A calcium-dependent component of the action potential in sympathetic nerve terminals in rat tail artery

1991 ◽  
Vol 418 (1-2) ◽  
pp. 102-108 ◽  
Author(s):  
P. �strand ◽  
L. Stj�rne
2007 ◽  
Vol 135 (1-2) ◽  
pp. 73-74
Author(s):  
John F.B. Morrison ◽  
Rajan Sheen ◽  
Subramanian Dhanasekaran

1980 ◽  
Vol 59 (s6) ◽  
pp. 445s-447s ◽  
Author(s):  
C. Chevillard ◽  
B. Saiag ◽  
M. Worcel

1. Hydrallazine relaxes the rat tail artery by a direct action on vascular smooth muscle cells, which appears to be modulated by the action of sympathetic nerve terminals. 2. There is a gradient of response to hydrallazine in arteries from normotensive Wistar rats, the proximal segments being poorly responsive. This gradient disappears after denervation with 6-hydroxydopamine in vitro. 3. Exogenously added purines inhibit noncompetitively the vasodilator response to hydrallazine in denervated segments from normotensive Wistar rats. Their order of potency is 2-Cl-adenosine > adenosine > ATP > inosine. 4. The effect of hydrallazine in innervated, poorly responsive segments is greatly potentiated by theophylline (50 μmol/l) and propranolol (5 μmol/l). These results, together with the effect of denervation, suggest that there are endogenous purines leaking from the nerve terminals under our experimental conditions. 5. Hydrallazine produces a marked inhibition of stimulus-induced contraction and 3H release after [3H]noradrenaline loading. The mechanism of this prejunctional action appears to be different from the mechanism of the postjunctional effect.


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