scholarly journals Expanding Role of Dopaminergic Inhibition in Hypercapnic Responses of Cultured Rat Carotid Body Cells: Involvement of Type II Glial Cells

2020 ◽  
Vol 21 (15) ◽  
pp. 5434 ◽  
Author(s):  
Erin M. Leonard ◽  
Colin A. Nurse
Keyword(s):  
Carotid Body ◽  
Cell Function ◽  
Atp Release ◽  
Purinergic Signalling ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Type I Cells ◽  
Type Ii Cell ◽  
I Cells

Dopamine (DA) is a well-studied neurochemical in the mammalian carotid body (CB), a chemosensory organ involved in O2 and CO2/H+ homeostasis. DA released from receptor (type I) cells during chemostimulation is predominantly inhibitory, acting via pre- and post-synaptic dopamine D2 receptors (D2R) on type I cells and afferent (petrosal) terminals respectively. By contrast, co-released ATP is excitatory at postsynaptic P2X2/3R, though paracrine P2Y2R activation of neighboring glial-like type II cells may boost further ATP release. Here, we tested the hypothesis that DA may also inhibit type II cell function. When applied alone, DA (10 μM) had negligible effects on basal [Ca2+]i in isolated rat type II cells. However, DA strongly inhibited [Ca2+]i elevations (Δ[Ca2+]i) evoked by the P2Y2R agonist UTP (100 μM), an effect opposed by the D2/3R antagonist, sulpiride (1–10 μM). As expected, acute hypercapnia (10% CO2; pH 7.4), or high K+ (30 mM) caused Δ[Ca2+]i in type I cells. However, these stimuli sometimes triggered a secondary, delayed Δ[Ca2+]i in nearby type II cells, attributable to crosstalk involving ATP-P2Y2R interactions. Interestingly sulpiride, or DA store-depletion using reserpine, potentiated both the frequency and magnitude of the secondary Δ[Ca2+]i in type II cells. In functional CB-petrosal neuron cocultures, sulpiride potentiated hypercapnia-induced Δ[Ca2+]i in type I cells, type II cells, and petrosal neurons. Moreover, stimulation of type II cells with UTP could directly evoke Δ[Ca2+]i in nearby petrosal neurons. Thus, dopaminergic inhibition of purinergic signalling in type II cells may help control the integrated sensory output of the CB during hypercapnia.

scholarly journals ULTRASTRUCTURE OF THE CAROTID BODY

1966 ◽  
Vol 30 (3) ◽  
pp. 563-578 ◽  
Author(s):  
T. J. Biscoe ◽  
W. E. Stehbens
Keyword(s):  
Blood Vessels ◽  
Schwann Cells ◽  
Carotid Body ◽  
Nerve Fibers ◽  
Nerve Endings ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Type I Cells ◽  
I Cells

An electron microscope investigation was made of the carotid body in the cat and the rabbit. In thin-walled blood vessels the endothelium was fenestrated. Larger vessels were surrounded by a layer of smooth muscle fibers. Among the numerous blood vessels lay groups of cells of two types covered by basement membranes. Aggregates of Type I cells were invested by Type II cells, though occasionally cytoplasmic extensions were covered by basement membrane only. Type I cells contained many electron-opaque cored vesicles (350 to 1900 A in diameter) resembling those in endocrine secretory cells. Type II cells covered nerve endings terminating on Type I cells and enclosed nerve fibers in much the same manner as Schwann cells. The nerve endings contained numerous microvesicles (∼500 A in diameter), mitochondria, glycogen granules, and a few electron-opaque cored vesicles. Junctions between nerve endings and Type I cells were associated with regions of increased density in both intercellular spaces and the adjoining cytoplasm. Cilia of the 9 + 0 fibril pattern were observed in Type I and Type II cells and pericytes. Nonmyelinated nerve fibers, often containing microvesicles, mitochondria, and a few electron-opaque cored vesicles (650 to 1000 A in diameter) were present in Schwann cells, many of which were situated close to blood vessels Ganglion cells near the periphery of the gland, fibrocytes, and segments of unidentified cells were also seen. It was concluded that, according to present concepts of the structure of nerve endings, those endings related to Type I cells could be efferent or afferent.

Type II epithelial cells are critical target for hyperoxia-mediated impairment of postnatal lung development

2006 ◽  
Vol 291 (5) ◽  
pp. L1101-L1111 ◽  
Author(s):  
Min Yee ◽  
Peter F. Vitiello ◽  
Jason M. Roper ◽  
Rhonda J. Staversky ◽  
Terry W. Wright ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cells ◽  
Lung Development ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Newborn Mice ◽  
Type I Cells ◽  
Type Ii Cell ◽  
I Cells

Type II epithelial cells are essential for lung development and remodeling, as they are precursors for type I cells and can produce vascular mitogens. Although type II cell proliferation takes place after hyperoxia, it is unclear why alveolar remodeling occurs normally in adults whereas it is permanently disrupted in newborns. Using a line of transgenic mice whose type II cells could be identified by their expression of enhanced green fluorescent protein and endogenous expression of surfactant proteins, we investigated the age-dependent effects of hyperoxia on type II cell proliferation and alveolar repair. In adult mice, type II cell proliferation was low during room air and hyperoxia exposure but increased during recovery in room air and then declined to control levels by day 7. Eight weeks later, type II cell number and alveolar compliance were indistinguishable from those in room air controls. In newborn mice, type II cell proliferation markedly increased between birth and postnatal day 7 before declining by postnatal day 14. Exposure to hyperoxia between postnatal days 1 and 4 inhibited type II cell proliferation, which resumed during recovery and was aberrantly elevated on postnatal day 14. Eight weeks later, recovered mice had 70% fewer type II cells and 30% increased lung compliance compared with control animals. Recovered mice also had higher levels of T1α, a protein expressed by type I cells, with minimal changes detected in genes expressed by vascular cells. These data suggest that perinatal hyperoxia adversely affects alveolar development by disrupting the proper timing of type II cell proliferation and differentiation into type I cells.

A morphometric study of the carotid body in chronically hypoxic rats

1984 ◽  
Vol 57 (5) ◽  
pp. 1430-1438 ◽  
Author(s):  
K. H. McGregor ◽  
J. Gil ◽  
S. Lahiri
Keyword(s):  
Blood Vessels ◽  
Carotid Body ◽  
Structural Changes ◽  
Volume Density ◽  
Morphometric Study ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Type I Cells ◽  
I Cells

We performed morphometric studies of carotid body in acutely and chronically hypoxic rats (inspired PO2 = 70 Torr, at sea level). Acute exposure was for the duration of about 10 min, and chronic exposure lasted for 28 days. We confirmed that the total volume of the organ increased by severalfold. At the light-microscopy level we found an enlargement of the volume density of the blood sinuses from 14 to 31% due to chronic hypoxia. The morphometric hematocrit increased from 39 to 70% paralleling changes in the conventionally measured venous hematocrit. These data do not show any specific plasma skimming in the carotid body blood vessels. With the electron microscope we found that the mean average volume of type I cells increased from 320 micron3 in controls to 1,120 micron3 in the chronically hypoxic rats without hyperplasia, whereas type II cells had increased in number without alteration in size. Qualitative observations revealed that the normal appearance of clusters of ovoid type I cells interspersed by capillaries had been transformed into a pattern of individual cells forming plates between expanded blood vessels with a large increase of contact area between the cells and vessels. Type II cells appeared to have proliferated without changes in individual size to cover the enlarged periphery of type I cells. The observed structural changes in the carotid body parenchyma and vasculature appear to be physiologically adaptive and provide further support for the idea that various elements in the organ are particularly sensitive to hypoxia.

Expression ofN-deacetylase/sulfotransferase and 3-O-sulfotransferase in rat alveolar type II cells

2000 ◽  
Vol 279 (2) ◽  
pp. L292-L301 ◽  
Author(s):  
Zhong-Yuan Li ◽  
Kazunori Hirayoshi ◽  
Yasuhiro Suzuki
Keyword(s):  
Heparan Sulfate ◽  
Protein A ◽  
Sodium Chlorate ◽  
Alveolar Type ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Type I Cells ◽  
Type Ii Cell ◽  
I Cells

Basal laminae beneath alveolar type I cells are suggested to contain highly sulfated heparan sulfate-containing proteoglycans (PGs), and cultured type II cells accumulate highly sulfated matrices. To characterize the regulation of PG synthesis during the transition from type II cells to type I cells, we examined mRNA expression of N-deacetylase/sulfotransferase (NST) and 3- O-sulfotransferase (3-OST), two enzymes specific for heparan sulfate synthesis. We found that both freshly isolated and cultured type II cells expressed NST and 3-OST as shown by in situ hybridization. Expression of surfactant-associated protein A, B, and C mRNAs, determined by semiquantitative PCR, decreased during culture. Expression of type I cell marker T1α mRNA increased except in cells cultured on an Engelbrecht-Holm-Swarm gel. Expression of NST was dependent on cell density and matrix and was intense in conditions where cells spread fully, whereas 3-OST expression was unchanged in the conditions examined. The PG sulfation inhibitor sodium chlorate significantly inhibited cultured type II cell spreading, and this inhibition was reversed by sodium sulfate. These results suggest that highly sulfated PGs modified by NST are necessary for the spreading of cells during transdifferentiation of type II cells to mature type I cells.

[Ca2+]i oscillations regulate type II cell exocytosis in the pulmonary alveolus

2000 ◽  
Vol 279 (1) ◽  
pp. L5-L13 ◽  
Author(s):  
Yugo Ashino ◽  
Xiaoyou Ying ◽  
Leland G. Dobbs ◽  
Jahar Bhattacharya
Keyword(s):  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Cells ◽  
Lung Inflation ◽  
Type I Cells ◽  
Lung Expansion ◽  
Type Ii Cell ◽  
I Cells

Pulmonary surfactant, a critical determinant of alveolar stability, is secreted by alveolar type II cells by exocytosis of lamellar bodies (LBs). To determine exocytosis mechanisms in situ, we imaged single alveolar cells from the isolated blood-perfused rat lung. We quantified cytosolic Ca2+ concentration ([Ca2+]i) by the fura 2 method and LB exocytosis as the loss of cell fluorescence of LysoTracker Green. We identified alveolar cell type by immunofluorescence in situ. A 15-s lung expansion induced synchronous [Ca2+]i oscillations in all alveolar cells and LB exocytosis in type II cells. The exocytosis rate correlated with the frequency of [Ca2+]i oscillations. Fluorescence of the lipidophilic dye FM1-43 indicated multiple exocytosis sites per cell. Intracellular Ca2+ chelation and gap junctional inhibition each blocked [Ca2+]i oscillations and exocytosis in type II cells. We demonstrated the feasibility of real-time quantifications in alveolar cells in situ. We conclude that in lung expansion, type II cell exocytosis is modulated by the frequency of intercellularly communicated [Ca2+]i oscillations that are likely to be initiated in type I cells. Thus during lung inflation, type I cells may act as alveolar mechanotransducers that regulate type II cell secretion.

scholarly journals Mechanical stretch activates piezo1 in caveolae of alveolar type I cells to trigger ATP release and paracrine stimulation of surfactant secretion from alveolar type II cells

2020 ◽  
Vol 34 (9) ◽  
pp. 12785-12804 ◽  
Author(s):  
Kathrin Diem ◽  
Michael Fauler ◽  
Giorgio Fois ◽  
Andreas Hellmann ◽  
Natalie Winokurow ◽  
...  
Keyword(s):  
Atp Release ◽  
Mechanical Stretch ◽  
Alveolar Type ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Surfactant Secretion ◽  
I Cells ◽  
Stimulation Of

Effects of oligohydramnios on lung growth and maturation in the fetal rat

2002 ◽  
Vol 282 (3) ◽  
pp. L431-L439 ◽  
Author(s):  
Joseph A. Kitterman ◽  
Cheryl J. Chapin ◽  
Jeff N. Vanderbilt ◽  
Nicolas F. M. Porta ◽  
Louis M. Scavo ◽  
...  
Keyword(s):  
Fetal Lung ◽  
Alveolar Type ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Lung Growth ◽  
Type I Cells ◽  
Fetal Lung Development ◽  
Fetal Rat ◽  
I Cells

Oligohydramnios (OH) retards fetal lung growth by producing less lung distension than normal. To examine effects of decreased distension on fetal lung development, we produced OH in rats by puncture of uterus and fetal membranes at 16 days of gestation; fetuses were delivered at 21 or 22 days of gestation. Controls were position-matched littermates in the opposite uterine horn. OH lungs had lower weights and less DNA, protein, and water, but no differences in saturated phosphatidylcholine, surfactant proteins (SP)-A and -B, and mRNA for SP-A, -B, -C, and -D. To evaluate effects on epithelial differentiation, we used RTI40 and RTII70, proteins specific in lung to luminal surfaces of alveolar type I and II cells, respectively. At 22 days of gestation, OH lungs had less RTI40 mRNA ( P < 0.05) and protein ( P < 0.001), but RTII70 did not differ from controls. With OH, type I cells (in proportion to type II cells) covered less distal air space perimeter ( P < 0.01). We conclude that OH, which retards lung growth, has little effect on surfactant and impedes formation of type I cells relative to type II cells.

A Study of the Enteric Plexuses in Some Amphibians

1951 ◽  
Vol s3-92 (17) ◽  
pp. 55-77
Author(s):  
MARGARET GUNN
Keyword(s):  
Myenteric Plexus ◽  
Proximal Part ◽  
Nerve Cells ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Nerve Fibres ◽  
Type I Cells ◽  
Splanchnic Nerves ◽  
I Cells

1. The extrinsic nerve-supply to the gut in the frog (Rana temporaria) is contained in the vagus and splanchnic nerves--both of which appear to contain parasympathetic and sympathetic fibres. 2. The vagus supplies the gut from the proximal part of the oesophagus to the most proximal part of the intestine. The splanchnic nerves supply the gut from the oesophagus to the rectum. 3. No vagal fibres accompany the splanchnic nerves. 4. A possible explanation is given for the variable effects produced on stimulation of the extrinsic nerves supplying the gut. 5. A plexus of nerve-fibres is present i n the submucosa which probably corresponds to Meissner's plexus of mammals, but no nerve-cells are present. 6. In the myenteric plexus the nerve-cells are commonly grouped int o ganglia in the oesophagus and stomach, but in theintestine the nerve-cells are fairly evenly distributed, distinct ganglia not being present. 7. Cells of three types have been found corresponding to Dogiel's three types. Type I cells are of two varieties: (a) large, strongly argyrophi l cells which are multi-polar possessing numerous short dendrites and a very prominent axon; (b)smaller cells having a prominent axon and often unipolar. Type I cells are enclosed in capsules. Type II cells are small multipolar cells with long dendrites. Type III cells are small multipolar cells with shorter dendrites and an axon bearing no collaterals. 8. Cells in the oesophagus and stomach are entirely of Type I. In the intestine these cells are present in fairly large numbers at the most proximal end, but throughout the rest of the intestine they only occur commonly close to the attachment of the mesentery, where they are found singly and fairly evenly spaced. 9. Cells of Types II and III occur only in the myenteric plexus of the intestine, where they are distributed fairly evenly, not forming distinct ganglia. 10. It is suggested that the Type II and III cells formed the original autonomic nerve plexus of the gut, the Type II cells being motor and the Type III sensory. The Type I cells are the post-ganglionic cells of the parasympathetic system and are an additional motor contribution to the plexus. 11. The endings of th e pre-ganglionic parasympathetic fibres on the ganglion cells may take any of three forms: (a) pericellular varicose endings which occur on the large variety of Typ e I cell; (b) pericapsular varicose endings which are borne by the smaller variety of Type I cell; and(c) club-shaped endings occurring on the larger Type I cells. 12. The type of synapse formed by the processes of cells of Types II and III consists of the simple endings of their processes on the cell bodies or dendrites of other cells, or the passing contact of their processes with the bodies of other cells. 13. Fine varicose fibrils have been observed on the surface of muscle-cells. These are presumably the distal ends of the cell processes and sympathetic fibres which form the motor endings. 14. The types of sensory endings which have been found are: (a) typical sensory varicose endings spread out in the submucosa of the oesophagus and rectum; those in the oesophagus originating from vagal fibres; and (b) Pacinian corpuscle in the sub-mucosa of the intestine. 15. The ‘interstitial cells of Cajal’ form an apparently anastomosing network in the gut-wall which appears to be distinct from the anastomosing Schwann plasmodium which covers the nerve-fibres.

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