Effects of adrenaline, angiotensin and calcium on spontaneously active and potassium-depolarized rat portal veins.
1) Adrenaline and angiotensin increased both frequency and developed tension of spontaneously active rat isolated portal veins. Adrenaline 10(-7) M and angiotensin 10(-9) M, produced a maximal increment of the amplitude of twitch contraction. Greater concentrations elicited a tetanic state, which in all cases had the same amplitude as the maximal effects obtained on single twitches. This suggests that there exists a dissociation between membrane and electrical phenomena, so that the highest intensity of the contractile system activity is attained at agonist concentrations lower than those which result in maximal decrease of membrane stability. (2) Increasing K to a 106 mM final concentration caused a persistent contracture. Adrenaline and angiotensin exhibited pharmaco-mechanical properties, as later addition of both substances produced an increase of the contracture tension. (3) Ca dose-response curves were performed on previously Ca-depleted veins, after the addition of K 106 mM, K-plus-adrenaline or K-plus-angiotensin. Both substances made the Ca responses rise steeply, as evidenced by the leftward shift of ED50. This provides support to the belief that pharmacomechanical coupling is mediated through an increase of the membrane permeability to Ca.
D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D002118:Calcium / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D004837:Epinephrine / Q000494:pharmacology*; D005260:Female; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D011169:Portal Vein / Q000187:drug effects* / Q000502:physiology; D011188:Potassium / Q000494:pharmacology*; D051381:Rats
D000804:Angiotensin II; D011188:Potassium; D002118:Calcium; D004837:Epinephrine