Article date: October 1991
By: S.F. Liu, D.E. Crawley, T.W. Evans, P.J. Barnes, in Volume 104, Issue 2, pages 565-569
Electrical field stimulation (EFS) of guinea‐pig isolated pulmonary artery induced a frequency‐dependent contraction. This was abolished by tetrodotoxin (1 μm) and prevented by phentolamine and prazosin (both 1 μm), indicating a role for α1‐adrenoceptors activated by noradrenaline (NA) released from perivascular adrenergic nerves.
l‐NG‐monomethyl arginine (l‐NMMA, 0.3–100 μm) caused a concentration‐dependent enhancement of the EFS‐induced contraction with a 3.4 ± 0.5 fold increase at 100 μm (n = 6). The augmenting effect of 30 μm l‐NMMA on the contraction to EFS was completely reversed by 100–300 μm l‐arginine, but not by an identical concentration of d‐arginine.
The contractile response to exogenous NA was similarly enhanced by 30 μm l‐NMMA (2.9 ± 0.6 fold increase, n = 5).
The contractile responses to exogenous phenylephrine and prostaglandin F2α which matched the contraction to EFS (4 Hz) were equally augmented by 30 μm l‐NMMA.
In vessel rings submaximally contracted with the thromboxane analogue U44069 (2 μm), the selective α2‐adrenoceptor agonist UK14304 induced concentration‐dependent relaxation, which was abolished by removal of endothelium. NA had little relaxant effect on these precontracted vessel rings unless in the presence of prazosin (1 μm).
Indomethacin had no significant effect on the contractile response to EFS or NA, indicating that vasodilator cyclo‐oxygenase products such as prostacyclin are not involved in modulating these responses.
Our results suggest that endogenous nitric oxide inhibits the contractile response to adrenergic nerve stimulation in the guinea‐pig pulmonary artery by a postjunctional mechanism, but release of prostacyclin does not modulate these responses. Basal release of nitric oxide from endothelial cells may account for this inhibition.
Electrical field stimulation (EFS) of guinea‐pig isolated pulmonary artery induced a frequency‐dependent contraction. This was abolished by tetrodotoxin (1 μm) and prevented by phentolamine and prazosin (both 1 μm), indicating a role for α1‐adrenoceptors activated by noradrenaline (NA) released from perivascular adrenergic nerves.
l‐NG‐monomethyl arginine (l‐NMMA, 0.3–100 μm) caused a concentration‐dependent enhancement of the EFS‐induced contraction with a 3.4 ± 0.5 fold increase at 100 μm (n = 6). The augmenting effect of 30 μm l‐NMMA on the contraction to EFS was completely reversed by 100–300 μm l‐arginine, but not by an identical concentration of d‐arginine.
The contractile response to exogenous NA was similarly enhanced by 30 μm l‐NMMA (2.9 ± 0.6 fold increase, n = 5).
The contractile responses to exogenous phenylephrine and prostaglandin F2α which matched the contraction to EFS (4 Hz) were equally augmented by 30 μm l‐NMMA.
In vessel rings submaximally contracted with the thromboxane analogue U44069 (2 μm), the selective α2‐adrenoceptor agonist UK14304 induced concentration‐dependent relaxation, which was abolished by removal of endothelium. NA had little relaxant effect on these precontracted vessel rings unless in the presence of prazosin (1 μm).
Indomethacin had no significant effect on the contractile response to EFS or NA, indicating that vasodilator cyclo‐oxygenase products such as prostacyclin are not involved in modulating these responses.
Our results suggest that endogenous nitric oxide inhibits the contractile response to adrenergic nerve stimulation in the guinea‐pig pulmonary artery by a postjunctional mechanism, but release of prostacyclin does not modulate these responses. Basal release of nitric oxide from endothelial cells may account for this inhibition.
DOI: 10.1111/j.1476-5381.1991.tb12469.x
View this article