Effects of exercise training on responsiveness of the mesenteric arterial bed to phenylephrine and KCl in male rats.

1. We aimed to determine whether there are any changes in responsiveness of the mesenteric arterial beds to phenylephrine (Phe) and KCl in exercise-trained rats, and whether vascular endothelium and/or vascular smooth muscle play a role in these changes. 2. Adult male rats were subjected to a swimming schedule every day for 28-33 days. Studies were performed in vitro using Krebs perfused mesenteric arterial beds. 3. Maximum perfusion pressure responses to KCl and Phe of the mesenteric arterial beds from exercise-trained rats were significantly lower than those from sedentary controls. However, these differences disappeared after blocking the nitric oxide synthase by NG-nitro-L-arginine (L-NOARG). 4. 3-[(3-cholamidopropyl)-dimethylammonio]-1-propanesulphonate (CHAPS, 3 mg ml(-1), 2 min infusion) caused a significant increase in maximum perfusion pressure responses to KCl to the same extent in both exercise-trained and sedentary control rats. CHAPS caused about a 4.5 fold leftward shift of the curve with no change in maximum response to Phe for the mesenteric arterial beds from sedentary control rats, but not for those obtained from exercise-trained rats. However, these differences were abolished in the presence of L-NOARG. 5. Indomethacin did not alter the dose-response curves to KCl or Phe in either swimming or control groups. 6. These results suggest that there was a lower vascular responsiveness to KCl and Phe in exercise-trained rats at rest. The decrease in reactivities to KCl or decrease in sensitivity to Phe after having endothelium impairment by CHAPS of the mesenteric arterial beds of exercise-trained rats were due to an increase in both spontaneous release and upregulation of phenylephrine-stimulated release of nitric oxide from both the vascular endothelium and the vascular smooth muscle cells, and may not be a consequence of an increase in vasodilator prostaglandins by the vascular bed.