TY - JOUR
T1 - THE MECHANISM OF α‐ADRENERGIC INHIBITION OF CATECHOLAMINE RELEASE
AU - COHEN, JACKIE
AU - ECKSTEIN, LEAH
AU - GUTMAN, YEHUDA
PY - 1980/1
Y1 - 1980/1
N2 - The effect of α‐adrenoceptor agonists on membrane adenosine triphosphatase (ATPase) activity was studied in membranes from the bovine adrenal medulla and the rat submaxillary gland. α‐Adrenoceptor agonists (10−7 to 10−5 m) enhanced significantly Na,K‐ATPase activity but not Mg‐ATPase activity in adrenal medulla. This effect was not observed in membranes from phaeochromocytoma. Phenylephrine (10−5 m), naphazoline (10−5 m) and clonidine (10−5 m) caused a significant increase of the activity of Na,K‐ATPase (but not of Mg‐ATPase) in the submaxillary gland. The enhancement became more prominent after ligature of the submaxillary duct but disappeared completely after superior cervical ganglionectomy. Thus, the effect of the α‐adrenoceptor agonists was due to an action on adrenergic nerve terminals in the submaxillary gland. Phenylephrine and naphazoline did not affect 45Ca uptake but enhanced the rate of 45Ca efflux from adrenal medullary slices in vitro. Phenylephrine enhanced the rate of 45Ca efflux from slices of submaxillary gland (with previous ligation of the duct); this was blocked by phentolamine and sympathetic denervation. Therefore phenylephrine was acting on the adrenergic nerve terminals. It is suggested that the inhibition by α‐adrenoceptor agonists of the exocytotic release of catecholamines from adrenergic nerve terminals and from chromaffin cells may be due to activation of the sodium pump, which results in enhancement of calcium efflux, causing a reduction of free intracellular Ca2+. 1980 British Pharmacological Society
AB - The effect of α‐adrenoceptor agonists on membrane adenosine triphosphatase (ATPase) activity was studied in membranes from the bovine adrenal medulla and the rat submaxillary gland. α‐Adrenoceptor agonists (10−7 to 10−5 m) enhanced significantly Na,K‐ATPase activity but not Mg‐ATPase activity in adrenal medulla. This effect was not observed in membranes from phaeochromocytoma. Phenylephrine (10−5 m), naphazoline (10−5 m) and clonidine (10−5 m) caused a significant increase of the activity of Na,K‐ATPase (but not of Mg‐ATPase) in the submaxillary gland. The enhancement became more prominent after ligature of the submaxillary duct but disappeared completely after superior cervical ganglionectomy. Thus, the effect of the α‐adrenoceptor agonists was due to an action on adrenergic nerve terminals in the submaxillary gland. Phenylephrine and naphazoline did not affect 45Ca uptake but enhanced the rate of 45Ca efflux from adrenal medullary slices in vitro. Phenylephrine enhanced the rate of 45Ca efflux from slices of submaxillary gland (with previous ligation of the duct); this was blocked by phentolamine and sympathetic denervation. Therefore phenylephrine was acting on the adrenergic nerve terminals. It is suggested that the inhibition by α‐adrenoceptor agonists of the exocytotic release of catecholamines from adrenergic nerve terminals and from chromaffin cells may be due to activation of the sodium pump, which results in enhancement of calcium efflux, causing a reduction of free intracellular Ca2+. 1980 British Pharmacological Society
UR - http://www.scopus.com/inward/record.url?scp=0019208975&partnerID=8YFLogxK
U2 - 10.1111/j.1476-5381.1980.tb10918.x
DO - 10.1111/j.1476-5381.1980.tb10918.x
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C2 - 6110452
AN - SCOPUS:0019208975
SN - 0007-1188
VL - 71
SP - 135
EP - 142
JO - British Journal of Pharmacology
JF - British Journal of Pharmacology
IS - 1
ER -