Table I.

Airway relaxation induced by NOC-5 and its modulation by related compounds

Experimental conditions Relaxation (% of maximal contraction) 
 Peak Sustained n 
5-HT–contracted airways    
NOC-5 (10 µM) 44 ± 6 12 ± 3 
SNAP (50 µM) 49 ± 12 17 ± 9 
NOC-5 + ZAP (10 µM) 49 ± 8 46 ± 6b 
NOC-5 + ODQ (5 µM) 4 ± 2a 2 ± 1b 
NOC-5 + Rp-8-pCPT-cGMPS (20 µM) 5 ± 3a 3 ± 2b 
ACH-contracted airways    
NOC-5 (10 µM) 40 ± 7 11 ± 6 
NOC-5 + ZAP (10 µM) 46.4 ± 8.7 45.7 ± 7.9b 
NOC-5 + VAR (1 µM) 53.1 ± 9.8 52.3 ± 9.2b 
Experimental conditions Relaxation (% of maximal contraction) 
 Peak Sustained n 
5-HT–contracted airways    
NOC-5 (10 µM) 44 ± 6 12 ± 3 
SNAP (50 µM) 49 ± 12 17 ± 9 
NOC-5 + ZAP (10 µM) 49 ± 8 46 ± 6b 
NOC-5 + ODQ (5 µM) 4 ± 2a 2 ± 1b 
NOC-5 + Rp-8-pCPT-cGMPS (20 µM) 5 ± 3a 3 ± 2b 
ACH-contracted airways    
NOC-5 (10 µM) 40 ± 7 11 ± 6 
NOC-5 + ZAP (10 µM) 46.4 ± 8.7 45.7 ± 7.9b 
NOC-5 + VAR (1 µM) 53.1 ± 9.8 52.3 ± 9.2b 

PDE-5 inhibitors: ZAP and vardenifil (VAR); sGC inhibitor (ODQ); PKG inhibitor (Rp-8-pCPT-cGMPS). The peak and sustained relaxation of airways in response to NOC-5 in the absence or presence of ZAP, ODQ, and Rp-8-pCPT-cGMPS calculated from experiments similar to those shown in Figs. 2 and 3.

a

P < 0.05 compared to peak relaxation induced by NOC-5 alone.

b

P < 0.05 compared to sustained relaxation induced by NOC-5 alone.

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