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SANTOS, L. M. O. Adrenergic mechanisms in the retrotrapezoid nucleus in breathing control. 2015. 83 p. Masters thesis (Pharmacology) Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, 2015. Retrotrapezoid nucleus (RTN) is a region located in the ventrolateral medulla and is known to contribute to central chemoreception, inspiration and active expiration. Previous studies showed the presence of catecholaminergic varicosities in the RTN region and also showed that noradrenaline can increase respiratory rate by the activation of alpha-1 adrenergic receptors in the pre-Bötzinger complex. The aim of this study was to investigate the cardiorespiratory effects produced by the activation of adrenergic receptors in RTN and the source of cathecolaminergic inputs to this region. A dense neuronal projection (41 ± 8%) from A7 to RTN was revealed using retrograde tracer FluorGold. In urethane-anaesthetized, vagotomized and artificial ventilated male Wistar rats (n=110), pulsatile arterial pressure (PAP), diaphragm (DiaEMG) and abdominal (AbdEMG) muscle activities were recorded. Unilateral injection of noradrenaline produced a transient dose-dependent inhibition of DiaEMG (Frequency: 1 μM: 1.4 ± 0.9 %; 2.5 μM: 1.5 ± 2.5%; 5 μM: 2.7 ± 2.4 %; 25 μM: 4.6 ± 2.4%; 50 μM: 5.7 ± 3.8 %; 250 μM: 10.2 ± 4.3 %; 500 μM: 14.5 ± 6.8 and 1000 μM: 26.8 ± 10.7%; p < 0.05) (Amplitude: 1 μM: 1.8 ± 0.8 %; 2.5 μM: 2.8 ± 2.4 %; 5 μM: 6.4 ± 2.7 %; 25 μM: 12.4 ± 3.4 %; 50 μM: 34.1 ± 4.9 %; 250 μM: 40.6 ± 4.1 %; 500 μM: 47.7 ± 2.9 % and 1000 μM: 65.0 ± 2.0 %; p < 0.05), but did not change PAP and AbdEMG. These results were replicated by the injection of moxonidine (alpha-2 adrenergic and imidazoline receptors agonist) into RTN. The inspiratory inhibitory effects produced by noradrenaline into the RTN were attenuated by pre-injection of yohimbine (alpha-2 receptors antagonist) and were not affect by the blockade of alpha-1 or beta-adrenergic receptors into the RTN. We found that unilateral injection of phenilephrine (Phe, alpha-1 adrenergic receptors agonist) into the RTN increased DiaEMG amplitude by 62.1 ± 8.1% e DiaEMG frequency by 75.5 ± 18.6%. Phe was also able to generate active expiration and did not change blood pressure. The respiratory responses elicited by phe were eliminated by previous injections of prazosin (alpha-1 receptors antagonist) within the RTN. These results confirm that alpha-1 receptors also signaling at the level of the RTN regulating respiratory activity. We conclude that A7 region in the brainstem is the main source of cathecolamines to the RTN. The results of this study support the idea that RTN has pontine adrenergic inputs that modulate RTN neurons activity through activation of alpha-1 and alpha-1 adrenergic receptors.

Mecanismos adrenérgicos no núcleo retrotrapezóide no controle respiratório.