Protection of presynaptic ?-adrenoceptors against irreversible blockade by phenoxybenzamine: preservation of the modulatory effects of exogenous noradrenaline and yohimbine

1987 ◽  
Vol 336 (2) ◽  
pp. 155-160 ◽  
Author(s):  
N. Limberger ◽  
Th H�lting ◽  
K. Starke
1989 ◽  
Vol 67 (9) ◽  
pp. 1146-1150 ◽  
Author(s):  
D. W. Cheung

Recent studies of the peripheral sympathetic nervous system indicate the presence of other vasoactive transmitters in addition to noradrenaline. There is now evidence suggesting ATP to be a co-transmitter of noradrenaline mediating the excitatory junction potential and the phentolamine-resistant component of the vasopressor response. In hypertension, changes in the neural regulation at both pre- and post-synaptic levels have been observed. In the spontaneously hypertensive rat (SHR), abnormal feedback regulation through presynaptic adrenoceptors and increases in release and uptake by the perivascular nerves are well characterized. Whether similar changes in the ATP release mechanism occur in the SHR and other forms of hypertension remain to be determined. A more important role for ATP in the neural regulation of the SHR tail artery has been proposed. In future studies, the possible contribution of co-transmitters to the responses should be taken into consideration.Key words: hypertension, noradrenaline, ATP, sympathetic nervous system.


1976 ◽  
Vol 51 (s3) ◽  
pp. 423s-426s ◽  
Author(s):  
S. Z. Langer

1. Two presynaptic mechanisms appear to be involved in the regulation of noradrenaline release during nerve stimulation. The first one, mediated by β-adrenoceptors, operates at low frequencies of nerve stimulation, leading to an increase in transmitter release. The second one, mediated through α-adrenoceptors, is triggered when higher concentrations of the transmitter are reached in the synaptic cleft, leading to inhibition of transmitter release, probably through a restriction in the availability of calcium for the secretory process. 2. It is postulated that part of the anti-hypertensive effects of drugs like clonidine, α-methyldopa and β-receptor-blocking agents may be related to their long-term effects on presynaptic adrenoceptors.


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