Abstract

The present article contains a brief review on the role of vasopressinergic projections to the nucleus tractus solitarii in the genesis of reflex bradycardia and in the modulation of heart rate control during exercise. The effects of vasopressin on exercise tachycardia are discussed on the basis of both the endogenous peptide content changes and the heart rate response changes observed during running in sedentary and trained rats. Dynamic exercise caused a specific vasopressin content increase in dorsal and ventral brainstem areas. In accordance, rats pretreated with the peptide or the V1 blocker into the nucleus tractus solitarii showed a significant potentiation or a marked blunting of the exercise tachycardia, respectively, without any change in the pressure response to exercise. It is proposed that the long-descending vasopressinergic pathway to the nucleus tractus solitarii serves as one link between the two main neural controllers of circulation, i.e., the central command and feedback control mechanisms driven by the peripheral receptors. Therefore, vasopressinergic input could contribute to the adjustment of heart rate response (and cardiac output) to the circulatory demand during exercise.

Highlights

  • Mechanisms governing the reflex control of the circulation and their integration at the bulbar level have been extensively studied

  • paraventricular nucleus (PVN) SON ME PP DBS ventral brainstem (VBS) SC Plasma ns ns ns ns ns (+1.2 x) ns (+3.2 x) ns ns ns ns ns ns ⇑ 43 x*+ ⇑ 6 x*+ ns ns the baroreceptor reflex through V2 receptors accessible from the blood, while neuronal V1 receptors show highly specific responses such as inhibition of the reflex bradycardia by the neurohormone released into the cerebrospinal fluid, but displacement of the operating point of the reflex by the neurotransmitter vasopressin released directly in the NTS upon stimulation of projections originating in the PVN

  • Preliminary results (Michelini LC, unpublished observations) on loading of baroreceptors in the presence of sympathetic or vagal blockade showed that vasopressin administration into the NTS was able to displace the bradycardic response toward higher heart rate values only in rats blocked with atropine, suggesting that vasopressin in the NTS facilitates the sympathetic pathway or favors the inhibition of sympathetic withdrawal that usually occurs during transient blood pressure increases

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Summary

Introduction

Mechanisms governing the reflex control of the circulation and their integration at the bulbar level have been extensively studied (see reviews 1-4). Conveyed by different sets of receptors such as baroreceptors, chemoreceptors, cardiopulmonary receptors, and others. To maintain blood pressure and adjust flow efficiently, the central nervous system (CNS) processes peripheral information about pressure levels, blood gases, pH, blood volume, temperature, etc. This information is integrated in different areas and at different levels of the CNS to provide adequate changes of sympathetic and parasympathetic tone to the heart and blood vessels, the main effectors of the circulatory system

Importance of baroreceptors and the genesis of reflex bradycardia
EAA AMB
Is reflex bradycardia always observed during a pressure increase?
Reflex control of the circulation
VP content immediately after acute exercise
Vasopressin in the NTS and its modulatory effect on exercise tachycardia
Conclusions
ANS Reflex control of the circulation
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