TY - JOUR
T1 - Positive inotropic response to α-adrenergic stimulation in an electrically driven rat left atrium
T2 - The role of extracellular calcium
AU - Shavit, Gabriel
AU - Gitter, Simon
AU - Barak, Yaacov
AU - Vidne, Bernardo A.
AU - Oron, Yoram
PY - 1986
Y1 - 1986
N2 - We studied the positive inotropic response induced by α-adrenergic receptor stimulation in an electrically driven rat left atrium. α-Adrenergic stimulation resulted in a prolonged positive inotropic response that reached its maximum within 5-7 min. The kinetics of the onset of the positive inotropic response were different for pure α-adrenergic, pure β-adrenergic, and mixed adrenergic stimulation. The positive inotropic responses to α- and β-adrenergic agonists were not additive. The relative inotropic response to α-adrenergic stimulation decreased when external calcium concentration was increased and disappeared when external calcium concentration was raised to 7.0 mM. The divalent cation ionophore A23187 (1 μM) produced a threefold increase of the contractility of the atrial preparation at 1.0 mM extracellular calcium, and no further α-adrenergic response was observed in its presence. Calcium channel antagonists verapamil and nifedipine markedly inhibited the response to α-adrenergic stimulation, with little effect on the β-adrenergic stimulation, at a calcium concentration of 0.5 mM. The inhibitory effect of calcium channel antagonists could be fully reversed by increasing the extracellular calcium concentration. Our data suggest that the α-adrenergic contractile response in the rat atrium involves the mobilization of extracellular calcium through verapamil-sensitive calcium channels in a mechanism different from that for the β-adrenergic response.
AB - We studied the positive inotropic response induced by α-adrenergic receptor stimulation in an electrically driven rat left atrium. α-Adrenergic stimulation resulted in a prolonged positive inotropic response that reached its maximum within 5-7 min. The kinetics of the onset of the positive inotropic response were different for pure α-adrenergic, pure β-adrenergic, and mixed adrenergic stimulation. The positive inotropic responses to α- and β-adrenergic agonists were not additive. The relative inotropic response to α-adrenergic stimulation decreased when external calcium concentration was increased and disappeared when external calcium concentration was raised to 7.0 mM. The divalent cation ionophore A23187 (1 μM) produced a threefold increase of the contractility of the atrial preparation at 1.0 mM extracellular calcium, and no further α-adrenergic response was observed in its presence. Calcium channel antagonists verapamil and nifedipine markedly inhibited the response to α-adrenergic stimulation, with little effect on the β-adrenergic stimulation, at a calcium concentration of 0.5 mM. The inhibitory effect of calcium channel antagonists could be fully reversed by increasing the extracellular calcium concentration. Our data suggest that the α-adrenergic contractile response in the rat atrium involves the mobilization of extracellular calcium through verapamil-sensitive calcium channels in a mechanism different from that for the β-adrenergic response.
KW - Extracellular calcium
KW - Nifedipine
KW - Rat left atrium
KW - Verapamil
KW - α-Adrenergic stimulation
UR - http://www.scopus.com/inward/record.url?scp=0022571758&partnerID=8YFLogxK
U2 - 10.1097/00005344-198603000-00015
DO - 10.1097/00005344-198603000-00015
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C2 - 2422471
AN - SCOPUS:0022571758
VL - 8
SP - 324
EP - 331
JO - Journal of Cardiovascular Pharmacology
JF - Journal of Cardiovascular Pharmacology
SN - 0160-2446
IS - 2
ER -