CO2 transduction in avian intrapulmonary chemoreceptors is critically dependent on transmembrane Na+/H+ exchange

2003 ◽  
Vol 284 (6) ◽  
pp. R1551-R1559 ◽  
Author(s):  
Steven C. Hempleman ◽  
Thomas P. Adamson ◽  
Rowin S. Begay ◽  
Irene C. Solomon
Keyword(s):  
Carbonic Anhydrase ◽  
Intracellular Ph ◽  
Action Potentials ◽  
Single Unit ◽  
Intrapulmonary Chemoreceptors ◽  
Dose Dependent Decrease ◽  
Dimethyl Amiloride ◽  
Dose Dependent ◽  
Unit Action

Avian intrapulmonary chemoreceptors (IPC) are vagal respiratory afferents that are inhibited by high lung Pco 2 and excited by low lung Pco 2. Previous work suggests that increased CO2 inhibits IPC by acidifying intracellular pH (pHi) and that pHi is determined by a kinetic balance between the rate of intracellular carbonic anhydrase-catalyzed CO2 hydration/dehydration and transmembrane extrusion of acids and/or bases by various exchangers. Here, the role of amiloride-sensitive Na+/H+ exchange (NHE) in the IPC CO2 response was tested by recording single-unit action potentials from IPC in anesthetized ducks, Anas platyrhynchos. For each of the IPC tested, blockade of the NHE using dimethyl amiloride (DMA) elicited a marked (>50%) dose-dependent decrease in mean IPC discharge ( P < 0.05), suggesting that NHE is important for pHi regulation and CO2 transduction in IPC. In addition, activation of the NHE using 12-O-tetradecanoylphorbol 13-acetate stimulated six of the seven IPC tested, although the overall effect was not statistically significantly ( P = 0.07). Taken together, these findings suggest that CO2 transduction in IPC is dependent on transmembrane NHE although it is likely to be much slower than carbonic anhydrase-catalyzed hydration-dehydration of CO2.

Single-unit recordings of arterial chemoreceptors from mouse petrosal ganglia in vitro

2000 ◽  
Vol 88 (4) ◽  
pp. 1489-1495 ◽  
Author(s):  
David F. Donnelly ◽  
Ricardo Rigual
Keyword(s):  
Mouse Model ◽  
Carotid Body ◽  
Unit Activity ◽  
Action Potentials ◽  
Single Unit ◽  
Gene Deletions ◽  
Suction Electrode ◽  
Single Unit Recordings ◽  
Unit Action

A preparation was developed that allows for the recording of single-unit chemoreceptor activity from mouse carotid body in vitro. An anesthetized mouse was decapitated, and each carotid body was harvested, along with the sinus nerve, glossopharyngeal nerve, and petrosal ganglia. After exposure to collagenase/trypsin, the cleaned complex was transferred to a recording chamber where it was superfused with oxygenated saline. The ganglia was searched for evoked or spontaneous unit activity by using a glass suction electrode. Single-unit action potentials were 57 ± 10 (SE) ( n = 16) standard deviations above the recording noise, and spontaneous spikes were generated as a random process. Decreasing superfusate[Formula: see text] to near 20 Torr caused an increase in spiking activity from 1.3 ± 0.4 to 14.1 ± 1.9 Hz ( n = 16). The use of mice for chemoreceptor studies may be advantageous because targeted gene deletions are well developed in the mouse model and may be useful in addressing unresolved questions regarding the mechanism of chemotransduction.

scholarly journals A regenerative microchannel device for recording multiple single-unit action potentials in awake, ambulatory animals

2015 ◽  
Vol 43 (3) ◽  
pp. 474-485 ◽  
Author(s):  
Akhil Srinivasan ◽  
John Tipton ◽  
Mayank Tahilramani ◽  
Adel Kharbouch ◽  
Eric Gaupp ◽  
...  
Keyword(s):  
Action Potentials ◽  
Single Unit ◽  
Microchannel Device ◽  
Unit Action

Cardiovascular effects of microinjection of low doses of serotonin into the NTS of unanesthetized rats

1997 ◽  
Vol 272 (4) ◽  
pp. R1135-R1142 ◽  
Author(s):  
J. C. Callera ◽  
L. G. Bonagamba ◽  
C. Sevoz ◽  
R. Laguzzi ◽  
B. H. Machado
Keyword(s):  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Cardiovascular Reflexes ◽  
Low Doses ◽  
Reflex Bradycardia ◽  
Baseline Values ◽  
Dose Dependent Decrease ◽  
Baroreceptor Activation ◽  
Dose Dependent

In the present study, we analyzed in conscious rats the effects of microinjections of serotonin (5-HT; pmol range) into the nucleus of the solitary tract (NTS) on basal mean arterial pressure (MAP) and heart rate (HR) and also on the reflex bradycardia induced by the activation of the baro- and chemoreflex evaluated 1 min after 5-HT microinjection into the NTS. The data show that unilateral microinjection of 5-HT in the picomolar range into the NTS of unanesthetized rats produced a dose-dependent decrease in MAP and HR, which was blocked by previous microinjection of ketanserin (250 pmol/50 nl) into the NTS. The changes in MAP and HR induced by 5-HT were of very short duration, with a return to baseline values a few seconds later. The cardiovascular responses to baro- or chemoreflex activation 1 min after 5-HT microinjection into the NTS did not differ from the control, indicating that low doses of 5-HT produced no effect on the cardiovascular reflexes tested at that time. The present data show that, as also observed in anesthetized rats, the microinjection of picomolar doses of 5-HT into the NTS elicits the typical cardiovascular responses to baroreceptor activation. These effects, hypotension and bradycardia, seem to be mediated by 5-HT2 receptors because both were blocked by a selective 5-HT2 receptor antagonist. However, since microinjection of 5-HT (1 pmol) into the NTS produced no changes in the cardiovascular responses to the baro- and chemoreflex activated 1 min later, the role of 5-HT2 receptors in the processing of the cardiovascular afferent messages in the NTS remains to be elucidated.

scholarly journals Activation of the NPY Y5 receptor regulates both feeding and energy expenditure

1999 ◽  
Vol 277 (5) ◽  
pp. R1428-R1434 ◽  
Author(s):  
Joyce J. Hwa ◽  
Melanie B. Witten ◽  
Patricia Williams ◽  
Lorraine Ghibaudi ◽  
Jun Gao ◽  
...  
Keyword(s):  
Food Intake ◽  
Energy Expenditure ◽  
Receptor Subtype ◽  
Receptor Subtypes ◽  
Interscapular Brown Adipose Tissue ◽  
Peptide Analogs ◽  
Brown Adipose ◽  
Dose Dependent Decrease ◽  
Dose Dependent

Intracerebroventricular (ICV) administration of neuropeptide Y (NPY) has been shown to decrease energy expenditure, induce hypothermia, and stimulate food intake. Recent evidence has suggested that the Y5 receptor may be a significant mediator of NPY-stimulated feeding. The present study attempts to further characterize the role of NPY Y5-receptor subtypes in feeding and energy expenditure regulation. Satiated Long-Evans rats with temperature transponders implanted in the interscapular brown adipose tissue (BAT) displayed a dose-dependent decrease in BAT temperature and an increase in food intake after ICV infusion of NPY. Similar effects were induced by ICV administration of peptide analogs of NPY that activate the Y5 receptor, but not by analogs that activate Y1, Y2, or Y4 receptors. Furthermore, ICV infusion of the Y5 selective agonistd-[Trp32]-NPY significantly reduced oxygen consumption and energy expenditure of rats as measured by indirect calorimetry. These data suggest that the NPY Y5-receptor subtype not only mediates the feeding response of NPY but also contributes to brown fat temperature and energy expenditure regulation.

scholarly journals Heterologous expression of rab4 reduces glucose transport and GLUT4 abundance at the cell surface in oocytes

1997 ◽  
Vol 324 (2) ◽  
pp. 455-459 ◽  
Author(s):  
Silvia MORA ◽  
Ingrid MONDEN ◽  
Antonio ZORZANO ◽  
Konrad KELLER
Keyword(s):  
Cell Surface ◽  
Glucose Transport ◽  
Glucose Transporter ◽  
Glucose Transporters ◽  
Inhibitory Effect ◽  
Trafficking Pathway ◽  
Independent Mechanism ◽  
Dose Dependent Decrease ◽  
Dose Dependent

To evaluate the role of the small rab GTP-binding proteins in glucose transporter trafficking, we have heterologously co-expressed rab4 or rab5 and GLUT4 or GLUT1 glucose transporters in Xenopus oocytes. Co-injection of rab4 and GLUT4 cRNAs resulted in a dose-dependent decrease in glucose transport; this effect was specific for rab4, since co-injection of an inactive rab4 mutant or rab5 cRNA did not have any effect on glucose transport. The effect of rab4 was selective for GLUT4, since no effect was detected in GLUT1-expressing oocytes. The inhibitory effect of rab4 on GLUT4-induced glucose transport was not the result of a change in overall cellular levels of GLUT4 glucose transporters. However, rab4 expression caused a marked decrease in the abundance of GLUT4 transporters present at the cell surface. Finally, rab4 and inhibitors of PtdIns 3-kinase showed additive effects in decreasing glucose transport in GLUT4-expressing oocytes. We conclude that rab4 plays an important role in the regulation of the intracellular GLUT4 trafficking pathway, by contributing to the intracellular retention of GLUT4 through a PtdIns 3-kinase-independent mechanism.

scholarly journals The Role of Carbonic Anhydrase 9 in Regulating Extracellular and Intracellular pH in Three-dimensional Tumor Cell Growths

2009 ◽  
Vol 284 (30) ◽  
pp. 20299-20310 ◽  
Author(s):  
Pawel Swietach ◽  
Shalini Patiar ◽  
Claudiu T. Supuran ◽  
Adrian L. Harris ◽  
Richard D. Vaughan-Jones
Keyword(s):  
Carbonic Anhydrase ◽  
Tumor Cell ◽  
Intracellular Ph ◽  
Three Dimensional ◽  
Carbonic Anhydrase 9

Prostaglandin E2 synthesis after oxidant stress is dependent on cell glutathione content

1994 ◽  
Vol 266 (5) ◽  
pp. C1392-C1399 ◽  
Author(s):  
S. L. Hempel ◽  
D. A. Wessels
Keyword(s):  
Arachidonic Acid ◽  
Oxidant Stress ◽  
Glutathione Depletion ◽  
Pge2 Synthesis ◽  
3T3 Fibroblasts ◽  
Intracellular Glutathione ◽  
Dose Dependent Decrease ◽  
Dose Dependent ◽  
Predominant Effect

The role of glutathione in protecting prostaglandin (PG) generation after exposure of fibroblasts to oxidant stress was investigated. Exposure of 3T3 fibroblasts to H2O2, followed by washing and then 20 microM arachidonic acid, caused a dose-dependent decrease in PG synthesis as assessed by radioimmunoassay. PGE2 production decreased from 3.7 +/- 1.1 to 0.15 +/- 0.04 pmol/microgram protein, and prostacyclin (PGI2) formation decreased from 0.56 +/- 0.03 to 0.06 +/- 0.03 pmol/microgram protein after exposure to 200 microM H2O2. Decreasing intracellular glutathione with 50 micrograms/ml 1,3-bis(chloroethyl)-1-nitrosourea (BCNU) enhanced the H2O2-induced decrease in PGE2 synthesis. Another glutathione-depleting agent, 1-chloro-2,4-dinitrobenzene (CDNB), also potentiated the H2O2-induced decrease in PGE2 formation. However, although PGI2 production was decreased by H2O2, neither BCNU nor CDNB potentiated this decrease. Without oxidant stress, extreme glutathione depletion decreased PGE2 synthesis and caused PGI2 synthesis to exceed PGE2. In summary, oxidant stress decreases both PGE2 and PGI2 formation. However, the primary effect of decreasing cell glutathione during oxidant stress is a reduction in PGE2 formation, not PGI2. This implies that the predominant effect of glutathione depletion during oxidant stress is on the PGE2 isomerase(s) and not PGH synthase or PGI2 synthase.

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