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- Publisher Website: 10.1152/japplphysiol.00684.2003
- Scopus: eid_2-s2.0-0942276798
- PMID: 14527966
- WOS: WOS:000187888400055
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Article: Regulation of the angiotensin-converting enzyme activity by a time-course hypoxia in the carotid body
Title | Regulation of the angiotensin-converting enzyme activity by a time-course hypoxia in the carotid body |
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Authors | |
Keywords | Angiotensin II Captopril Chronic hypoxia Renin-angiotensin system |
Issue Date | 2004 |
Publisher | American Physiological Society. |
Citation | Journal Of Applied Physiology, 2004, v. 96 n. 2, p. 809-813 How to Cite? |
Abstract | Chronic hypoxia activates a local angiotensin-generating system in the carotid body. Here, we test the hypothesis that the activity of the critical enzyme for this system, angiotensin-converting enzyme (ACE), in the carotid body is subject to regulation by a time-course hypoxia. Results from the carotid body assays showed that ACE activity was markedly increased under the hypoxic stress of 7-, 14-, 21-, and 28-day exposures. The changes in ACE activity of 7-day (15.00 vs. 30.95 × 10-5 nmol·μ g-1·min-1). 14-day (8.73 vs. 30.25 × 10 -5 nmol·μg-1·min-1), and 21-day (11.41 vs. 31.83 × 10-5 nmol·μg -1·min-1) hypoxia treatments were enhanced significantly. However, ACE activity in 28-day (13.18 vs. 24.53 × 10 -5 nmol·μg-1·min-1) hypoxia treatment was observed to increase insignificantly when compared with results in the respective control groups. Captopril inhibited all rises in ACE activity in both the control and experimental groups. Results clearly indicate an activation of the enzymatic activity of ACE, the critical enzyme for determining the conversion of angiotensin I into the physiologically active angiotensin II, by chronic hypoxia in the carotid body. An increase in the ACE activity may increase the local production of angiotensin II in the carotid body and thus its agonist action at the AT1 receptor. This may be important in the modulation of cardiopulmonary adaptation in the hypoxic ventilatory response as well as for electrolyte and water homeostasis during chronic hypoxia. |
Persistent Identifier | http://hdl.handle.net/10722/81339 |
ISSN | 2023 Impact Factor: 3.3 2023 SCImago Journal Rankings: 1.042 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Lam, SY | en_HK |
dc.contributor.author | Fung, ML | en_HK |
dc.contributor.author | Leung, PS | en_HK |
dc.date.accessioned | 2010-09-06T08:16:31Z | - |
dc.date.available | 2010-09-06T08:16:31Z | - |
dc.date.issued | 2004 | en_HK |
dc.identifier.citation | Journal Of Applied Physiology, 2004, v. 96 n. 2, p. 809-813 | en_HK |
dc.identifier.issn | 8750-7587 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/81339 | - |
dc.description.abstract | Chronic hypoxia activates a local angiotensin-generating system in the carotid body. Here, we test the hypothesis that the activity of the critical enzyme for this system, angiotensin-converting enzyme (ACE), in the carotid body is subject to regulation by a time-course hypoxia. Results from the carotid body assays showed that ACE activity was markedly increased under the hypoxic stress of 7-, 14-, 21-, and 28-day exposures. The changes in ACE activity of 7-day (15.00 vs. 30.95 × 10-5 nmol·μ g-1·min-1). 14-day (8.73 vs. 30.25 × 10 -5 nmol·μg-1·min-1), and 21-day (11.41 vs. 31.83 × 10-5 nmol·μg -1·min-1) hypoxia treatments were enhanced significantly. However, ACE activity in 28-day (13.18 vs. 24.53 × 10 -5 nmol·μg-1·min-1) hypoxia treatment was observed to increase insignificantly when compared with results in the respective control groups. Captopril inhibited all rises in ACE activity in both the control and experimental groups. Results clearly indicate an activation of the enzymatic activity of ACE, the critical enzyme for determining the conversion of angiotensin I into the physiologically active angiotensin II, by chronic hypoxia in the carotid body. An increase in the ACE activity may increase the local production of angiotensin II in the carotid body and thus its agonist action at the AT1 receptor. This may be important in the modulation of cardiopulmonary adaptation in the hypoxic ventilatory response as well as for electrolyte and water homeostasis during chronic hypoxia. | en_HK |
dc.language | eng | en_HK |
dc.publisher | American Physiological Society. | en_HK |
dc.relation.ispartof | Journal of Applied Physiology | en_HK |
dc.subject | Angiotensin II | en_HK |
dc.subject | Captopril | en_HK |
dc.subject | Chronic hypoxia | en_HK |
dc.subject | Renin-angiotensin system | en_HK |
dc.title | Regulation of the angiotensin-converting enzyme activity by a time-course hypoxia in the carotid body | en_HK |
dc.type | Article | en_HK |
dc.identifier.openurl | http://library.hku.hk:4550/resserv?sid=HKU:IR&issn=8750-7587&volume=96&issue=2&spage=809&epage=813&date=2004&atitle=Regulation+of+the+angiotensin-converting+enzyme+activity+by+a+time-course+hypoxia+in+the+carotid+body | en_HK |
dc.identifier.email | Fung, ML: fungml@hkucc.hku.hk | en_HK |
dc.identifier.authority | Fung, ML=rp00433 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1152/japplphysiol.00684.2003 | en_HK |
dc.identifier.pmid | 14527966 | en_HK |
dc.identifier.scopus | eid_2-s2.0-0942276798 | en_HK |
dc.identifier.hkuros | 88099 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-0942276798&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 96 | en_HK |
dc.identifier.issue | 2 | en_HK |
dc.identifier.spage | 809 | en_HK |
dc.identifier.epage | 813 | en_HK |
dc.identifier.isi | WOS:000187888400055 | - |
dc.publisher.place | United States | en_HK |
dc.identifier.scopusauthorid | Lam, SY=7402279518 | en_HK |
dc.identifier.scopusauthorid | Fung, ML=7101955092 | en_HK |
dc.identifier.scopusauthorid | Leung, PS=7401748938 | en_HK |
dc.identifier.issnl | 1522-1601 | - |