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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ventral medullary surface (VMS) is a site of the medullary chemoreceptor neurons which sense excess protons (H+) derived from hypercapnia and facilitate respiration. We hypothesized that expression of genes involved in H+-sensitivity is higher in the VMS than in other central nervous system areas. By using the differential display technique, we differentiated the mRNAs of VMS neurons from those of cerebral cortical neurons. Seventeen clones of interest were isolated, and sequence analysis revealed that one of these clones had an encoding nuclear transcription factor, MafG. MafG is a member of Maf protein family, and the founding member of the family (v-Maf) was originally discovered as the transduced transforming component of avian musculoaponeurotic fibrosarcoma virus, AS42. The rat MafG was composed of 162 amino acid residues and was conserved among the primary structures of various species. Expression of rat mafG mRNA is high in the VMS, heart and skeletal muscle while the cerebral cortex, cerebellum, liver, stomach and intestine show moderate expression. To determine whether the expression of mafG mRNA is induced by hypercapnic stimulation, 7% CO2 in air was inhaled to rats for 5 min. We found that the hypercapnic stimulation induced the gene expression of mafG. These results suggest that MafG may be involved in H+-sensitivity and respiratory regulation in the VMS.
Mol Cell Biochem 2000 Jan
PMID:Cloning of MafG homologue from the rat brain by differential display and its expression after hypercapnic stimulation. 1072 42

The effects of hyperoxic hypercapnia on cardiovascular and ventilatory variables and blood gas and acid/base parameters were examined in conscious and anesthetized spontaneously breathing (ASB) channel catfish, Ictalurus punctatus. These separate experiments were designed to determine: (1) if channel catfish show a ventilatory response to hypercapnic acidosis when blood O(2) content is maintained in conscious animals; and (2) whether branchial receptors innervated by cranial nerves IX and X mediate this response. The combination of high O(2) and CO(2) tensions allowed the cardioventilatory effects of hypercapnic acidosis to be assessed independently of Root or Bohr mediated changes in blood O(2) content. In the absence of significant changes in dorsal or ventral aorta O(2) content, hyperoxic hypercapnia significantly stimulated ventilation, relative to hyperoxic exposure. Hypercapnic acidosis, however, had no significant effects on blood pressure or heart rate. Branchial denervation in ASB fish abolished the ventilatory response to hypercapnic acidosis. The results indicate that hypercapnic acidosis independently stimulates ventilation in channel catfish. This response is mediated by CO(2)/pH-sensitive branchial receptors innervated by cranial nerves IX and X.
Comp Biochem Physiol A Mol Integr Physiol 2000 Mar
PMID:Branchial chemoreceptors mediate ventilatory responses to hypercapnic acidosis in channel catfish. 1079 69

We have investigated whether translocation of constitutive low molecular weight stress proteins (alphaB-crystallin and HSP27) to the myofilament/cytoskeletal compartment occurs during ischemic preconditioning and assessed if this is causally associated with cardioprotection. Triton-insoluble preparations from fresh or aerobically perfused rat hearts (n=4/group) contained relatively little alphaB-crystallin (96 +/- 43 and 43 +/- 36 units respectively) or HSP27 (177 +/- 32 and 101 +/- 26 units respectively). Three preconditioning cycles of (5 min ischemia + 5 min reperfusion) increased the Triton-insoluble crystallin to 864 +/- 61 units (P<0.05) and HSP27 to 1353 +/- 53 units (P<0.05). Two hours of aerobic perfusion following the preconditioning protocol resulted the return of alphaB-crystallin and HSP27 to near control levels (189 +/- 14 units and 252 +/- 24 units, respectively). Stress protein translocation, comparable to that achieved by the IPC protocol was induced by aerobic perfusion with hypercarbic (pH 6.8) perfusion. Thus, three cycles of 5 min hypercarbia + 5 min normocarbia increased alphaB-crystallin to 628 +/- 30 units (P<0.05) and HSP27 to 1353 +/- 53 units. In parallel functional studies, the recovery of LVDP after 35 min ischemia and 60 min of reperfusion was 43 +/- 7% in the ischemic control group, 61 +/- 3% (P<0.05) in the preconditioned group and 42 +/- 6% in the hypercarbic group. Thus, translocation of alphaB-crystallin and/or is not of-itself sufficient to induce cardioprotection. Using a phospho-specific antibody, we have demonstrated that preconditioning not only translocates alphaB-crystallin but also increases its phosphorylation at Ser-59 by 9.7-fold compared to aerobic controls (1616 +/- 402 v 166 +/- 28 units respectively). In contrast, hypercarbia while eliciting a comparable translocation, failed to alter the phosphorylation state of alphaB-crystallin. Preconditioning-induced phosphorylation was significantly attenuated by 50 microM genistein (by 61%), 10 microM SB203580 (by 91%) and 10 microM bisindolylmaleimide (by 68%), but not by 10 microM PD98059 (by 4%). Our findings are consistent with the possibility that ischemic preconditioning may be mediated by phosphorylation and translocation of constitutive low molecular weight stress proteins, particularly alphaB-crystallin.
J Mol Cell Cardiol 2000 Jun
PMID:Ischemic preconditioning: a potential role for constitutive low molecular weight stress protein translocation and phosphorylation? 1088 50

The effects of hypercapnic acidosis and hypoxia on intracellular Ca(2+) concentration ([Ca(2+)](i)) were determined with Indo 1 in enzymatically isolated single type I cells from neonatal rat carotid bodies. Type I cells responded to graded hypoxic stimuli with graded [Ca(2+)](i) rises. The percentage of cells responding was also dependent on the severity of the hypoxic stimulus. Raising CO(2) from 5 to 10 or 20% elicited a significant increase in [Ca(2+)](i) in the same cells as those that responded to hypoxia. Thus both stimuli can be sensed by each individual cell. When combinations of hypoxic and acidic stimuli were given simultaneously, the responses were invariably greater than the response to either stimulus given alone. Indeed, in most cases, the response to hypercapnia was slightly potentiated by hypoxia. These data provide the first evidence that the classic synergy between hypoxic and hypercapnic stimuli observed in the intact carotid body may, in part, be an inherent property of the type I cell.
Am J Physiol Lung Cell Mol Physiol 2000 Jul
PMID:Interactions between hypoxia and hypercapnic acidosis on calcium signaling in carotid body type I cells. 1089

Ventilator strategies allowing for increases in carbon dioxide (CO(2)) tensions (hypercapnia) are being emphasized to ameliorate the consequences of inflammatory-mediated lung injury. Inflammatory responses lead to the generation of reactive species including superoxide (O(2)(-)), nitric oxide (.NO), and their product peroxynitrite (ONOO(-)). The reaction of CO(2) and ONOO(-) can yield the nitrosoperoxocarbonate adduct ONOOCO(2)(-), a more potent nitrating species than ONOO(-). Based on these premises, monolayers of fetal rat alveolar epithelial cells were utilized to investigate whether hypercapnia would modify pathways of.NO production and reactivity that impact pulmonary metabolism and function. Stimulated cells exposed to 15% CO(2) (hypercapnia) revealed a significant increase in.NO production and nitric oxide synthase (NOS) activity. Cell 3-nitrotyrosine content as measured by both HPLC and immunofluorescence staining also increased when exposed to these same conditions. Hypercapnia significantly enhanced cell injury as evidenced by impairment of monolayer barrier function and increased induction of apoptosis. These results were attenuated by the NOS inhibitor N-monomethyl-L-arginine. Our studies reveal that hypercapnia modifies.NO-dependent pathways to amplify cell injury. These results affirm the underlying role of.NO in tissue inflammatory reactions and reveal the impact of hypercapnia on inflammatory reactions and its potential detrimental influences.
Am J Physiol Lung Cell Mol Physiol 2000 Nov
PMID:Hypercapnia induces injury to alveolar epithelial cells via a nitric oxide-dependent pathway. 1105 37

The burrowing brittlestar Hemipholis elongata (Say) maintains a constant M(O2)of 3.79+/-1.47 micromol O(2) g(-1) h(-1) (for 0.2-0.3 g animals, mean+/-S.D., n=7), measured in the burrow, over a broad range of PO(2). Below the critical PO(2) of 37 mm Hg, M(O(2)) becomes dependent on the oxygen tension. M(O2) is a function of the size of H. elongata; the scaling exponent is 0. 83 and is similar to those reported for other echinoderms. The M(O2) of H. elongata is unaffected by removal from the burrow, by hypercapnia, by exposure to hydrogen sulfide, or by temperature change in the range from 20 to 32 degrees C. The relative insensitivity of H. elongata to these factors may be an adaptation to life in the highly variable estuarine and tidal creek environments where the animals are frequently found.
Comp Biochem Physiol A Mol Integr Physiol 2000 Oct
PMID:Respiration in the burrowing brittlestar, Hemipholis elongata say (Echinodermata, Ophiuroidea): a study of the effects of environmental variables on oxygen uptake. 1106 87

Periophthalmodon schlosseri is a mudskipper which uses the vascularized buccopharyngeal cavity as a respiratory organ. The fish construct mud burrows that contain hypoxic water, but store air inside the burrows. Because the burrow gas is frequently hypoxic and hypercapnic, the effects of altered respiratory gas concentrations on the aerial ventilation frequency (V(F)), inspiratory tidal volume (V(T)) and minute volume (V(M)=V(F)xV(T)) of P. schlosseri were studied by pneumotachography. Both total buccopharyngeal gas volume (V(BP)) and V(T) scaled significantly with body mass (mass exponents=1.10 and 1.03, respectively), and V(T)/V(BP) was 0.54+/-0. 05 (S.E.M., n=6). V(BP), expressed as a percentage of body volume, was much higher (16%) than in other air-breathing gobies (2-4%). When fish respired in normoxic air and water, V(F) was 0.25+/-0.04 breaths min(-1), V(T) 7.6+/-0.6 ml 100 g(-1), and V(M) 1.80+/-0.18 ml 100 g(-1) min(-1). Aquatic hypoxia did not significantly affect V(F), V(T), or V(M). In both moderate (P(O(2))=10 kPa) and severe (P(O(2))=5 kPa) aerial hypoxia, V(F) and V(M) increased significantly. V(T) increased significantly only during severe aerial hypoxia. In aerial hypercapnia, V(F) and V(M) increased significantly.
Comp Biochem Physiol A Mol Integr Physiol 2000 Nov
PMID:Aerial ventilatory responses of the mudskipper, Periophthalmodon schlosseri, to altered aerial and aquatic respiratory gas concentrations. 1111 38

Extracellular afferent neural activity was recorded in vivo from cranial nerve IX (glossopharyngeal) from mechanoreceptors in the first gill arch of anesthetized, spontaneously breathing channel catfish (Ictalurus punctatus). Single unit and paucifiber recordings show that both phasic and tonic receptors were active during normal ventilation. Phasic receptors were characterized as having a burst of activity during some phase of the ventilatory cycle. Most of these occurred during peak adduction or peak abduction. Phasic receptors were not active during spontaneous apnic periods. Tonic receptors were always active, even during apneas, firing frequency was modulated by breathing movements with peak activity occurring during adduction. Flow-sensitive mechanoreceptors were identified in anesthetized, paralyzed catfish. These receptors decreased activity when the ventilatory water flow was stopped. Hypercapnia (5% CO(2) in air) stimulated ventilatory rate and amplitude but had no effect on mechanoreceptor activity. The discharge characteristics of branchial mechanoreceptors indicate that they could be involved in the timing and coordination of ventilatory movements and maintenance of the 'gill curtain' to minimize ventilatory dead space. Unlike ventilatory mechanoreceptors in the air breathing organs of gar and lungs of lungfish and tetrapods, branchial mechanoreceptors were insensitive to hypercapnia.
Comp Biochem Physiol A Mol Integr Physiol 2001 Jan
PMID:Branchial mechanoreceptor activity during spontaneous ventilation in channel catfish. 1113 45

This paper reviews the effects of exercise and hypercapnia on blood flow to the splanchnic circulation. Brief struggling behaviours are known to decrease blood flow to the gut (GBF). Likewise, prolonged swimming in unfed fish has been shown to reduce GBF in proportion to the increased oxygen uptake. Therefore, the normal postprandial increase in GBF theoretically should be impaired whenever fish are active. However, indirect evidence suggests that GBF is spared to some degree when fed fish swim continuously but at a cost (10-15%) to their critical swimming speed. Severe respiratory acidosis can be created by the new intensive aquaculture settings that use oxygen injection into re-circulated water. The only study so far to examine the effects of severe hypercapnia on GBF and its regulation showed that routine GBF and alpha-adrenergic control of GBF remained normal in unfed white sturgeon (Acipenser transmontanus). However, severe hypercapnia produced a hyperactive state and increased sensitivity of GBF to struggling. As a result, routine GBF was maintained for a short period of time. Thus, environmental changes such as severe hypercapnia can indirectly impact GBF through altered struggling behaviour, but the implications of the overall reduction in GBF to food assimilation have yet to be established.
Comp Biochem Physiol A Mol Integr Physiol 2001 Mar
PMID:Gut blood flow in fish during exercise and severe hypercapnia. 1124 44

Experimental results consistently show that the respiratory control system is plastic, such that environmental factors and experience can modify its performance. Such plasticity may represent basic neurobiological principles of learning and memory, whereby intermittent sensory stimulation produces long-term alterations (i.e. facilitation or depression) in synaptic transmission depending on the timing and intensity of the stimulation. In this review, we propose that intermittent chemosensory stimulation produces long-term changes in respiratory motor output via specific neuromodulatory systems. This concept is based on recent data suggesting that intermittent hypoxia produces a net long-term facilitation of respiratory output via the serotonergic system, whereas intermittent hypercapnia produces a net long-term depression by a mechanism associated with the noradrenergic system. There is suggestive evidence that, although both respiratory stimuli activate both modulatory systems, the balance is different. Thus, these opposing modulatory influences on respiratory motor control may provide a 'push-pull' system, preventing unchecked and inappropriate fluctuations in ventilatory drive.
Comp Biochem Physiol A Mol Integr Physiol 2001 Sep
PMID:Plasticity in respiratory motor control: intermittent hypoxia and hypercapnia activate opposing serotonergic and noradrenergic modulatory systems. 1154 68


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