PubMed · 3453793
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K Kyösola, T Mattila, A Harjula, H Kyösola, T Waris. 1987. [Cardiac "catecholamine challenge"].. https://pubmed.ncbi.nlm.nih.gov/3453793/
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A major difficulty of recording from peripheral sympathetic nerves is that microvolt values reflect characteristics of the recording conditions and limit comparisons between different experimental groups. In this study we assessed methods of calibrating renal sympathetic nerve activity (RSNA) in conscious rabbits. Calibration values were obtained from maximum RSNA responses to nasopharyngeal stimulation, airjet stress or unloading baroreceptors. Curves relating RSNA to blood pressure were produced by raising and lowering blood pressure with vasoactive drugs. To assess whether normalization would eliminate differences between RSNA curves which were most likely due to recording conditions, rabbits were first divided into two groups with high or low basal microvolt levels of RSNA, then again into two groups with high or low heart rate. In both cases, curves were similar if values were normalized by nasopharyngeal stimulation or by the upper plateau value. In hypertensive rabbits, where the baroreflex is suppressed, only the nasopharyngeal method showed this attenuated pattern. This method also eliminated the 50% decay in basal RSNA measured over 5 weeks. We conclude that expressing RSNA in terms of the maximum response to nasopharyngeal stimulation provides a calibration method suitable for comparing nerve activity over the long term as well as showing valid differences in baroreflex curves between different experimental groups.
The selective monoamine oxidase-B inhibitor selegiline (deprenyl) causes sympathomimetic effects and is metabolised to R(-)-methamphetamine and R(-)-amphetamine. The new monoamine oxidase-B inhibitor rasagiline is devoid of sympathomimetic effects and is metabolised to R(+)-1-aminoindan. Sympathomimetic effects of methamphetamine and 1-aminoindan enantiomers were compared in the rat vas deferens. R(-)-methamphetamine and S(+)-methamphetamine caused initial potentiation and subsequent inhibition of the field stimulation-induced twitch response of isolated rat vas deferens (0.1 Hz). EC(50) values for inhibition of twitch in prazosin-treated vas deferens were 0.36+/-0.13 and 1.64+/-0.10 microM (mean+/-S.E.M.) for S(+)- and R(-)-methamphetamine, respectively. There was no difference between S(+)-methamphetamine and R(-)-methamphetamine in potentiation of postsynaptic contractile response to noradrenaline. R(+)- and S(-)-1-aminoindan increased twitch response only at concentrations above 30 microM. R(-)-methamphetamine has similar potency to S(+)-methamphetamine in potentiation of noradrenaline-mediated responses and can therefore play a role in the sympathomimetic effects of selegiline.
Previously, we reported that the alpha(1A)-adrenoceptor, but not the alpha(1D)-adrenoceptor, mediates pupillary dilation elicited by sympathetic nerve stimulation in rats. This study was undertaken to further characterize the alpha-adrenoceptor subtypes mediating pupillary dilation in response to both neural and agonist activation. Pupillary dilator response curves were generated by intravenous injection of norepinephrine in pentobarbital-anesthetized rats. Involvement of alpha(1)-adrenoceptors was established as mydriatic responses were inhibited by systemic administration of nonselective alpha-adrenoceptor antagonists, phentolamine (0.3-3 mg/kg) and phenoxybenzamine (0.03-0.3 mg/kg), as well as by the selective alpha(1)-adrenoceptor antagonist, prazosin (0.3 mg/kg). The alpha(2)-adrenoceptor antagonist, rauwolscine (0.5 mg/kg), was without antagonistic effects. alpha(1A)-Adrenoceptor selective antagonists, 2-([2,6-dimethoxyphenoxyethyl]aminomethyl)-1,4-benzodioxane (WB-4101; 0.1-1 mg/kg) and 5-methylurapidil (0.1-1 mg/kg), the alpha(1B)-adrenoceptor selective antagonist, 4-amino-2-[4-[1-(benzyloxycarbonyl)-2(S)- [[(1,1-dimethylethyl)amino]carbonyl]-piperazinyl]-6,7-dimethoxyquinazoline (L-765314; 0.3-1 mg/kg), as well as the alpha(1D)-adrenoceptor selective antagonist, 8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5]decane-7,9-dione (BMY-7378; 1 mg/kg), were used to delineate the adrenoceptor subtypes involved. Mydriatic responses to norepinephrine were significantly antagonized by intravenous administration of both WB-4101 and 5-methylurapidil, but neither by L-765314 nor by BMY-7378. L-765314 (0.3-3 mg/kg, i.v.) was also ineffective in inhibiting the mydriasis evoked by cervical sympathetic nerve stimulation. These results suggest that alpha(1B)-adrenoceptors do not mediate sympathetic mydriasis in rats, and that the alpha(1A)-adrenoceptor is the exclusive subtype mediating mydriatic responses in this species.