Presence and physiological role of presynaptic inhibitory α2-adrenoreceptors in guinea pig atria

Nature ◽  
1981 ◽  
Vol 294 (5842) ◽  
pp. 671-671 ◽  
Author(s):  
S. Z. LANGER
1988 ◽  
Vol 412 (5) ◽  
pp. 554-556 ◽  
Author(s):  
B. Belles ◽  
J. Hescheler ◽  
W. Trautwein ◽  
K. Blomgren ◽  
J. O. Karlsson

1978 ◽  
Vol 48 (1) ◽  
pp. 107-116 ◽  
Author(s):  
Dietrich Reinhardt ◽  
Reinhard Butzheinen ◽  
Otto-Erich Brodde ◽  
Hans Joachim Schümann

1986 ◽  
Vol 64 (5) ◽  
pp. 575-580
Author(s):  
Onkar N. Tripathi ◽  
M. Mehrotra ◽  
B. N. Dhawan

The role of the calcium channel in the first large contraction (postvagal potentiation, PVP) of the atria at the end of the inhibitory phase of its response (IPR) to vagal stimulation has been investigated by studying the effects of agents acting on the calcium channel (e.g., Ca2+, Mn2+, La3+, and D-600) or sarcoplasmic reticulum (SR) (e.g., deoxycholate (DOC)). IPR was potentiated by high [Ca2+]o (3–16 mM) and also by the calcium channel blockers, Mn2+ (1 μM–0.5 mM), La3+ (0.1 μM–0.5 mM), D-600 (1.0–10 μM), and DOC (1 μM–0.5 mM). PVP was also potentiated by enhanced [Ca2+]o, but the PVP ratio, which employs a correction for the simultaneous changes in the force of spontaneous contraction was inhibited. This indicated greater potentiation of contractility during spontaneous activity by Ca2+ than during PVP. Mn2+, La3+, and D-600 and even DOC in the above concentrations inhibited PVP but increased the PVP ratio. High concentrations of DOC (>1 mM), which disrupt SR, strongly inhibited PVP. It is concluded that the calcium channel plays a more prominent role in spontaneous contractions than in PVP in guinea pig atria. PVP is suggested to be generated by excessive triggered release of Ca2+ from SR leading to a marked increase in [Ca2+]i. The calcium channel and the calcium trapped in the glycocalyx also play significant roles in PVP.


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