Cardiovascular Responses to Catecholamines and Interactions with Endothelin-1 and Adenine Nucleosides in the Pericardium of the Dog Heart (original) (raw)
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Naunyn-schmiedebergs Archives of Pharmacology, 1982
The positive inotropic effects of catecholamines were studied on samples of ventricular myocardium taken from patients undergoing open heart surgery. The adenylyl cyclase and binding of 3H-(−)-bupranolol were examined in membrane particles prepared from similarly obtained samples. The equilibrium dissociation constant (K D ) for (−)-bupranolol was estimated in 4 ways: blockade of the positive inotropic effects of catecholamines, blockade of the stimulation of the adenylyl cyclase by catecholamines, saturation binding of 3H-(−)-bupranolol, inhibition of the binding of 3H-(−)-bupranolol by its unlabeled stereoisomers. The estimates of K D fall in the range 0.5–1.4 nmol/l. The stereo-selectivity ratio (K D (+)-isomer/K D (−)-isomer) is 73. Both values for bupranolol are very similar in cat and man. The inotropic potency of (−)-noradrenaline is nearly 2 orders of magnitude higher in cat heart tissues than in tissues from human hearts. The difference in inotropic potencies between species is only partially accounted for by the five-fold lower potency of (−)-noradrenaline for the human heart adenylyl cyclase as compared to the cat enzyme.
Catecholamines in coronary sinus and peripheral plasma during pacing- induced angina in man
Circulation, 1979
Subscriptions: Information about subscribing to Circulation is online at by guest on July 9, 2011 http://circ.ahajournals.org/ Downloaded from CATECHOLAMINE RESPONSE TO ANGINA/Schwartz et al. 32. Palacious 1, Johnson RA, Newell JB, Powell WJ Jr: Left ventricular end-diastolic pressure volume relationships with experimental acute global ischemia. Circulation 53: 428, 1976 33. Forrester JS, Diamond G, Parmley WW, Swan HJC: Early increase in left ventricular compliance after myocardial infarction. J Clin Invest 51: 598, 1972 34. Tyberg JV, Forrester JS, Wyatt HL, Goldner SJ, Parmley WW, Swan HJC: An analysis of segmental ischemic dysfunction utilizing the pressure-length loop. Circulation 49: 748, 1974 35. Theroux P, Ross J Jr, Franklin D, Kemper WS, Sasayama S: Regional myocardial function in the conscious dog during acute coronary occlusion and responses to morphine, propranolol, nitroglycerin, and lidocaine. Circulation 53: 302, 1976 36. Theroux P, Ross J Jr, Franklin D, Covell JW, Bloor CM, Sasayama S: Regional myocardial function and dimensions early and late after myocardial infarction in the unanesthetized dog. Circ Res 40: 158, 1977 37. Crozatier B, Ashraf M, Franklin D, Ross J Jr: Sarcomere length in experimental myocardial infarction: evidence for sarcomere overstretch in dyskinetic ventricular regions. J Mol Cell Cardiol 9: 785, 1977 38. Theroux P, Franklin D, Ross J Jr, Kemper WS: Regional myocardial function during acute coronary artery occlusion and its modification by pharmacologic agents in the dog. Circ Res 35: 896, 1974 39. Waters DD, Da Luz P, Wyatt HL, Swan HJC, Forrester JS: Early changes in regional and global left ventricular function induced by graded reductions in regional coronary perfusion. Am frequently during pacing-induced angina, cannot be demonstrated during exercise-induced angina, since metabolic evidence of ischemia is obscured by elevated arterial lactate concentrations."' 12 In relationship to anaerobic glycolysis, a decrease of myocardial tissue content of high-energy phosphates, ATP and CP, has been demonstrated.'13-5 An increase in myocardial tissue content'517, 37 and a coronary venous release of the diffusible ATP catabolites adenosine, inosine and hypoxanthine, have been shown19 20 22 23 in animals after temporary coronary occlusion. 43 by guest on July 9, 2011
Acta physiologica Scandinavica, 1999
In this study our aims were to investigate the presence and source of catecholamines in pericardial fluid of normotensive, reserpine-treated and spontaneously hypertensive rats. We found that noradrenaline is the only detectable catecholamine present in rat pericardial fluid. The effect of reserpine 6, 12, and 24 h after pre-treatment with 5 mg kg−1 (8.2 μmol kg−1) i.p. shows that the concentration of noradrenaline in pericardial fluid reflects the amount of noradrenaline released within the heart rather than the amount of noradrenaline in plasma. Using spontaneously hypertensive rats (SHR) as a model for primary hypertension we could show that the level of pericardial noradrenaline is approximately threefold in the pericardial fluid of the SHRs when compared to respective values of age-matched normotensive Wistar–Kyoto rats (WKY), suggesting that there was an increased noradrenaline overflow in the hearts of the SHRs. In conclusion, determination of the noradrenaline concentration in the pericardial fluid might provide a new method for estimating the release of noradrenaline in the heart.
Journal of Cardiovascular Electrophysiology, 1999
Catecholamine Facilitated Reentry. Introduction: Adenosine has no direct clectrophysiologic function in ventricnlar tissue, but in the presence of cyclic adenosine monophosphate (cAMP), stinuilatiun exerts a potent antiadrenergic etTect. This effect has l>een exploited in the recognition and treatment of ventricular tachycardia (VT) due to cAMP-mediated triggered activity and automaticity, which are respectively terminated and suppressed by adenosine. However, the effects of adenosine on calecholamine-facilitated reentrant VT are unknown. A pivotal issue is whether termination of VT with adenosine is mechanism specific, or whether it represents a nonspecific antiadrenergic effect. The purpose of this study, therefore, was to define the effects of adenosine in a well-characterized group of patients with catecholamine-facilitated reentrant VT.
Naunyn-schmiedebergs Archives of Pharmacology, 2004
The function of β-adrenoceptors was investigated in ventricular myocardium obtained from patients undergoing open heart surgery. Dopamine increased contractile force up to 1/2 and 1/4 of the maximum increase caused by (−)-noradrenaline or (−)-adrenaline in right and left ventricular preparations, respectively. β-adrenoceptors were labelled with 3H-(−)-bupranolol. For 3/4 of the receptors (β1) the affinity of (−)-noradrenaline was 20 times higher than for the remaining 1/4 (β2). (−)-Adrenaline and dopamine appeared to be nonselective for β1 and β2. Dopamine was able to stimulate the adenylate cyclase only up to 1/3 of the maximum stimulation caused by (−)noradrenaline and (−)-adrenaline. Increases in contractile force by (−)-noradrenaline were closely associated with small increases of cyclase activity through β1-adrenoceptors, consistent with a common link. The experiments on human myocardium were compared with similar experiments on feline myocardium. Feline ventricle exhibited a 20- to 30-fold higher sensitivity to catecholamines as activators of contractile force than did human ventricle. However, the binding affinities for catecholamines were similar in cat and man. A 3 h exposure of human and feline ventricular myocardium to (−)-isoprenaline caused desensitization by uncoupling β-adrenoceptors from the adenylate cyclase. Desensitization reduced the maximum contractile response to (−)-isoprenaline in human but not in feline ventricle. The more efficient activation of contractile force by (−)-noradrenaline in cat, compared to man, appears to be related to a 2-fold higher density of β1-adrenoceptors, a 6-fold higher production of cyclic AMP per β1-adrenoceptor and possibly to a more effective use of cyclic AMP for contraction.
European Journal of Pharmacology, 1992
We investigated the /32-adrenoceptor-mcdiated effects of atrial and vcntricular effective rcfractory period (ERP), SA node paccmaker activity, and AV conductivity induccd by sympathetic nerve stimulation or epinephrine infusion in anesthetized dogs. A /3:-adrenoceptor antagonist, ICI 118,551 up to 100 ~tg/kg, i.v,, inhibited the positive chronotropic and dromotropic responses to sympathetic stimulation but did not shorten the atrial or ventricular ERP. ICI 118,551 also attenuated the positive chronotropic and dromotropic responses and the shortcning of atrial ERP in response to epinephrine but not the shortening of ventricular ERP. A selective ,~l-adrenoceptor antagonist, atenolol, inhibited each electrical cardiac response to sympathetic stimulation and epinephrine infusion in a similar manner. These results suggest that/3e-adrenoceptor-mediated electrical cardiac responses to endogenous catecholamines also exist in addition to the predominant /31-adrenoccptor-mediated responses, and that the order of the proportion of/3:-adrenoceptor-mcdiated cardiac effects was SA node pacemaker activity >> AV conductivity = atrial ERP >> vcntricular ERP in the dog hear!.