PubMed · 9196836
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T Kamibayashi, K Harasawa, M Maze. 1997. Alpha-2 adrenergic agonists.. https://doi.org/10.1007/bf03022261
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A method is presented for monitoring the coupling of the alpha(2)-adrenoceptor, as well as other receptors, to their G proteins using the GTP-induced shift in agonist affinity states. In tissue sections GTP, but not ATP, induces a robust decrease in agonist affinity of greater than 100-fold, which is much larger than previously found in membrane preparations. A sensitive and easy procedure to monitor the extent of coupling is to compare the amount of [(3)H]RX821002 binding remaining in the presence of 100 nM brimonidine in the absence and presence of 100 microM GTP. This method should be especially applicable for determining the extent of coupling of receptors to their G proteins in multiple brain regions using autoradiographic procedures.
Excitatory junctional potentials (EJPs) elicited with brief duration (10 s) electrical field stimulation of guinea-pig mesenteric arteries were nearly abolished at all frequencies by pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS, 30 microM) but persisted following reserpinization. Suramin (100 microM) enhanced EJPs at 0.2-0.5 Hz responses and reduced them at 2-32 Hz. Phentolamine (1 microM) and yohimbine (0.1 microM) enhanced EJPs at 0.2-8 Hz but not at 16-32 Hz. Oxymetazoline (0.3 microM) reduced EJPs at 0.2-0.5 Hz but not at 1-32 Hz. Following reserpinization, EJPs were enhanced at 0.2-2 Hz but not at 4-32 Hz. Clonidine (0.1 microM) was without effect at all frequencies in control arteries but reduced EJPs at 0.2-2 Hz in reserpine-treated arteries. In conclusion, pre-junctional alpha(2)-adrenoceptors modulate ATP release during low frequency, brief duration sympathetic nerve stimulation.
In the present study we examined the effect of alpha-adrenergic regulation of active transepithelial Na+ absorption across the isolated frog skin epithelium. alpha-Adrenergic stimulation was achieved by addition of the adrenergic agonist noradrenaline in the presence of the beta-adrenergic blocker propranolol. alpha-Adrenergic stimulation inhibited basal as well as antidiuretic hormone (ADH)-stimulated Na+ transport. The ADH-induced increase in Na+ transport was accompanied by a membrane depolarisation due to an increase in the apical Na+ permeability. The subsequent application of noradrenaline inhibited the Na+ transport and repolarised the membrane potential, suggesting that alpha-adrenergic stimulation had reduced the apical Na+ permeability. The inhibition was abolished by the alpha2-adrenergic antagonist yohimbine whereas it was insensitive to the alpha1-adrenergic antagonist prazosin. alpha-Adrenergic stimulation had no effect on the cytosolic free [Ca2+] ([Ca2+]i). Incubation of the epithelium in the presence of ADH increased the cellular adenosine 3',5'-cyclic monophosphate (cAMP) content, an increase which was abolished by alpha-adrenergic activation. The effect of alpha-adrenergic stimulation on cAMP production was abolished by the alpha2-adrenergic antagonist yohimbine. We conclude that the noradrenaline-induced inhibition of the ADH-stimulated Na+ absorption and cAMP content is mediated by activation of alpha2-adrenoceptors. The data further indicate that the principal cells of the epithelium do not express alpha1-adrenoceptors. The noradrenaline-induced inhibition of the ADH-stimulated Na+ transport was concentration dependent, with 0.24+/-0.03 microM eliciting a half-maximal response. This alpha2-adrenergic-mediated down-regulation of Na+ absorption is achieved at a concentration of noradrenaline which begins to activate the NaCl secretion via the skin glands. The alpha2-adrenoceptors therefore appear to have considerable physiological importance.