title: Effects of exercise training on responsiveness of the mesenteric arterial bed to phenylephrine and KCl in male rats.
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.
authors.affiliation: Department of Physiology, Faculty of Science, Prince of Songkla University, Hat-Yai, Thailand 90112, USA.
authors.forename: C
authors.initials: C
authors.lastname: Jansakul
authors.forename: P
authors.initials: P
authors.lastname: Hirunpan
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000494:pharmacology*; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D001835:Body Weight / Q000187:drug effects / Q000502:physiology; D002793:Cholic Acids / Q000494:pharmacology; D003902:Detergents / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000187:drug effects; D004791:Enzyme Inhibitors / Q000494:pharmacology; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D008638:Mesenteric Arteries / Q000187:drug effects / Q000502:physiology*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D052250:Nitric Oxide Synthase Type III; D019335:Nitroarginine / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology*; D010805:Physical Conditioning, Animal / Q000502:physiology*; D011189:Potassium Chloride / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D013550:Swimming
chemical_list: D000316:Adrenergic alpha-Agonists; D000894:Anti-Inflammatory Agents, Non-Steroidal; D002793:Cholic Acids; D003902:Detergents; D004791:Enzyme Inhibitors; D010656:Phenylephrine; D019335:Nitroarginine; D011189:Potassium Chloride; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III; C496316:Nos3 protein, rat; C028213:3-((3-cholamidopropyl)dimethylammonium)-1-propanesulfonate; D007213:Indomethacin