Neuronal Control of Breathing: Sex and Stress Hormones

Abstract

There is a growing public awareness that hormones can have a significant impact on most biological systems, including the control of breathing. This review will focus on the actions of two broad classes of hormones on the neuronal control of breathing: sex hormones and stress hormones. The majority of these hormones are steroids; a striking feature is that both groups are derived from cholesterol. Stress hormones also include many peptides which are produced primarily within the paraventricular nucleus of the hypothalamus (PVN) and secreted into the brain or into the circulatory system. In this article we will first review and discuss the role of sex hormones in respiratory control throughout life, emphasizing how natural fluctuations in hormones are reflected in ventilatory metrics and how disruption of their endogenous cycle can predispose to respiratory disease. These effects may be mediated directly by sex hormone receptors or indirectly by neurotransmitter systems. Next, we will discuss the origins of hypothalamic stress hormones and their relationship with the respiratory control system. This relationship is 2-fold: (i) via direct anatomical connections to brainstem respiratory control centers, and (ii) via steroid hormones released from the adrenal gland in response to signals from the pituitary gland. Finally, the impact of stress on the development of neural circuits involved in breathing is evaluated in animal models, and the consequences of early stress on respiratory health and disease is discussed.

Ventilatory, metabolic, and thermal responses to hypercapnia in female rats: effects of estrous cycle, ovariectomy, and hormonal replacement

“…Hypercapnia caused a significant increase in the V E/V O 2 [hypercapnia effect: P Ͻ 0.001; F (3,22) ϭ 85.6; no interaction], and, again, no difference was found between groups (Fig. 4).…”

“…All groups had lower V O 2 during hypercapnia [hypercapnia effect: P ϭ 0.0127; F (3,22) ϭ 6.8; no interaction], and no differences were observed between the groups in different stages of the estrous cycle. Hypercapnia caused a significant increase in the V E/V O 2 [hypercapnia effect: P Ͻ 0.001; F (3,22) ϭ 85.6; no interaction], and, again, no difference was found between groups (Fig.…”

“…3). Hypercapnia caused an increase in V E in all groups [hypercapnia effect: P Ͻ 0.0001; F (3,22) ϭ 131.7; no interaction] due to an increase in VT [hypercapnia effect: P Ͻ 0.0001; F (3,22) ϭ 84.6; no interaction] and fR [hypercapnia effect: P Ͻ 0.0001; F (3,22) ϭ 301.1; no interaction]. There was no difference in the hypercapnic ventilatory response between groups in the different phases of the estrous cycle, as seen in Fig.…”

“…They can also influence peripheral or central chemoreceptors (5), which suggests an important hormonal role in the breathing control (3). Most of the experiments in respiratory control, however, are performed in male rats.…”

“…premotor neurons (13), rhythm generating neurons (3). They can also influence peripheral or central chemoreceptors (5), which suggests an important hormonal role in the breathing control (3).…”