Interaction of Isoflurane and Sevoflurane with α- and β-adrenoceptor Stimulations in Rat Myocardium 

1998 ◽  
Vol 88 (5) ◽  
pp. 1249-1258 ◽  
Author(s):  
Jean-Luc Hanouz ◽  
Pierre-Yves Gueugniaud ◽  
Yves Lecarpentier ◽  
Pierre Coriat ◽  
Bruno Riou
Keyword(s):  
Positive Inotropic Effect ◽  
Left Ventricular ◽  
Control Groups ◽  
Inotropic Effects ◽  
Beta Adrenoceptor ◽  
Calcium Stimulation ◽  
Positive Inotropic Effects ◽  
Inotropic Responses ◽  
Negative Inotropic Effects

Background Halothane potentiates the positive inotropic effects of alpha- and beta-adrenoceptor stimulations but impairs the positive lusitropic effect of beta-adrenoceptor stimulations. However, the interactions of isoflurane and sevoflurane with alpha- and beta-adrenoceptor stimulation have not been entirely defined. Methods The effects of 1 minimum alveolar concentration isoflurane and sevoflurane on the inotropic responses induced by phenylephrine (10(-8) to 10(-4) M) or isoproterenol (10(-8 to 10(-4) M) were studied in rat left ventricular papillary muscles in vitro (Krebs-Henseleit solution, 29 degrees C; pH, 7.4; 0.5 mM calcium; stimulation frequency, 12 pulses/min). The positive lusitropic effects of alpha- and beta-adrenoceptor stimulations were studied under isotonic and isometric conditions. Data are mean percentages of baseline +/- SEM. Results In control groups, phenylephrine (134 +/- 8%; P < 0.05) and isoproterenol (171 +/- 7%; P < 0.05) induced a positive inotropic effect. Isoflurane enhanced the positive inotropic effects of phenylephrine (185 +/- 10%; P < 0.05) and of isoproterenol (203 +/- 11%; P < 0.05). Sevoflurane enhanced the positive inotropic effects of phenylephrine (187 +/- 10%; P < 0.05) and of isoproterenol (228 +/- 11%; P < 0.05). These potentiations were similar to those previously reported with halothane. Isoflurane and sevoflurane did not modify the positive lusitropic effects under low and high loads of isoproterenol. Conclusion Although isoflurane and sevoflurane have moderate negative inotropic effects, they potentiated the positive inotropic effects of alpha- and beta-adrenoceptor stimulations but did not modify the positive lusitropic effects of beta-adrenoceptor stimulation.

Interaction of Halogenated Anesthetics with Dobutamine in Rat Myocardium

1999 ◽  
Vol 90 (6) ◽  
pp. 1663-1670. ◽  
Author(s):  
Pierre-Yves Gueugniaud ◽  
Jean-Luc Hanouz ◽  
Jean-Marc Martino ◽  
Yves Lecarpentier ◽  
Pierre Coriat ◽  
...  
Keyword(s):  
Positive Inotropic Effect ◽  
Isometric Force ◽  
Left Ventricular ◽  
Inotropic Effect ◽  
Inotropic Effects ◽  
Beta Adrenoceptor ◽  
Alpha Adrenoceptor ◽  
Positive Inotropic Effects ◽  
Inotropic Responses

Background Halogenated anesthetics potentiate the positive inotropic effects of alpha- and beta-adrenoceptor stimulations, but their interactions with dobutamine remain unknown. Methods The effects of halothane, isoflurane, sevoflurane, and desflurane (1 and 2 minimum alveolar concentration) on the inotropic responses induced by dobutamine (10(-8)-10(-4) M) were studied in rat left ventricular papillary muscles in vitro. Inotropic effects were studied under low (isotony) and high (isometry) loads. The authors also studied the lusitropic effects in isotonic (R1) and isometric (R2) conditions. Data are the mean percentage of baseline +/- SD. Results Dobutamine induced a positive inotropic effect (active isometric force: 185+/-36%, P < 0.001) and a positive lusitropic effect under low load (R1: 78+/-9%, P < 0.001), but not under high load (R2: 95+/-21%, not significant). Halothane, isoflurane, and sevoflurane did not modify the positive inotropic effect of dobutamine. Even in the presence of alpha-adrenoceptor blockade, isoflurane did not potentiate the positive inotropic effect of dobutamine. Desflurane significantly enhanced the positive inotropic effect of dobutamine (active isometric force: 239+/-35%, P < 0.001), but this potentiation was abolished by pretreatment with reserpine. In contrast to halothane, isoflurane, sevoflurane, and desflurane did not significantly modify the lusitropic effects of dobutamine. Conclusions Halogenated anesthetics, except desflurane, did not modify the positive inotropic effects of dobutamine. Desflurane enhanced the positive inotropic effect of dobutamine, but this effect was related to the desflurane-induced release in intramyocardial catecholamine stores.

Interaction of Halothane with α- and β-Adrenoceptor Stimulations in Rat Myocardium

1997 ◽  
Vol 86 (1) ◽  
pp. 147-159 ◽  
Author(s):  
Jean-Luc Hanouz ◽  
Bruno MD Riou ◽  
Laurent Massias ◽  
Yves Lecarpentier ◽  
Pierre Coriat
Keyword(s):  
Positive Inotropic Effect ◽  
Negative Inotropic Effect ◽  
Left Ventricular ◽  
Inotropic Effect ◽  
Papillary Muscles ◽  
Inotropic Effects ◽  
Beta Adrenoceptor ◽  
Low Load ◽  
Positive Inotropic Effects

Background Halothane induces negative inotropic and lusitropic effects in myocardium. It has been suggested that halothane potentiates beta-adrenoceptor stimulation. However, its effects on the inotropic response to alpha-adrenoceptor stimulation and its effects on the lusitropic effects of alpha- and beta-adrenoceptor stimulation are unknown. Methods The effects of halothane (0.5 and 1 minimum alveolar concentration [MAC]) on the inotropic responses induced by phenylephrine (10(-8) to 10(-4) M) and isoproterenol (10(-8) to 10(-4) M) were studied in rat left ventricular papillary muscles in vitro (in Krebs-Henseleit solution at 29 degrees C, pH 7.40, with 0.5 mM calcium and stimulation frequency at 12 pulses/min). The lusitropic effects were studied in isotonic (R1) and isometric (R2) conditions. Results One MAC halothane induced a negative inotropic effect (54 +/- 3%, P < 0.05), increased R1 (109 +/- 3%, P < 0.05), and decreased R2 (88 +/- 2%, P < 0.05). In control groups, phenylephrine (137 +/- 7%, P > 0.05) and isoproterenol (162 +/- 6%, P < 0.05) induced a positive inotropic effect. Halothane did not significantly modify the positive inotropic effect of calcium, suggesting that it did not modify the inotropic reserve of papillary muscles. In contrast, 1 MAC halothane enhanced the positive inotropic effects of phenylephrine (237 +/- 19%, P < 0.05) and isoproterenol (205 +/- 11%, P < 0.05). Halothane did not modify the lusitropic effect of phenylephrine under high or low load. In contrast, 1 MAC halothane impaired the positive lusitropic effect of isoproterenol under low load (P < 0.05), whereas it did not modify the positive lusitropic effect of isoproterenol under high load. Conclusions At clinically relevant concentrations, halothane potentiated the positive inotropic effects of both alpha- and beta-adrenoceptor stimulation. Furthermore, halothane alters the positive lusitropic-effect of beta-adrenoceptor stimulation under low load.

Interaction of Halogenated Anesthetics with α- and β-Adrenoceptor Stimulations in Diabetic Rat Myocardium

2004 ◽  
Vol 101 (5) ◽  
pp. 1145-1152 ◽  
Author(s):  
Julien Amour ◽  
Jean-Stéphane David ◽  
Benoît Vivien ◽  
Pierre Coriat ◽  
Bruno Riou
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Positive Inotropic Effect ◽  
Diabetic Rats ◽  
Left Ventricular ◽  
Inotropic Effect ◽  
Diabetic Rat ◽  
Inotropic Effects ◽  
Beta Adrenoceptor ◽  
Alpha Adrenoceptor ◽  
Positive Inotropic Effects

Background Halogenated anesthetics potentiate the positive inotropic effects of alpha- and beta-adrenoceptor stimulations. Although diabetes mellitus induces significant myocardial abnormalities, the interaction of halogenated anesthetics and adrenoceptor stimulation in diabetic myocardium remains unknown. Methods Left ventricular papillary muscles were provided from healthy and streptozotocin-induced diabetic rats. Effects of 1 minimum alveolar concentration halothane, isoflurane, and sevoflurane on the inotropic and lusitropic responses of alpha (phenylephrine)- and beta (isoproterenol)-adrenoceptor stimulations were studied at 29 degrees C with 12 pulses/min. Data shown are mean percentage of baseline active force +/- SD. Results Phenylephrine induced comparable positive inotropic effects in healthy and diabetic rats (143 +/- 8 vs. 136 +/- 18%; not significant), but the potentiation by halogenated anesthetics was abolished in the diabetic rats (121 +/- 20, 130 +/- 20, and 123 +/- 20% for halothane, isoflurane, and sevoflurane, respectively; not significant). In diabetic rats, the positive inotropic effect of isoproterenol was markedly diminished (109 +/- 9 vs. 190 +/- 18%; P < 0.05), but its potentiation was preserved with isoflurane (148 +/- 21%; P < 0.05) and sevoflurane (161 +/- 40%; P < 0.05) but not with halothane (126 +/- 16%; not significant). Halothane induced a deleterious effect on the sarcoplasmic reticulum, as shown by its impairment in the lusitropic effect of isoproterenol, compared with isoflurane and sevoflurane. Conclusion Potentiation of the positive inotropic effect of alpha-adrenoceptor stimulation by halogenated anesthetics is abolished in diabetic rats. In contrast, potentiation of beta-adrenoceptor stimulation is preserved with isoflurane and sevoflurane but not with halothane, probably because of its deleterious effects on sarcoplasmic reticulum.

Interaction of Protamine with α- and β-Adrenoceptor Stimulations in Rat Myocardium

2001 ◽  
Vol 95 (5) ◽  
pp. 1226-1233 ◽  
Author(s):  
Jean-Stéphane David ◽  
Benoît Vivien ◽  
Yves Lecarpentier ◽  
Pierre Coriat ◽  
Bruno Riou
Keyword(s):  
Positive Inotropic Effect ◽  
Left Ventricular ◽  
Relaxation Response ◽  
Papillary Muscles ◽  
Active Force ◽  
Control Groups ◽  
Beta Adrenoceptor ◽  
Alpha Adrenoceptor ◽  
Sites Of Action ◽  
Inotropic Responses

Background Protamine alters the inotropic responses to beta-adrenoceptor stimulation, but its mechanism of action is not well-understood. Moreover, its interaction with alpha-adrenoceptor stimulation and the lusitropic (relaxation) response to beta-adrenoceptor stimulation remain unknown. Methods The effects of protamine (10 or 100 microg/ml) on the responses induced by phenylephrine and isoproterenol were studied in rat left ventricular papillary muscles. Inotropic and lusitropic effects were studied under low and high loads. The authors also studied the interaction of protamine with forskolin (50 microm) and dibutyryl 3',5'-cAMP (0.5 mm). Data are mean percentage of baseline active force +/- SD. Results In control groups, phenylephrine (135 +/- 17%, P < 0.05) and isoproterenol (185 +/- 44%, P < 0.05) induced a positive inotropic effect. Isoproterenol induced positive lusitropic effects under low and high loads. Protamine abolished the inotropic responses to alpha- (102 +/- 23%, not significant) and beta-adrenoceptor stimulations (99 +/- 17%, not significant) but did not modify the lusitropic responses to isoproterenol. Protamine abolished the inotropic responses to forskolin (89 +/- 6 vs. 154 +/- 20%, P < 0.05) and markedly decreased that of dibutyryl 3',5'-cAMP (132 +/- 31 vs. 167 +/- 30%, P < 0.05) but did not modify their lusitropic responses. Conclusions Protamine abolished the inotropic responses to alpha- and beta-adrenoceptor stimulations but preserved the lusitropic responses to beta-adrenoceptor stimulation. Although protamine may act at several sites on the adrenoceptor stimulation cascade, one of its main sites of action is situated downstream from cAMP-mediated phosphorylation.

Effects of Desflurane in Senescent Rat Myocardium

2006 ◽  
Vol 105 (5) ◽  
pp. 961-967 ◽  
Author(s):  
Sandrine Rozenberg ◽  
Sophie Besse ◽  
Julien Amour ◽  
Benoît Vivien ◽  
Benoît Tavernier ◽  
...  
Keyword(s):  
Negative Inotropic Effect ◽  
Left Ventricular ◽  
Inotropic Effect ◽  
Shortening Velocity ◽  
Adult Rats ◽  
Inotropic Effects ◽  
Beta Adrenoceptor ◽  
Low Load ◽  
Positive Effect ◽  
Negative Inotropic Effects

Background The myocardial negative inotropic effects of desflurane are less pronounced than those of other halogenated anesthetics, partly because of intramyocardial catecholamine store release. However, the effects of desflurane on aging myocardium are unknown, whereas aging is known to be associated with an attenuation of catecholamine responsiveness. Methods The effects of desflurane (1.9-9.3 vol%) were studied in left ventricular papillary muscle of adult and senescent rats (29 degrees C; 0.5 mm Ca; stimulation frequency 12 pulses/min). The inotropic effects were compared under low and high loads, using the maximum unloaded shortening velocity and maximum isometric active force, and without or with alpha- and beta-adrenoceptor blockade. Results Desflurane induced a moderate positive inotropic effect in adult rats but a negative inotropic effect in senescent rats. After alpha- and beta-adrenoceptor blockade, desflurane induced a comparable negative inotropic effect in adult and senescent rats. No lusitropic effect under low load was observed, whereas desflurane induced a slight but significant positive lusitropic effect under high load similar between the two groups of rats. This positive effect was abolished by adrenoceptor blockade. Conclusion The authors' study suggests that desflurane does not induce significant intramyocardial catecholamine release in senescent myocardium, a result that should be integrated in the well-known alteration in the catecholamine response during aging.

Inotropic responsiveness of atrial myocardium bathed in Tris- or bicarbonate-buffered solutions

1979 ◽  
Vol 237 (3) ◽  
pp. H318-H325
Author(s):  
L. R. Durrett ◽  
H. R. Adams
Keyword(s):  
Atrial Myocardium ◽  
Inotropic Effects ◽  
Time To Peak ◽  
Pulsus Alternans ◽  
Group A ◽  
Bicarbonate Solutions ◽  
Inotropic Influences ◽  
Inotropic Responses ◽  
Negative Inotropic Effects

Atrial muscle of guinea pigs was used to study the inotropic influences of substituting a tris(hydroxymethyl)-aminomethane-buffered solution aerated with 100% O2 for a bicarbonate-buffered solution aerated with 95% O2-5% CO2 under otherwise equivalent in vitro conditions. Basal values of isometric contractile tension and its first derivative (dT/dt) were smaller and time to peak tension and time to 90% relaxation were longer in Tris- than in bicarbonate-bathed muscles. Both groups responded similarly to changes in stimulation frequently (0.1--2.2 Hz) and Ca2+ concentration (1.0--7.0 mM); however, maximal inotropic responses to these variables were smaller in the Tris-bathed atria. The negative inotropic effects of D600 and gentamicin were greater in the Tris group. Tris-bathed atria developed pulsus alternans when exposed to Mn2+ or a reduced Ca2+ concentration, whereas pulsus alternans did not occur in the bicarbonate group. A transient increase in contractility occurred in bicarbonate-bathed atria after treatment with 0.125 mM Mn2+, but only a negative response occurred in the Tris group. Thus important, and seemingly Ca2+-dependent, differences exist between the inotropic influences of Tris and bicarbonate solutions that may affect the utility of Tris-buffered (and/or bicarbonate deprived) heart muscle for studying certain inotropic interventions.

Myocardial Effects of Halothane and Isoflurane in Hamsters with Hypertrophic Cardiomyopathy 

1997 ◽  
Vol 87 (6) ◽  
pp. 1406-1416 ◽  
Author(s):  
Benoit Vivien ◽  
Jean-Luc Hanouz ◽  
Pierre-Yves Gueugniaud ◽  
Yves Lecarpentier ◽  
Pierre Coriat ◽  
...  
Keyword(s):  
Isometric Force ◽  
Negative Inotropic Effect ◽  
Myocardial Contraction ◽  
Left Ventricular ◽  
Inotropic Effect ◽  
Inotropic Effects ◽  
Low Load ◽  
Cardiomyopathic Hamsters ◽  
Negative Inotropic Effects

Background The effects of halothane and isoflurane on myocardial contraction and relaxation in diseased myocardium are not completely understood. Methods The effects of equianesthetic concentrations of halothane and isoflurane on inotropy and lusitropy in left ventricular papillary muscles of healthy hamsters and those with genetically induced cardiomyopathy (strain BIO 14.6) were investigated in vitro (29 degrees C; pH 7.40; Ca2+ 2.5 mM; stimulation frequency, 3/min) in isotonic and isometric conditions. Results Halothane induced a negative inotropic effect that was greater in cardiomyopathic than in healthy hamsters (1.5 vol%, active isometric force (AF): 19 +/- 8% vs. 28 +/- 11% of control values; P < 0.05). Isoflurane induced a negative inotropic effect that was greater in cardiomyopathic than in healthy hamsters (2.0 vol%, AF: 64 +/- 13% vs. 75 +/- 11% of control values; P < 0.01). However, the negative inotropic effects of halothane and isoflurane were not different for cardiomyopathic or healthy hamsters when their concentrations were corrected for minimum alveolar concentration (MAC) values in each strain. Halothane induced a negative lusitropic effect under low load, which was more important in cardiomyopathic hamsters, suggesting a greater impairment in calcium uptake by the sarcoplasmic reticulum. In contrast, isoflurane induced a moderate positive lusitropic effect under low load in healthy but not in cardiomyopathic hamsters. Halothane and isoflurane induced no significant lusitropic effect under high load. Conclusions Halothane and isoflurane had greater negative inotropic effects in cardiomyopathic than in healthy hamsters. Nevertheless, no significant differences in their inotropic effects were noted when concentrations were correlated as a multiple of MAC in each strain.

Nitric oxide's role in the heart: control of beating or breathing?

2004 ◽  
Vol 287 (1) ◽  
pp. H8-H13 ◽  
Author(s):  
Walter J. Paulus ◽  
Jean G. F. Bronzwaer
Keyword(s):  
Troponin I ◽  
Left Ventricular ◽  
Coronary Perfusion ◽  
Stroke Work ◽  
Isolated Cardiomyocytes ◽  
Inotropic Effects ◽  
Diastolic Stiffness ◽  
Myocardial Energetics ◽  
Negative Inotropic Effects

Beneficial actions of nitric oxide (NO) in failing myocardium have frequently been overshadowed by poorly documented negative inotropic effects mainly derived from in vitro cardiac preparations. NO's beneficial actions include control of myocardial energetics and improvement of left ventricular (LV) diastolic distensibility. In isolated cardiomyocytes, administration of NO increases their diastolic cell length consistent with a rightward shift of the passive length-tension relation. This shift is explained by cGMP-induced phosphorylation of troponin I, which prevents calcium-independent diastolic cross-bridge cycling and concomitant diastolic stiffening of the myocardium. Similar improvements in diastolic stiffness have been observed in isolated guinea pig hearts, in pacing-induced heart failure dogs, and in patients with dilated cardiomyopathy or aortic stenosis and have been shown to result in higher LV preload reserve and stroke work. NO also controls myocardial energetics through its effects on mitochondrial respiration, oxygen consumption, and substrate utilization. The effects of NO on diastolic LV performance appear to be synergistic with its effects on myocardial energetics through prevention of myocardial energy wastage induced by LV contraction against late-systolic reflected arterial pressure waves and through prevention of diastolic LV stiffening, which is essential for the maintenance of adequate subendocardial coronary perfusion. A drop in these concerted actions of NO on diastolic LV distensibility and on myocardial energetics could well be instrumental for the relentless deterioration of failing myocardium.

scholarly journals Altered Contractile Response due to Increased β3-Adrenoceptor Stimulation in Diabetic Cardiomyopathy

2007 ◽  
Vol 107 (3) ◽  
pp. 452-460 ◽  
Author(s):  
Julien Amour ◽  
Xavier Loyer ◽  
Morgan Le Guen ◽  
Nejma Mabrouk ◽  
Jean-Stéphane David ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Diabetic Cardiomyopathy ◽  
Positive Inotropic Effect ◽  
Left Ventricular ◽  
Inotropic Effect ◽  
Inotropic Response ◽  
Beta Adrenoceptor ◽  
Adrenoceptor Antagonist

Background In the diabetic heart, the positive inotropic response to beta-adrenoceptor stimulation is altered and beta1 and beta2 adrenoceptors are down-regulated, whereas beta3 adrenoceptor is up-regulated. In heart failure, beta3-adrenoceptor stimulation induces a negative inotropic effect that results from endothelial nitric oxide synthase (NOS3)-derived nitric oxide production. The objective of our study was to investigate the role of beta3-adrenoceptor in diabetic cardiomyopathy. Methods beta-Adrenergic responses were investigated in vivo (dobutamine echocardiography) and in vitro (left ventricular papillary muscle) in healthy and streptozotocin-induced diabetic rats. The effect of beta3-adrenoceptor inhibition on the inotropic response was studied in vitro. Immunoblots and NOS activities were performed in heart homogenates (electron paramagnetic resonance) and isolated cardiomyocytes. Data are mean percentage of baseline +/- SD. Results The impaired positive inotropic effect was confirmed in diabetes both in vivo (121 +/- 15% vs. 160 +/- 16%; P < 0.05) and in vitro (112 +/- 5% vs. 179 +/- 15%; P < 0.05). In healthy rat, the positive inotropic effect was not significantly modified in presence of beta3-adrenoceptor antagonist (174 +/- 20%), nonselective NOS inhibitor (N -nitro-l-arginine methylester [l-NAME]; 183 +/- 19%), or selective NOS1 inhibitor (vinyl-l-N-5-(1-imino-3-butenyl)-l-ornithine [l-VNIO]; 172 +/- 13%). In diabetes, in parallel with the increase in beta3-adrenoceptor protein expression, the positive inotropic effect was partially restored by beta3-adrenoceptor antagonist (137 +/- 8%; P < 0.05), l-NAME (133 +/- 11%; P < 0.05), or l-VNIO (130 +/- 13%; P < 0.05). Nitric oxide was exclusively produced by NOS1 within diabetic cardiomyocytes. NOS2 and NOS3 proteins were undetectable. Conclusions beta3-Adrenoceptor is involved in altered positive inotropic response to beta-adrenoceptor stimulation in diabetic cardiomyopathy. This effect is mediated by NOS1-derived nitric oxide in diabetic cardiomyocyte.

Distinction of NPY receptors in vitro and in vivo. II. Differential effects of NPY and NPY-(18-36)

1990 ◽  
Vol 259 (1) ◽  
pp. H174-H180 ◽  
Author(s):  
N. A. Scott ◽  
M. C. Michel ◽  
J. H. Boublik ◽  
J. E. Rivier ◽  
S. Motomura ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Receptor Subtypes ◽  
Base Line ◽  
Hemodynamic Effects ◽  
Vascular Effects ◽  
Inotropic Effects ◽  
Npy Receptor ◽  
Negative Inotropic Effects

We have studied the hemodynamic effects of neuropeptide Y (NPY) and its COOH-terminal fragment NPY-(18–36) in conscious rats. Intra-arterial injection of NPY rapidly elevated systemic vascular resistance (SVR), which remained high for greater than 30 min. Cardiac output (CO) decreased, and it remained low for greater than 30 min. Accordingly, blood pressure rose only transiently and returned to base-line values within 5 min. The reduction of CO could be attributed to a decreased stroke volume with an only marginal reduction of heart rate. Thus a direct cardiodepressive effect of NPY rather than baroreflex activation appears to be the major cause of the reduced CO. In vitro experiments excluded the possibility that NPY has direct negative inotropic effects and suggest that its cardiodepressive action is caused by coronary vasoconstriction or by presynaptic inhibition of norepinephrine release. Intra-arterial injections of NPY-(18-36) caused different hemodynamic effects. NPY-(18–36) decreased CO in a manner similar to that seen with NPY but initially did not elevate SVR, resulting overall in a reduced blood pressure. Only later, when blood pressure was reduced, was an elevation of SVR observed, which could be associated with increased plasma levels of catecholamines, angiotensin II, vasopressin, and NPY. Thus NPY-(18–36) mimics the cardiac effects of NPY but does not elicit its vascular effects. As NPY-(18–36) discriminates between NPY receptor subtypes in vitro, we conclude that the cardiac and vascular effects of NPY are mediated by distinct receptor subtypes.

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