PMID- 11212964
OWN - NLM
STAT- MEDLINE
DCOM- 20010405
LR  - 20190822
IS  - 0263-6352 (Print)
IS  - 0263-6352 (Linking)
VI  - 19
IP  - 2
DP  - 2001 Feb
TI  - Angiotensin converting enzyme protects acetylcholine-induced relaxation from its 
      attenuation by formyl-methionyl-leucyl-phenylalanine in rat aorta.
PG  - 223-8
AB  - OBJECTIVE: A chemotactic tripeptide formyl-methionyl-leucyl-phenylalanine (fMLP) 
      attenuated acetylcholine (ACh)-induced relaxation. Because angiotensin converting 
      enzyme (ACE), which inactivates fMLP, is rich in vascular endothelial cells, we 
      examined whether endothelial cell ACE inhibits the attenuating effect of fMLP on 
      ACh-induced relaxation. DESIGN AND METHODS: ACh-induced relaxation was evaluated 
      in aortic rings from 9-week-old Sprague-Dawley rats. We examined the effects of 
      ACE, the ACE inhibitor captopril and/or fMLP on ACh-induced relaxation in aortas 
      from rats with or without dexamethasone treatment, which enhances ACE activity. 
      RESULTS: Pre-treatment with ACE did not alter ACh-induced relaxation in control 
      aortas but abolished the inhibitory effect of fMLP on ACh-induced relaxation 
      [maximal relaxation (Emax): 95.4 +/- 1.2 versus 75.5 +/- 1.9%, P < 0.05]. 
      Conversely, captopril enhanced the attenuation of ACh-induced relaxation by fMLP 
      (Emax: 62.5 +/- 3.3 versus 74.0 +/- 2.2%, P < 0.05), although captopril did not 
      affect ACh-induced relaxation in control aortas. In addition, fMLP did not 
      attenuate ACh-induced relaxation in aortas from dexamethasone-treated rats (Emax: 
      89.7 +/- 3.7 versus 85.2 +/- 3.8%, NS), which enhanced ACE activity of aortas 
      (3.37 +/- 0.25 versus 2.70 +/- 0.20 IU/mg protein, P < 0.05). CONCLUSION: 
      Endothelial-cell ACE attenuates the effect of fMLP on ACh-induced relaxation, 
      possibly by its cleavage.
FAU - Ando, K
AU  - Ando K
AD  - Department of Endocrinology and Nephrology, Faculty of Medicine, University of 
      Tokyo, Japan. katsua-tky@umin.ac.jp
FAU - Fujita, T
AU  - Fujita T
LA  - eng
PT  - Journal Article
PL  - Netherlands
TA  - J Hypertens
JT  - Journal of hypertension
JID - 8306882
RN  - 59880-97-6 (N-Formylmethionine Leucyl-Phenylalanine)
RN  - 7S5I7G3JQL (Dexamethasone)
RN  - 9G64RSX1XD (Captopril)
RN  - EC 3.4.15.1 (Peptidyl-Dipeptidase A)
RN  - N9YNS0M02X (Acetylcholine)
SB  - IM
MH  - Acetylcholine/*pharmacology
MH  - Animals
MH  - Aorta, Thoracic/*drug effects/physiology
MH  - Captopril/pharmacology
MH  - Dexamethasone/pharmacology
MH  - Endothelium, Vascular/physiology
MH  - In Vitro Techniques
MH  - Male
MH  - N-Formylmethionine Leucyl-Phenylalanine/*pharmacology
MH  - Peptidyl-Dipeptidase A/*pharmacology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Vasodilation/*drug effects
EDAT- 2001/02/24 12:00
MHDA- 2001/04/06 10:01
CRDT- 2001/02/24 12:00
PHST- 2001/02/24 12:00 [pubmed]
PHST- 2001/04/06 10:01 [medline]
PHST- 2001/02/24 12:00 [entrez]
AID - 10.1097/00004872-200102000-00008 [doi]
PST - ppublish
SO  - J Hypertens. 2001 Feb;19(2):223-8. doi: 10.1097/00004872-200102000-00008.