene-related peptide, and calbindin D28k in the lung of rats demonstrated that part of the pulmonary neuroepithelial bodies are selectively contacted by at least three different nerve fiber populations. The first antigen was detected using tyramide signal amplification, a very sensitive method allowing a dilution of the first primary antibody far beyond the detection limit of fluorescently labeled secondary antibodies. The second antigen was visualized by a fluorophore-conjugated secondary monovalent Fab antibody that at the same time blocks the access of the third secondary antibody to the second primary antibody. Moreover, the monovalence of the Fab fragment prevents the third primary antibody from binding with the second-step secondary antibody. The triple staining technique described here is generally applicable, uses commercially available products only, and allows the detection of three antigens in the same preparation with primary antibodies that are raised in the same species.

Animals↗
PubMed2003

Characterization of the nodulation plasmid encoded chemoreceptor gene mcpG from Rhizobium leguminosarum.

BACKGROUND: In general, chemotaxis in Rhizobium has not been well characterized. Methyl accepting chemotaxis proteins are sensory proteins important in chemotaxis of numerous bacteria, but their involvement in Rhizobium chemotaxis is unclear and merits further investigation. RESULTS: A putative methyl accepting chemotaxis protein gene (mcpG) of Rhizobium leguminosarum VF39SM was isolated and characterized. The gene was found to reside on the nodulation plasmid, pRleVF39d. The predicted mcpG ORF displayed motifs common to known methyl-accepting chemotaxis proteins, such as two transmembrane domains and high homology to the conserved methylation and signaling domains of well-characterized MCPs. Phenotypic analysis of mcpG mutants using swarm plates did not identify ligands for this putative receptor. Additionally, gene knockouts of mcpG did not affect a mutant strain's ability to compete for nodulation with the wild type. Notably, mcpG was found to be plasmid-encoded in all strains of R. leguminosarum and R. etli examined, though it was found on the nodulation plasmid only in a minority of strains. CONCLUSIONS: Based on sequence homology R. leguminosarum mcpG gene codes for a methyl accepting chemotaxis protein. The gene is plasmid localized in numerous Rhizobium spp. Although localized to the sym plasmid of VF39SM mcpG does not appear to participate in early nodulation events. A ligand for McpG remains to be found. Apparent McpG orthologs appear in a diverse range of proteobacteria. Identification and characterization of mcpG adds to the family of mcp genes already identified in this organism.

Amino Acid Sequence↗
PubMed2001

Acute oxygen sensing: diverse but convergent mechanisms in airway and arterial chemoreceptors.

Airway neuroepithelial bodies sense changes in inspired O2, whereas arterial O2 levels are monitored primarily by the carotid body. Both respond to hypoxia by initiating corrective cardiorespiratory reflexes, thereby optimising gas exchange in the face of a potentially deleterious O2 supply. One unifying theme underpinning chemotransduction in these tissues is K+ channel inhibition. However, the transduction components, from O2 sensor to K+ channel, display considerable tissue specificity yet result in analogous end points. Here we highlight how emerging data are contributing to a more complete understanding of O2 chemosensing at the molecular level.

Animals↗
PubMed1981

Ventilatory chemoreceptor response in parents of children at risk for sudden infant death syndrome.

We postulated that parents of infants who sustain near-death episodes associated with defective chemical regulation of breathing might share a similar defect. We, therefore, measured the ventilatory responses to progressive hypoxia and hypercapnia individually in eight sets of parents of infants who had sustained at least one near-death episode (apnea, cyanosis, pallor, limpness, and responsive only to mouth-to-mouth resuscitation); each infant had a ventilatory response to CO2 which was more than 2 S.D. below the mean normal. Ventilatory function measured by vital capacity forced expiratory volume 1.0 and flow curves was normal in each group. Responses to hypercapnia and hypoxemia in both fathers and mothers were similar to 11 pairs of controls. Ventilation during CO2 rebreathing normalized for surface area increased 0.87 liter/min/mm Hg in fathers, 0.94 in controls, 0.87 in mothers, and 0.75 in controls. Ventilation during progressive hypoxemia increased 88 liter/min/1 divided by mm Hg in fathers, 92 in controls, 86 in mothers, and 101 in controls. None of these differences was significant.

Adult↗