Document Detail

Temporal increase in the reactivity of pulmonary vasculature to substance P in chronically hypoxic rats.
MedLine Citation:
PMID:  11832408     Owner:  NLM     Status:  MEDLINE    
We previously demonstrated that the pulmonary vascular response to substance P (SP) increased in chronically hypoxic rats. This study explored the temporal increase in reactivity of the pulmonary vascular response to SP and its underlying mechanisms. First, young female Wistar rats were exposed to sea level (SL) or simulated high altitude (HA) for 15 h/day for 3 days, 1 wk, 2 wk, and 4 wk. Lungs were isolated and perfused with 4% bovine serum albumin in Krebs-Henseleit buffer solution. SP (1.5 x 10(-4) M) induced significant increases in pulmonary arterial pressure (P(pa)), venous pressure (P(v)), capillary pressure (P(c)), arterial resistance (R(a)), and filtration coefficient (K(fc)) in SL lungs. Increases in P(pa) and R(a) were significantly augmented in HA lungs, with a temporal increase trend peaking at 2 wk of HA exposure. The selective neurokinin (NK) type 1 (NK1) receptor antagonist SR-14033 significantly attenuated SP-induced increases in P(pa), P(v), P(c), R(a), and K(fc) in SL lungs. In lungs exposed to HA for 2 wk, SR-14033 suppressed the effect of SP on P(pa). Also, chronic hypoxia induced significant increases in NK1 receptors and NK1 receptor mRNA, with a temporal trend. We conclude that chronic hypoxia temporally augments SP-induced vascular responses, which are closely associated with increases in NK1 receptors and gene expression.
Yih-Loong Lai; Szu-Jung Chu; Ming-Chieh Ma; Chau-Fong Chen
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  American journal of physiology. Regulatory, integrative and comparative physiology     Volume:  282     ISSN:  0363-6119     ISO Abbreviation:  Am. J. Physiol. Regul. Integr. Comp. Physiol.     Publication Date:  2002 Mar 
Date Detail:
Created Date:  2002-02-08     Completed Date:  2002-03-15     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  100901230     Medline TA:  Am J Physiol Regul Integr Comp Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  R858-64     Citation Subset:  IM    
Department of Physiology, National Taiwan University College of Medicine, Taipei 100, Taiwan.
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MeSH Terms
Anoxia / physiopathology*
Blood Pressure / drug effects
Blood Vessels / drug effects
Capillaries / physiopathology
Chronic Disease
Piperidines / pharmacology
Pulmonary Circulation / drug effects*
Quinuclidines / pharmacology
RNA, Messenger / metabolism
Rats, Wistar
Receptors, Neurokinin-1 / genetics,  metabolism
Receptors, Neurokinin-2 / antagonists & inhibitors
Substance P / pharmacology*
Time Factors
Reg. No./Substance:
0/Piperidines; 0/Quinuclidines; 0/RNA, Messenger; 0/Receptors, Neurokinin-1; 0/Receptors, Neurokinin-2; 153050-21-6/SR 140333; 33507-63-0/Substance P

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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