PubMed · 9328035
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P Soares-da-Silva, M A Vieira-Coelho. 1998. Nonneuronal dopamine.. https://doi.org/10.1016/s1054-3589(08)60884-4
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OBJECTIVE: This study was undertaken to determine whether stimulation of sympathetic cardiac nerves induces release of the thrombolytic enzyme tissue-type plasminogen activator (t-PA) in the coronary vascular bed. METHODS AND RESULTS: Anesthetized pigs were studied in an open chest model. Bilateral vagotomy was performed, and sympathetic cardiac nerves were activated by electrical stimulation (1 and 8 Hz). To evaluate possible mediating effects of increased heart rate and enhanced local blood flow, tachycardia was induced by pacing and hyperemia by local infusion of sodium nitroprusside and clevedipine. Furthermore, to study the effects of alpha- and beta-adrenergic receptor stimulation, phenylephrine and isoprenaline were infused locally. In response to low- and high-frequency sympathetic stimulation, mean coronary net release of total t-PA increased approximately 6- and 25-fold, respectively. Active t-PA showed a similar response pattern. Neither tachycardia nor coronary hyperemia stimulated t-PA release. In contrast, beta-adrenergic stimulation by isoprenaline induced an approximately 6-fold increase in coronary t-PA release, whereas no significant change in release rates occurred in response to alpha-adrenergic stimulation by phenylephrine. CONCLUSIONS: Stimulation of cardiac sympathetic nerves induces a marked coronary release of t-PA, and part of this response may be mediated through stimulation of beta-adrenergic receptors.
The possible participation of the central noradrenergic system in the expression of the ejaculatory reflex of the rat was explored by evaluating the effects of the alpha(2)-adrenoceptor antagonist, yohimbine, on the exhausted coital reflex model. Male sexually experienced Wistar rats, subjected to the coital reflex exhaustion paradigm received a single i.v. injection of yohimbine (10 microg/animal), immediately after reaching exhaustion. Enhancement of noradrenergic transmission by yohimbine provoked the immediate expression of a single ejaculatory genital motor pattern (GMP) similar to a first reflexively evoked one, but in the absence of urethral mechanical stimulation. Pre-treatment with clonidine (10 microg/animal) completely prevented the yohimbine-induced GMP, implying that its effect was exerted upon alpha(2)-adrenoceptors. Clonidine treatment per se induced the expression of a single GMP, similar to a last reflexively evoked one, that was completely blocked by pre-treatment with prazosin (1 microg/animal) indicating that it was due to the alpha(1) properties of clonidine. Administration of prazosin previous to yohimbine did not interfere with the expression of the GMP but attenuated it, suggesting the involvement of alpha(1)-adrenoceptors in the yohimbine-induced motor response. Data reveal a facilitatory influence of the noradrenergic system on ejaculatory function mediated by both alpha(1)- and alpha(2)-adrenoceptors and support the notion of yohimbine acting at a spinal level.