Why the study?
Does cobalt chloride microinjection into the vlPAG modulate the tachycardic response to baroreflex activation in male Wistar rats?
Does cobalt chloride microinjection into the vlPAG modulate the tachycardic response to baroreflex activation in male Wistar rats?
Neurotransmission in the ventrolateral periaqueductal grey matter modulates the tachycardic response of the baroreflex, demonstrating complex brain-heart circuitry control.
Hypothesis-generating for vlPAG in baroreflex control; leaves open human translation and clinical relevance.
Baroreflex activity is a neural mechanism responsible for short‐term adjustments in blood pressure ( BP ). Several supramedullary areas, which send projections to the medulla, are able to control this reflex. In this context, the ventrolateral part of the periaqueductal grey matter (vl PAG ), which is a mesencephalic structure, has been suggested to regulate the cardiovascular system. However, its involvement in baroreflex control has never been addressed. Therefore, our hypothesis is that the vl PAG neurotransmission is involved in baroreflex cardiac activity. Male Wistar rats had stainless steel guide cannulae unilaterally or bilaterally implanted in the vl PAG . Afterward, a catheter was inserted into the femoral artery for BP and HR recording. A second catheter was implanted into the femoral vein for baroreflex activation. When the nonselective synaptic blocker cobalt chloride (CoCl 2 ) was unilaterally injected into the vl PAG , in either the left or the right hemisphere, it increased the tachycardic response to baroreflex activation. However, when CoCl 2 was bilaterally microinjected into the vl PAG it decreased the tachycardic response to baroreflex stimulation. This work shows that vl PAG neurotransmission is involved in modulation of the tachycardic response of the baroreflex. Moreover, we suggest that the interconnections between the vl PAG of both hemispheres are activated during baroreflex stimulation. In this way, our work helps to improve the understanding about brain–heart circuitry control, emphasizing the role of the autonomic nervous system in such modulation.
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Lagatta et al. (2016) studied this question.
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