Alpha 2-adrenoceptors activate dihydropyridine-sensitive calcium channels via Gi-proteins and protein kinase C in rat portal vein myocytes.

N. Lepr�tre, J. Mironneau
Pflugers Arch.. 1994-12-01; 429(2): 253-261
DOI: 10.1007/bf00374320

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1. Pflugers Arch. 1994 Dec;429(2):253-61.

Alpha 2-adrenoceptors activate dihydropyridine-sensitive calcium channels via
Gi-proteins and protein kinase C in rat portal vein myocytes.

Leprêtre N(1), Mironneau J.

Author information:
(1)Laboratoire de Physiologie Cellulaire et Pharmacologie, France.

The presence of functional alpha 2-adrenoceptors was investigated in isolated
smooth muscle cells from rat portal vein using the nystatin-perforated
patch-clamp technique. The free cytoplasmic calcium concentration ([Ca2+]i) was
estimated using emission from the dye Fura-2. Activation of alpha 2-adrenoceptors
by clonidine (an alpha 2-adrenoceptor agonist) or noradrenaline (a non-selective
alpha-adrenoceptor agonist), both in the presence of 0.1 microM prazosin to block
alpha 1-adrenoceptors, caused a slow and sustained increase in [Ca2+]i which was
inhibited by 0.1 microM rauwolscine (an alpha 2-adrenoceptor antagonist). A
similar Ca2+ response was obtained with oxymetazoline (a selective alpha
2A-adrenoceptor agonist) suggesting that the increase in [Ca2+]i resulted from
activation of the alpha 2A-adrenoceptor subtype. The increase in [Ca2+]i did not
occur in calcium-free solution or in the presence of oxodipine (a
voltage-dependent calcium channel blocker), indicating that it depended on a
calcium influx. The alpha 2A-adrenoceptor-activated calcium influx was unchanged
after complete release of the stored calcium induced by applications of ryanodine
and caffeine. In addition, no accumulation of inositol trisphosphate was detected
in the presence of 0.1 microM prazosin. Taken together, these results indicate
that alpha 2A-adrenoceptor activation does not stimulate phosphoinositide
turnover and subsequent calcium release from intracellular stores. Whole-cell
patch-clamp experiments showed that alpha 2A-adrenoceptor activation promoted
calcium influx through voltage-dependent L-type channels.(ABSTRACT TRUNCATED AT
250 WORDS)

DOI: 10.1007/BF00374320
PMID: 7892112 [Indexed for MEDLINE]

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