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Carotid Body AT(4) Receptor Expression and its Upregulation in Chronic Hypoxia.

Fung ML, Lam SY, Wong TP, Tjong YW, Leung PS - Open Cardiovasc Med J (2007)

Bottom Line: Specific fluorescein-labeled Ang IV binding sites and positive staining of AT(4) immunoreactivity were mainly found in lobules in the carotid body.To examine if Ang IV induces intracellular Ca(2+) response in the carotid body, cytosolic calcium ([Ca(2+)](i)) was measured by spectrofluorimetry in fura-2-loaded glomus cells dissociated from CH and Nx carotid bodies.Exogenous Ang IV elevated [Ca(2+)](i) in the glomus cells and the Ang IV response was significantly greater in the CH than the Nx group.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, University of Hong Kong, Pokfulam, Hong Kong.

ABSTRACT
Hypoxia regulates the local expression of angiotensin-generating system in the rat carotid body and the me-tabolite angiotensin IV (Ang IV) may be involved in the modulation of carotid body function. We tested the hypothesis that Ang IV-binding angiotensin AT(4) receptors play a role in the adaptive change of the carotid body in hypoxia. The expression and localization of Ang IV-binding sites and AT(4) receptors in the rat carotid bodies were studied with histochemistry. Specific fluorescein-labeled Ang IV binding sites and positive staining of AT(4) immunoreactivity were mainly found in lobules in the carotid body. Double-labeling study showed the AT(4) receptor was localized in glomus cells containing tyrosine hydroxylase, suggesting the expression in the chemosensitive cells. Intriguingly, the Ang IV-binding and AT(4) immunoreactivity were more intense in the carotid body of chronically hypoxic (CH) rats (breathing 10% oxygen for 4 weeks) than the normoxic (Nx) control. Also, the protein level of AT(4) receptor was doubled in the CH comparing with the Nx group, supporting an upregulation of the expression in hypoxia. To examine if Ang IV induces intracellular Ca(2+) response in the carotid body, cytosolic calcium ([Ca(2+)](i)) was measured by spectrofluorimetry in fura-2-loaded glomus cells dissociated from CH and Nx carotid bodies. Exogenous Ang IV elevated [Ca(2+)](i) in the glomus cells and the Ang IV response was significantly greater in the CH than the Nx group. Hence, hypoxia induces an upregulation of the expression of AT(4) receptors in the glomus cells of the carotid body with an increase in the Ang IV-induced [Ca(2+)]i elevation. This may be an additional pathway enhancing the Ang II action for the activation of chemoreflex in the hypoxic response during chronic hypoxia.

No MeSH data available.


Related in: MedlinePlus

The expression and localization of AT4 receptor-immunoreactivity in (A) Nx and (B) CH rat carotid body. Note the intensity of staining is at a high level in the CH comparing with that of the Nx group. Sections with tyrosine hydroxylase (TH) for the Nx and CH carotid bodies are shown in C and D. E and F are overlays of the AT4 receptor- and TH-stainings. Calibration bars are 20 and 50 μm, respectively, for low (A, C, E) and high magnification (B, D, F).
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Figure 2: The expression and localization of AT4 receptor-immunoreactivity in (A) Nx and (B) CH rat carotid body. Note the intensity of staining is at a high level in the CH comparing with that of the Nx group. Sections with tyrosine hydroxylase (TH) for the Nx and CH carotid bodies are shown in C and D. E and F are overlays of the AT4 receptor- and TH-stainings. Calibration bars are 20 and 50 μm, respectively, for low (A, C, E) and high magnification (B, D, F).

Mentions: The localization of protein expression of the AT4 receptors in the carotid body is shown in Fig. (2). Positive staining of AT4 receptor-immunoreactivity was obtained in Nx and CH carotid bodies (Fig. 2C,D). The immunostaining was localized in lobules of the carotid body, which was also positively stained with TH-immunoreactivity (Fig. 2A,B), confirming that the AT4 receptor expression was in the chemosensitive glomus cell. Additionally, the intensity of the staining was at a high level in the CH comparing with that of the Nx group, indicating an increase in AT4 receptor expression in the CH carotid body.


Carotid Body AT(4) Receptor Expression and its Upregulation in Chronic Hypoxia.

Fung ML, Lam SY, Wong TP, Tjong YW, Leung PS - Open Cardiovasc Med J (2007)

The expression and localization of AT4 receptor-immunoreactivity in (A) Nx and (B) CH rat carotid body. Note the intensity of staining is at a high level in the CH comparing with that of the Nx group. Sections with tyrosine hydroxylase (TH) for the Nx and CH carotid bodies are shown in C and D. E and F are overlays of the AT4 receptor- and TH-stainings. Calibration bars are 20 and 50 μm, respectively, for low (A, C, E) and high magnification (B, D, F).
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Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2570565&req=5

Figure 2: The expression and localization of AT4 receptor-immunoreactivity in (A) Nx and (B) CH rat carotid body. Note the intensity of staining is at a high level in the CH comparing with that of the Nx group. Sections with tyrosine hydroxylase (TH) for the Nx and CH carotid bodies are shown in C and D. E and F are overlays of the AT4 receptor- and TH-stainings. Calibration bars are 20 and 50 μm, respectively, for low (A, C, E) and high magnification (B, D, F).
Mentions: The localization of protein expression of the AT4 receptors in the carotid body is shown in Fig. (2). Positive staining of AT4 receptor-immunoreactivity was obtained in Nx and CH carotid bodies (Fig. 2C,D). The immunostaining was localized in lobules of the carotid body, which was also positively stained with TH-immunoreactivity (Fig. 2A,B), confirming that the AT4 receptor expression was in the chemosensitive glomus cell. Additionally, the intensity of the staining was at a high level in the CH comparing with that of the Nx group, indicating an increase in AT4 receptor expression in the CH carotid body.

Bottom Line: Specific fluorescein-labeled Ang IV binding sites and positive staining of AT(4) immunoreactivity were mainly found in lobules in the carotid body.To examine if Ang IV induces intracellular Ca(2+) response in the carotid body, cytosolic calcium ([Ca(2+)](i)) was measured by spectrofluorimetry in fura-2-loaded glomus cells dissociated from CH and Nx carotid bodies.Exogenous Ang IV elevated [Ca(2+)](i) in the glomus cells and the Ang IV response was significantly greater in the CH than the Nx group.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, University of Hong Kong, Pokfulam, Hong Kong.

ABSTRACT
Hypoxia regulates the local expression of angiotensin-generating system in the rat carotid body and the me-tabolite angiotensin IV (Ang IV) may be involved in the modulation of carotid body function. We tested the hypothesis that Ang IV-binding angiotensin AT(4) receptors play a role in the adaptive change of the carotid body in hypoxia. The expression and localization of Ang IV-binding sites and AT(4) receptors in the rat carotid bodies were studied with histochemistry. Specific fluorescein-labeled Ang IV binding sites and positive staining of AT(4) immunoreactivity were mainly found in lobules in the carotid body. Double-labeling study showed the AT(4) receptor was localized in glomus cells containing tyrosine hydroxylase, suggesting the expression in the chemosensitive cells. Intriguingly, the Ang IV-binding and AT(4) immunoreactivity were more intense in the carotid body of chronically hypoxic (CH) rats (breathing 10% oxygen for 4 weeks) than the normoxic (Nx) control. Also, the protein level of AT(4) receptor was doubled in the CH comparing with the Nx group, supporting an upregulation of the expression in hypoxia. To examine if Ang IV induces intracellular Ca(2+) response in the carotid body, cytosolic calcium ([Ca(2+)](i)) was measured by spectrofluorimetry in fura-2-loaded glomus cells dissociated from CH and Nx carotid bodies. Exogenous Ang IV elevated [Ca(2+)](i) in the glomus cells and the Ang IV response was significantly greater in the CH than the Nx group. Hence, hypoxia induces an upregulation of the expression of AT(4) receptors in the glomus cells of the carotid body with an increase in the Ang IV-induced [Ca(2+)]i elevation. This may be an additional pathway enhancing the Ang II action for the activation of chemoreflex in the hypoxic response during chronic hypoxia.

No MeSH data available.


Related in: MedlinePlus