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Am J Physiol Regul Integr Comp Physiol 282: R858-R864, 2002; doi:10.1152/ajpregu.00429.2001
0363-6119/02 $5.00
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Vol. 282, Issue 3, R858-R864, March 2002

Temporal increase in the reactivity of pulmonary vasculature to substance P in chronically hypoxic rats

Yih-Loong Lai, Szu-Jung Chu, Ming-Chieh Ma, and Chau-Fong Chen

Department of Physiology, National Taiwan University College of Medicine, Taipei 100, Taiwan

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 × 10-4 M) induced significant increases in pulmonary arterial pressure (Ppa), venous pressure (Pv), capillary pressure (Pc), arterial resistance (Ra), and filtration coefficient (Kfc) in SL lungs. Increases in Ppa and Ra 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 Ppa, Pv, Pc, Ra, and Kfc in SL lungs. In lungs exposed to HA for 2 wk, SR-14033 suppressed the effect of SP on Ppa. 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.

pulmonary hypertension; tachykinins; gene expression


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