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  • Title: Effects of exercise training on responsiveness of the mesenteric arterial bed to phenylephrine and KCl in male rats.
    Author: Jansakul C, Hirunpan P.
    Journal: Br J Pharmacol; 1999 Aug; 127(7):1559-66. PubMed ID: 10455310.
    Abstract:
    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.
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