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Hormones and Neurochemicals in the Regulation of Breathing

Jerome A. Dempsey, E. Burt Olson, James B. Skatrud

10.1002/cphy.cp030207

Source: Supplement 11: Handbook of Physiology, The Respiratory System, Control of Breathing

Originally published: 1986

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Hormones
1.1 Progesterone
1.2 Thyroid Hormone
1.3 Estrogens and Androgens
1.4 Angiotensin
2 Neurochemicals
2.1 Monoamines
2.2 Amino Acids
2.3 Peptides
Figure 1. Figure 1.

Arterial (or arterialized blood) pH and partial pressure of CO2 in arterial blood () during normal menstrual cycle and pregnancy. Symbols represent data from different studies: • 259; ▪ 354; ▵ 305; ▴ 94; + 132; □ 219; x 212; ▿ 227; ◯ 24,79. ⊙, Plasma progesterone concentration during menstrual cycle 346 or pregnancy 171.
Figure 2. Figure 2.

Effects of exogenous and endogenous progesterone in various physiological states on relationship of expired minute ventilation () to and to CO2 elimination (). Solid lines show calculated relationship according to alveolar air equation [ (a constant)]. Open symbols, values at rest; closed symbols, values during mild or moderate exercise, ◯ and •, normal control 340; ⋄ and ♦, 2 wk of MPA therapy 340; □ and ▪, term pregnancy 187,305; ▿, high altitude (3, 100 m), nonpregnant to term pregnancy 267,268; +, NREM sleep, control 339; and ⊕, NREM sleep with MPA therapy 339. Chronic metabolic acidosis in normal subjects is also shown (▵, ▴) as example of non‐progesterone‐induced chronic hyperventilation 119,291. Note that at rest or at any given (rest or exercise), the lower the starting (or preprogesterone) (e.g., at high altitude), the greater the ventilatory response needed (to progesterone stimulus) to cause further reduction in . Similar principle applies in superimposed ventilatory depression; e.g., effect of sleep on in controls vs. subjects treated with MPA. During exercise, resting is defended equally well in controls and subjects with chronic hyperventilation caused by exogenous or endogenous progesterone, requiring greater ventilatory response to any given increment in metabolic rate in hypocapnic vs. normocapnic state. Increased gain of ventilatory response (Δ:Δ) is not unique to progesterone‐induced hyperventilation but also occurs in metabolic acidosis 119,291 and with chronic depletion of serotonin in CNS of goats 261. Conversely chronic hypoventilation (and hypercapnia), as in metabolic alkalosis (ref. 291 and J. B. Skatrud, unpublished observations) or carotid body denervation 261, results in depressed ventilatory response to exercise (Δ:Δ) in order to defend resting as well as it does in control state (not shown). BTPS, at body temperature, ambient pressure, and saturated with H2O vapor; STPD, at standard temperature and pressure, dry.
Figure 3. Figure 3.

Effects of alterations in total body metabolic rate in humans on relationship of to and to . Open symbols, values at rest; closed symbols, values during mild or moderate exercise. ⋄ and →⋄, hyperthyroidism to euthyroidism 366; ◯ and •, hypothyroidism to ▿ and ▾, euthyroidism 341; ▵ and ▴, Luft's syndrome 87; and ⊕, control to 2 h‐9 days salicylate ingestion 317. Note was maintained with changed resting metabolic rate in altered thyroid states and from rest‐to‐exercise in any state. This contrasts with the mild but consistent hypocapnia with prolonged (2 h‐9 days) salicylate administration. Also, contrast ventilatory responses to exercise, when at rest there is isocapnic hyperpnea induced by thyroid hormone or Luft's syndrome, vs. hypocapnic hyperventilation induced by progesterone (and other drugs, see Fig. 2). Although both conditions increase resting , resting or set point decreases only in latter state (i.e., increased ). As alveolar air equation dictates, enhanced ventilatory response to exercise is required to maintain near resting levels in new hypocapnic steady state (caused by progesterone), but not in maintained normocapnia that occurs during changes in thyroid hormone levels or Luft's syndrome.
Figure 4. Figure 4.

Horizontal (top) and sagittal (bottom) projections of rat brain proposed by Pelligrino et al. 303,304. A: selected landmarks for respiratory‐related activity. Shaded areas: rostral (R), intermediate (I), and caudal (C) chemosensitive areas on ventral surface of medulla 329,330. H, hypothalamus; HG, hypoglossal nucleus; IO, inferior olivary nucleus; NAC, nucleus amygdaloideus centralis; NAcc, nucleus accumbens; NAm, nucleus ambiguus; NC, nucleus caudatus; NP, nucleus parabrachialis; NTS, nucleus tractus solitarius; SN, substantia nigra. B: dopamine (DA) pathways superimposed on A. Stippled areas indicate DA cell bodies in regions of SN and medial eminence; terminal fields not detailed. C: norepinephrine (NE) pathways superimposed on A. Stippled areas indicate accepted location of NE cell bodies; terminal fields not detailed. [Data from Dahlstrom and Fuxe 62, Swanson and Hartman 353, and Ungerstedt 365.] D: serotonin (5‐HT) pathways superimposed on A. Stippled areas indicate 5‐HT cell bodies; terminal fields not detailed. [Data from Fuxe and co‐workers 62,122.] E: epinephrine (E) pathways superimposed on A. Stippled areas indicate E cell bodies; terminal fields not detailed. [Data from Hökfelt et al. 159.]

Data from Dahlstrom and Fuxe 62 and Ungerstedt 365


Figure 1.

Arterial (or arterialized blood) pH and partial pressure of CO2 in arterial blood () during normal menstrual cycle and pregnancy. Symbols represent data from different studies: • 259; ▪ 354; ▵ 305; ▴ 94; + 132; □ 219; x 212; ▿ 227; ◯ 24,79. ⊙, Plasma progesterone concentration during menstrual cycle 346 or pregnancy 171.



Figure 2.

Effects of exogenous and endogenous progesterone in various physiological states on relationship of expired minute ventilation () to and to CO2 elimination (). Solid lines show calculated relationship according to alveolar air equation [ (a constant)]. Open symbols, values at rest; closed symbols, values during mild or moderate exercise, ◯ and •, normal control 340; ⋄ and ♦, 2 wk of MPA therapy 340; □ and ▪, term pregnancy 187,305; ▿, high altitude (3, 100 m), nonpregnant to term pregnancy 267,268; +, NREM sleep, control 339; and ⊕, NREM sleep with MPA therapy 339. Chronic metabolic acidosis in normal subjects is also shown (▵, ▴) as example of non‐progesterone‐induced chronic hyperventilation 119,291. Note that at rest or at any given (rest or exercise), the lower the starting (or preprogesterone) (e.g., at high altitude), the greater the ventilatory response needed (to progesterone stimulus) to cause further reduction in . Similar principle applies in superimposed ventilatory depression; e.g., effect of sleep on in controls vs. subjects treated with MPA. During exercise, resting is defended equally well in controls and subjects with chronic hyperventilation caused by exogenous or endogenous progesterone, requiring greater ventilatory response to any given increment in metabolic rate in hypocapnic vs. normocapnic state. Increased gain of ventilatory response (Δ:Δ) is not unique to progesterone‐induced hyperventilation but also occurs in metabolic acidosis 119,291 and with chronic depletion of serotonin in CNS of goats 261. Conversely chronic hypoventilation (and hypercapnia), as in metabolic alkalosis (ref. 291 and J. B. Skatrud, unpublished observations) or carotid body denervation 261, results in depressed ventilatory response to exercise (Δ:Δ) in order to defend resting as well as it does in control state (not shown). BTPS, at body temperature, ambient pressure, and saturated with H2O vapor; STPD, at standard temperature and pressure, dry.



Figure 3.

Effects of alterations in total body metabolic rate in humans on relationship of to and to . Open symbols, values at rest; closed symbols, values during mild or moderate exercise. ⋄ and →⋄, hyperthyroidism to euthyroidism 366; ◯ and •, hypothyroidism to ▿ and ▾, euthyroidism 341; ▵ and ▴, Luft's syndrome 87; and ⊕, control to 2 h‐9 days salicylate ingestion 317. Note was maintained with changed resting metabolic rate in altered thyroid states and from rest‐to‐exercise in any state. This contrasts with the mild but consistent hypocapnia with prolonged (2 h‐9 days) salicylate administration. Also, contrast ventilatory responses to exercise, when at rest there is isocapnic hyperpnea induced by thyroid hormone or Luft's syndrome, vs. hypocapnic hyperventilation induced by progesterone (and other drugs, see Fig. 2). Although both conditions increase resting , resting or set point decreases only in latter state (i.e., increased ). As alveolar air equation dictates, enhanced ventilatory response to exercise is required to maintain near resting levels in new hypocapnic steady state (caused by progesterone), but not in maintained normocapnia that occurs during changes in thyroid hormone levels or Luft's syndrome.



Figure 4.

Horizontal (top) and sagittal (bottom) projections of rat brain proposed by Pelligrino et al. 303,304. A: selected landmarks for respiratory‐related activity. Shaded areas: rostral (R), intermediate (I), and caudal (C) chemosensitive areas on ventral surface of medulla 329,330. H, hypothalamus; HG, hypoglossal nucleus; IO, inferior olivary nucleus; NAC, nucleus amygdaloideus centralis; NAcc, nucleus accumbens; NAm, nucleus ambiguus; NC, nucleus caudatus; NP, nucleus parabrachialis; NTS, nucleus tractus solitarius; SN, substantia nigra. B: dopamine (DA) pathways superimposed on A. Stippled areas indicate DA cell bodies in regions of SN and medial eminence; terminal fields not detailed. C: norepinephrine (NE) pathways superimposed on A. Stippled areas indicate accepted location of NE cell bodies; terminal fields not detailed. [Data from Dahlstrom and Fuxe 62, Swanson and Hartman 353, and Ungerstedt 365.] D: serotonin (5‐HT) pathways superimposed on A. Stippled areas indicate 5‐HT cell bodies; terminal fields not detailed. [Data from Fuxe and co‐workers 62,122.] E: epinephrine (E) pathways superimposed on A. Stippled areas indicate E cell bodies; terminal fields not detailed. [Data from Hökfelt et al. 159.]

Data from Dahlstrom and Fuxe 62 and Ungerstedt 365
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Article Title: Hormones and Neurochemicals in the Regulation of Breathing
 

How to Cite

Jerome A. Dempsey, E. Burt Olson, James B. Skatrud. Hormones and Neurochemicals in the Regulation of Breathing. Compr Physiol 2011, Supplement 11: Handbook of Physiology, The Respiratory System, Control of Breathing: 181-221. First published in print 1986. doi: 10.1002/cphy.cp030207