Effect of contraction on the subsequent responsiveness and maximum contractility of the rabbit ear artery and saphenous vein in vitro.
The purpose of this study was to investigate the effect of prior agonist-induced contraction of vascular smooth muscle on its subsequent responsiveness and maximum contractility. Repeated exposure of the rabbit ear artery to equieffective histamine (Hist) or KCl concentrations increased subsequent norepinephrine (NE) responsiveness and maximum contractility in comparison to rested controls. Tissues exposed in a similar manner to an equieffective serotonin concentration responded to NE more than did controls, but less than Hist- and KCl-pretreated tissues. Prior exposure to NE or KCl increased Hist responsiveness and maximum contractility. However, NE pretreatment did not increase serotonin or KCl responsiveness. The increased responsiveness and maximum contractility lasted for at least 90 and 390 min., respectively. When ear arteries were exposed to agonists in the presence of NaNO2 or papaverine the increase in responsiveness was either reduced or absent. Everted arteries repeatedly exposed to Hist demonstrated an increased tonic phase contraction to NE; there was no change in the initial transient phase of contraction. Exposure of the saphenous vein to Hist oe KCl had no effect on subsequent NE responsiveness; however, maximum contractility was increased. The present results suggest that (1) contraction brought about by agonist drugs can result in two separate phenomena -- increased responsiveness and increased maximum contractility; (2) the increased responsiveness may mask underlying alpha-adrenoceptor desensitization which may be agonist specific; (3) an event following agonist-receptor binding is responsible for increased responsiveness and increased maximum contractility; (4) the mechanism for increased responsiveness may be due to an increased coupling between receptor activation and membrane permeability to calcium; (5) agonist contraction in the saphenous vein and ear artery may be regulated by different mechanisms.
D000818:Animals; D001158:Arteries / Q000187:drug effects*; D004423:Ear / Q000098:blood supply; D005260:Female; D006632:Histamine / Q000494:pharmacology; D066298:In Vitro Techniques; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology; D010208:Papaverine / Q000494:pharmacology; D011817:Rabbits; D012501:Saphenous Vein / Q000187:drug effects*; D012977:Sodium Nitrite / Q000494:pharmacology; D013997:Time Factors; D014661:Vasoconstriction / Q000187:drug effects*
D006632:Histamine; D010208:Papaverine; D012977:Sodium Nitrite; D009638:Norepinephrine