Indications for the Involvement of a Hemoprotein as an Oxygen Pressure Sensor Protein in the Carotid Body

Author(s):  
H. Acker
Author(s):  
David F. Wilson ◽  
Sergei A. Vinogradov ◽  
Anil Mokashi ◽  
Anna Pastuszko ◽  
Sukhamay Lahiri ◽  
...  

Physiology ◽  
1995 ◽  
Vol 10 (5) ◽  
pp. 211-216 ◽  
Author(s):  
H Acker ◽  
D Xue

An NAD(P)H oxidase-generating H2O2 dependent on PO2 is proposed as an O2 sensor protein in type I cells of the carotid body, regulating potassium channel open probability as well as tyrosine hydroxylase gene expression. The proposed signal cascade also is important in other O2-sensing cells.


1995 ◽  
Vol 78 (5) ◽  
pp. 1904-1909 ◽  
Author(s):  
W. Kummer ◽  
H. Acker

We demonstrate, by means of immunohistochemistry, that type I cells of human, guinea pig, and rat carotid bodies react with antisera raised against the subunits p22phox, gp91phox, p47phox, and p67phox of the NAD(P)H oxidase isolated from human neutrophil granulocytes. The findings support previous photometric studies that indicate that carotid body type I cells possess a putative oxygen sensor protein that is similar to the neutrophil NAD(P)H oxidase and consists of a hydrogen peroxide generating low-potential cytochrome b558 with cofactors regulating the electron transfer to oxygen.


1984 ◽  
Vol 61 (5) ◽  
pp. 634-634
Author(s):  
David E. Jones ◽  
Charles B. Watson ◽  
Carol Goetter

1990 ◽  
Vol 272 (3) ◽  
pp. 743-747 ◽  
Author(s):  
A R Cross ◽  
L Henderson ◽  
O T G Jones ◽  
M A Delpiano ◽  
J Hentschel ◽  
...  

The rat carotid body tissue reveals a photometrically measurable haem signal with absorbance maxima at 560 nm, 518 nm and 425 nm, suggesting the presence of a b-type cytochrome; this was confirmed by pyridine haemochrome and CO spectra. The quantity of cytochrome b was estimated to be 310 pmol.mg of protein-1. This haem is capable of H2O2 formation, which can be inhibited by 10 microM-diphenyliodonium (DPI). The hypoxia-induced increase in nervous chemoreceptor discharge and the reduction of FAD and NAD(P)+ were also inhibited by DPI (10 microM). These results suggest that an oxidase such as the NAD(P)H oxidase of neutrophils may act as a pO2 sensor protein in the rat carotid body, probably inducing the pO2 chemoreceptor process by H2O2 formation.


1991 ◽  
Vol 261 (4) ◽  
pp. C614-C622 ◽  
Author(s):  
W. L. Rumsey ◽  
R. Iturriaga ◽  
D. Spergel ◽  
S. Lahiri ◽  
D. F. Wilson

The relationship between oxygen pressure (PO2) in the carotid body and carotid sinus nerve discharge was evaluated in the isolated perfused/superfused cat carotid body using the oxygen-dependent quenching of phosphorescence. Images of phosphorescence intensity arising from Pd-coproporphyrin within the microcirculation of the carotid body provided measurements of intravascular PO2. These measurements were substantiated by determining phosphorescence life-time. The carotid body was perfused in the isolated state via the common carotid artery with N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid-buffered Tyrode solution, pH 7.4, at a constant pressure of 80 mmHg. Superfusion was maintained with similar media equilibrated with 100% argon. PO2 in the exchange vessels was markedly less than that in the perfusate entering the carotid artery, 23 +/- 3 and 45 +/- 3 Torr for normoxic (111 +/- 15 Torr) and hyperoxic (345 +/- 72 Torr) perfusates, respectively. Chemosensory discharge rose slowly in response to a brief interruption of perfusate flow as PO2 steadily declined from either of these capillary PO2 values to approximately 10 Torr. Between approximately 10 and 3 Torr, chemosensory discharge increased strikingly, concomitant with an enhanced rate of oxygen disappearance, from -36 +/- 4 to -69 +/- 13 (92% change) and -28 +/- 3 to -48 +/- 3 (71% change) Torr/s for normoxic and hyperoxic perfusates, respectively. As PO2 fell below approximately 3 Torr, oxygen disappearance slowed and neural activity decayed. Thus the relationships between microvascular PO2 and chemosensory discharge and between oxygen disappearance and neural discharge suggest that oxygen metabolism in the carotid body determines the expression of oxygen chemoreception.


1988 ◽  
Vol 167 (1-2) ◽  
pp. 309-316 ◽  
Author(s):  
M. Ristov ◽  
GJ. Sinadinovski ◽  
M. Mitreski

Author(s):  
Fadhil Al-Lami ◽  
R.G. Murray

Although the fine structure of the carotid body has been described in several recent reports, uncertainties remain, and the morphological effects of anoxia on the carotid body cells of the cat have never been reported. We have, therefore, studied the fine structure of the carotid body both in normal and severely anoxic cats, and to test the specificity of the effects, have compared them with the effects on adrenal medulla, kidney, and liver of the same animals. Carotid bodies of 50 normal and 15 severely anoxic cats (9% oxygen in nitrogen) were studied. Glutaraldehyde followed by OsO4 fixations, Epon 812 embedding, and uranyl acetate and lead citrate staining, were the technics employed.We have called the two types of glomus cells enclosed and enclosing cells. They correspond to those previously designated as chemoreceptor and sustentacular cells respectively (1). The enclosed cells forming the vast majority, are irregular in shape with many processes and occasional peripheral densities (Fig. 1).


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