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  • 1
    Electronic Resource
    Electronic Resource
    An α-Adrenoceptor Facilitating the Stimulation-Evoked Acetylcholine Release in the Rat Perfused Heart (1990)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 604 (1990), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1990.tb32037.x
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Desensitization of inhibitory prejunctional α2-adrenoceptors and putative imidazoline receptors on rabbit heart sympathetic nerves (1993)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 348 (1993), S. 127-133 
    Details
    ISSN: 1432-1912
    Keywords: Sympathetic neurotransmission ; Prejunctional receptors ; α2-Autoreceptor and autoinhibition ; Imidazoline receptor ; Desensitization
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To find out whether sympathetic nerves of the rabbit heart possess pharmacologically relevant prejunctional imidazoline receptors different from α-autoreceptors, the inhibition by oxymetazoline, aganodine and BDF 6143 (4-chloro-2-[2-imidazoline-2-ylamino]-isoindoline hydrochloride) of endogenous noradrenaline overflow evoked by stimulation of extrinsic postganglionic sympathetic nerves (0.66 Hz, 80 pulses) was investigated. In addition we wanted to find out whether either type of these prejunctional receptors undergoes desensitization upon pre-exposure to respective agonists. The α2-adrenoceptor agonist oxymetazoline inhibited the evoked noradrenaline overflow (2.9 nmol/l, IC50; about 90010, maximum inhibition). The inhibition was antagonized by rauwolscine (−log KB 8.20). This confirms the presence of α2-autoreceptors. Endogenous noradrenaline activated autoinhibition to a small extent as indicated by a rauwolscine-induced increase in evoked overflow by less than 2-fold. The α2- and imidazoline receptor agonist aganodine inhibited the evoked noradrenaline overflow (2.4 nmol/l, IC50; about 80%, maximum inhibition). The inhibition was antagonized by rauwolscine with a potency (−log KB 6.75), about 1/30 of that found at the α2-autoreceptor. Neither an α2-selective low concentration of rauwolscine nor the α1-adrenoceptor antagonist prazosin, nor SKF 104078, a mixed α1/2-antagonist, reduced the aganodine effect. The α2-adrenoceptor antagonist and imidazoline receptor agonist BDF 6143 inhibited the evoked noradrenaline overflow (18 nmol/l, IC50; about 70% maximum inhibition). The inhibition was insensitive to a low rauwolscine concentration. In hearts pre-exposed for 30 min (followed by washout; rauwolscine 0.1 μmol/l added later on to minimize presynaptic α2-adrenoceptor activation or blockade by drugs persisting in the biophase) to oxymetazoline 10 μmol/l, aganodine 2 μmol/l or BDF 6143 10 μmol/l, the inhibitory effects of oxymetazoline 30 nmol/l and aganodine 10 nmol/l were concomitantly reduced. No significant reduction of the agonist effect was seen after pre-exposure to BDF 6143 2 μmol/l. Pre-exposure to BDF 6143 10 μmol/l shifted the concentration for half-maximum inhibition to the right and depressed the maximum effect of both, oxymetazoline and aganodine, but did not affect the inhibitory action of the muscarinic agonist methacholine. It is concluded that inhibitory prejunctional α2-autoreceptors and putative imidazoline receptors coexist on postganglionic sympathetic nerves of the rabbit heart. They are both subject to desensitization upon exposure to a high agonist concentration. The findings are compatible with a mutual cross-desensitization under the conditions investigated.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00164788
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  • 3
    Electronic Resource
    Electronic Resource
    Characterization of sensory neurotransmission and its inhibition via α2B-adrenoceptors and via non-α2-receptors in rabbit iris (1993)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 347 (1993), S. 394-401 
    Details
    ISSN: 1432-1912
    Keywords: Sensory nerves ; Prejunctional receptors ; α2-adrenoceptor subtypes ; imidazoline receptor ; neurokinin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To find out whether, and which type of, adrenoceptors mediate prejunctional inhibition of sensory neurotransmitter release from trigeminal fibres, the modulation of twitch response to electrical field stimulation on rabbit isolated iris was investigated. Evoked iris sphincter contractions consisted of a minor fast cholinergic and a large slow component. The latter was unaffected by atropine and guanethidine, hence nonadrenergic noncholinergic in nature (NANC), but nearly completely abolished by capsaicin pretreatment and by the neurokinin receptor antagonist spantide. The response was probably not mediated by NK2 receptors as SR 48,968, an NK2 selective nonpeptide antagonist, failed to reduce the response to the release of the endogenous neurokinin(s) (and exogenous substance P), but in part due to NK1 receptor activation as shown by a reduction of response by CP 96,345, an NK1 selective non-peptide antagonist, and in part perhaps mediated by NK3 receptors. A small neurokinin receptor antagonist- and capsaicin-insensitive NANC contraction is probably not mediated by CGRP receptors. The α2-adrenoceptor agonist oxymetazoline inhibited the evoked NANC response (22 nmol/1, IC20; about 40%, maximum inhibition) without affecting the cholinergic response (up to 1 μmol/1) or the postjunctional iris sensitivity to exogenous substance P. The inhibition was antagonized by rauwolscine (apparent -log KB 8.04) and by the relatively α2B-adrenoceptor selective antagonist ARC-239 (-log KB 8.51). The α2- and imidazoline receptor agonist aganodine inhibited the evoked NANC response (0.25 μmol/l, IC20; about 30%, maximum inhibition) without affecting the postjunctional substance P responses. Rauwolscine 0.3 μmol/l failed to antagonize this effect. It is concluded that the release of sensory neurotransmitter(s) from trigeminal fibres in the rabbit eye may be inhibited by α2B-adrenoceptors and by a non-α2-receptor, perhaps an imidazoline receptor.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00165389
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  • 4
    Electronic Resource
    Electronic Resource
    Characterization of the prejunctional muscarinic receptors mediating inhibition of evoked release of endogenous noradrenaline in rabbit isolated vas deferens (1994)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 349 (1994), S. 1-10 
    Details
    ISSN: 1432-1912
    Keywords: Key words: Endogenous noradrenaline release – Rabbit vas deferens – Prejunctional muscarinic inhibition – Muscarinic receptor subtypes – Prejunctional purinoceptors – P2 purinoceptor antagonist – Prostanoids
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. The aim of the present study was to characterize the prejunctional modulation of evoked release of endogenous noradrenaline in rabbit vas deferens by the use of muscarinic receptor agonists and subtype-prefering antagonists.   Vasa deferentia of the rabbit were stimulated electrically by trains of 120 pulses delivered at 4 Hz or trains of 30 pulses at 1 Hz. The inhibition by muscarinic agonists of the stimulation-evoked overflow of endogenous noradrenaline in the absence and presence of antagonists was used to determine affinity constants for antagonists. These values were compared with those observed at putative M1 receptors inhibiting neurogenic twitch contractions in the rabbit vas deferens and with affinity data obtained at M1(m1)–M4(m5) receptors in functional studies and binding experiments.   The evoked overflow of noradrenaline from sympathetic nerves was enhanced by the A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), the P2 purinoceptor antagonist pyridoxalphosphate-6-azophenyl-29,49-disulfonic acid (PPADS) and indomethacin, indicating a tonic inhibition by endogenous A1 and P2 purinoceptor agonists and prostanoids, respectively. The stimulation-evoked overflow at 4 Hz was not sensitive to inhibition by the muscarinic agonists methacholine or 4-(4-chlorophenylcarbamoyloxy)-2-butynyltrimethylammonium iodide (4-Cl-McN-A-343). In contrast, at a stimulation frequency of 1 Hz the evoked noradrenaline release was decreased by muscarinic agonists (EC50): arecaidine propargyl ester (0.062 μM), 4-Cl-McN-A-343 (0.32 μM), 4-(4-fluorophenylcarbamoyloxy)-2-butynyl-N-methyl-pyrrolidinium tosylate (4-F-PyMcN+; 0.48 μM) and methacholine (0.86 μM). The affinity constants of most of the muscarinic antagonists [atropine: pKB = 9.47; (R)-trihexyphenidyl: pKB = 9.18; pirenzepine: pA2 = 7.68; methoctramine: pKB = 6.90] are consistent with estimates of these antagonists at M1(m1) receptors determined in various functional and binding studies. The high antagonistic potency of pirenzepine and (R)-trihexyphenidyl and the agonistic activity of 4-F-PyMcN+ argue for the involvement of M1, and against that of M2 and M3 receptors in the inhibition of evoked noradrenaline overflow. However, the high apparent pKB of 8.30 for himbacine is not in accordance with an M1 receptor; by contrast, it would be compatible with the presence of M2 or M4 receptors. The potencies of the tested muscarinic agonists and antagonists largely agree with those obtained for the inhibition of neurogenic twitch responses (0.05 Hz) in the rabbit vas deferens. In conclusion, the rabbit vas deferens is endowed with prejunctional muscarinic receptors mediating heteroinhibition of noradrenaline release that are probably of the same subtype as the putative M1 receptors inhibiting neurogenic twitch contractions, and are not of the M2, M3 or m5 subtype.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00178199
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  • 5
    Electronic Resource
    Electronic Resource
    Characterization of the prejunctional muscarinic receptors mediating inhibition of evoked release of endogenous noradrenaline in rabbit isolated vas deferens (1994)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 349 (1994), S. 1-10 
    Details
    ISSN: 1432-1912
    Keywords: Endogenous noradrenaline release ; Rabbit vas deferens ; Prejunctional muscarinic inhibition ; Muscarinic receptor subtypes ; Prejunctional purinoceptors ; P2 purinoceptor antagonist ; Prostanoids
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The aim of the present study was to characterize the prejunctional modulation of evoked release of endogenous noradrenaline in rabbit vas deferens by the use of muscarinic receptor agonists and subtype-prefering antagonists. Vasa deferentia of the rabbit were stimulated electrically by trains of 120 pulses delivered at 4 Hz or trains of 30 pulses at 1 Hz. The inhibition by muscarinic agonists of the stimulation-evoked overflow of endogenous noradrenaline in the absence and presence of antagonists was used to determine affinity constants for antagonists. These values were compared with those observed at putative M1 receptors inhibiting neurogenic twitch contractions in the rabbit vas deferens and with affinity data obtained at M1(m1)-M4(m5) receptors in functional studies and binding experiments. The evoked overflow of noradrenaline from sympathetic nerves was enhanced by the Al receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), the P2 purinoceptor antagonist pyridoxalphosphate-6-azophenyl-2′,4′-disulfonic acid (PPADS) and indomethacin, indicating a tonic inhibition by endogenous A1 and P2 purinoceptor agonists and prostanoids, respectively. The stimulation-evoked overflow at 4 Hz was not sensitive to inhibition by the muscarinic agonists methacholine or 4-(4-chlorophenylcarbamoyloxy)-2-butynyltrimethylammonium iodide (4-Cl-McN-A-343). In contrast, at a stimulation frequency of 1 Hz the evoked noradrenaline release was decreased by muscarinic agonists (EC50): arecaidine propargyl ester (0.062 μM), 4-Cl-McN-A-343 (0.32 μM), 4-(4-fluorophenylcarbamoyloxy)-2-butynylN-methyl-pyrrolidinium tosylate (4-F-PyMcN+; 0.48 μM) and methacholine (0.86 μM). The affinity constants of most of the muscarinic antagonists [atropine: pKB = 9.47; (R)-trihexyphenidyl: pKB = 9.18; pirenzepine: pA2 = 7.68; methoctramine: pKB = 6.90] are consistent with estimates of these antagonists at M1(m1) receptors determined in various functional and binding studies. The high antagonistic potency of pirenzepine and (R)-trihexyphenidyl and the agonistic activity of 4-F-PyMcN+ argue for the involvement of M1, and against that of M2 and M3 receptors in the inhibition of evoked noradrenaline overflow. However, the high apparent pKB of 8.30 for himbacine is not in accordance with an M1 receptor; by contrast, it would be compatible with the presence of M2 or M4 receptors. The potencies of the tested muscarinic agonists and antagonists largely agree with those obtained for the inhibition of neurogenic twitch responses (0.05 Hz) in the rabbit vas deferens. In conclusion, the rabbit vas deferens is endowed with prejunctional muscarinic receptors mediating heteroinhibition of noradrenaline release that are probably of the same subtype as the putative M1 receptors inhibiting neurogenic twitch contractions, and are not of the M2, M3 or m5 subtype.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00178199
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    Paper (German National Licenses)
    Fulltext
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