Effect of swimming on vascular reactivity to phenylephrine and KC1 in male rats
Authors: Jansakul C. 
Published: July 2012

The present study aimed to examine whether there is any change in vascular responsiveness to phenylephrine and KC1 during exercise, and whether the vascular endothelium plays a role in these changes.

Adult male rats were subjected to a swimming schedule every day for 5–6 weeks. Studies were performed in vitro on thoracic aortae.

Maximum contractile response to phenylephrine of endothelium‐intact thoracic aortic rings (passive tension 1.0 g) obtained from swimming rats (1.2 ±0.2 g, n = 8) was lower than that of sedentary control rats (2.1 ±0.2 g, n = 8). When the endothelium was removed, however, the dose‐response curves of both groups of rats were shifted to the left with an increase in maximum responses and they were no longer significantly different (max. tension, swimming rats: 3.2 ±0.3 g, n = 6, control rats: 3.4 ±0.4 g, n = 5).

Indomethacin did not significantly alter the dose‐response curves. A similar effect to that obtained by removal of the endothelium was observed when methylene blue and indomethacin were both added.

Passive tension in the range of 2.5‐3.0 g, caused a significant increase in active tension developed to phenylephrine (1 μm for endothelium‐intact and 0.1 μm for endothelium‐denuded) of thoracic aortic rings of both swimming and sedentary control rats compared to their corresponding groups when using passive tension of 1.0–1.5 g.

The reduction in responses to phenylephrine of endothelium‐intact thoracic aortic rings of swimming rats persisted with the use of a passive tension of 3.0 g. The presence of 300 μm NG‐nitro‐L‐arginine (L‐NOARG) caused a significant leftward shift of the curve with an increase in maximum responses when a passive tension of either 1.0 or 3.0 g was applied to the rings. However, for the rings with a passive tension of 1.0 g, L‐NOARG caused a smaller increase in maximal contractile responses to phenylephrine of the rings of sedentary controls than those of swimming rats.

There was no difference in the dose‐response curves to depolarizing concentrations of KC1 (20, 40, 80 and 120 mM) of endothelium‐intact thoracic aortic rings from swimming and sedentary control rats. When the endothelium was removed, however, the dose‐response curves of both groups of animals were shifted to the left with an increase in maximum responses. Moreover, the responses to KC1 of endothelium‐denuded thoracic aortic rings of swimming rats were greater than those of sedentary control rats.

These results suggest that there were changes in vascular responsiveness to phenylephrine and KC1 during exercise. The fall in sensitivity to phenylephrine with no change in KC1 responses, and the increase in maximum responses to phenylephrine in the presence of L‐NOARG in endothelium‐intact aortae (passive tension 1.0 g) from swimming rats, were due to an increase in spontaneous release and upregulation of phenylephrine‐stimulated release of EDRF/NO, and may not be a consequence of an increase in prostaglandins or a decrease in the production of endothelial constrictors by vascular endothelium. EDRF/NO may play an important role in modulating local vasodilatation.