Respiratory and Electrolyte Effects Induced by Estrogen and Progesterone

Goodland, Ruth L.; Reynolds, John G.; McCoord, Augusta B.; Pommerenke, W.T.

doi:10.1016/s0015-0282(16)31327-9

Cited by 65 publications

(20 citation statements)

References 19 publications

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“…This effect of estrogen on the sensitivity of central neurons to progesterone is believed to be a consequence of induction of intracellular progesterone receptors by estrogen (5). A synergism of estrogen and progesterone in the respiratory response has been suggested in some earlier studies, although the results are equivocal (32)(33)(34)(35)(36)(37). In one such study a significant increase in ventilation was found only 526 PROGESTERONE STIMULATION OF RESPIRATION Endo • 1990 Voll26«Nol in OVX rats that received both estrogen and progestin; however, the absolute level of ventilation was not significantly greater with joint estrogen administration than when progestin was administered alone (32).…”

Section: Discussionmentioning

confidence: 98%

The Stimulation of Respiration by Progesterone in Ovariectomized Cat Is Mediated by an Estrogen-Dependent Hypothalamic Mechanism Requiring Gene Expression*

1990

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The central site of action and the cellular mechanism by which progesterone stimulates respiration were studied in ovariectomized cats that were anesthetized, paralyzed, and ventilated and in which respiratory sensory feedback mechanisms were either eliminated or controlled. Phrenic nerve activity served as an index of central respiratory output. Progesterone did not stimulate respiration in ovariectomized cats not pretreated with estrogen. In contrast, repeated doses of progesterone (0.1-1.0 microgram/kg, iv, cumulative) caused a sustained (greater than 45 min) dose-dependent facilitation of phrenic nerve activity in animals primed 3 days before study with 17 beta-estradiol (20 micrograms/kg, sc). Estrogen exposure is, therefore, a prerequisite for the respiratory response to progesterone in ovariectomized cats. This estrogen-dependent respiratory response to progesterone was attenuated in animals pretreated with either the estrogen receptor antagonist CI628 or the progesterone receptor antagonist RU486, indicating that the respiratory response is mediated by both estrogen and progesterone receptors. Inhibitors of protein (anisomycin) and RNA (actinomycin-D) synthesis caused a diminution of the respiratory response to progesterone, implicating a requirement for gene expression in the response. Midcollicular decerebration (which removed the diencephalon) attenuated, whereas decortication (which spared the diencephalon) did not affect the respiratory response to progesterone. Thus, the diencephalon appears to be a critical neuroanatomical substrate for the response. These results indicate that the respiratory response to progesterone is mediated, at a hypothalamic site, via a genomic mechanism with characteristics consistent with the prototypic mechanism for progesterone actions.

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Section: Discussionmentioning

confidence: 98%

The Stimulation of Respiration by Progesterone in Ovariectomized Cat Is Mediated by an Estrogen-Dependent Hypothalamic Mechanism Requiring Gene Expression*

1990

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“…Other workers have found that exogenously administered estradiol has no effect on respiration in either human subjects (26,27) or rats (16). Koepchen (28) reported that exogenously administered testosterone had no acute effects on ventilation.…”

Section: Discussionmentioning

confidence: 99%

Progesterone stimulates respiration through a central nervous system steroid receptor-mediated mechanism in cat.

Bayliss

Millhorn

Gallman

et al. 1987

Proc. Natl. Acad. Sci. U.S.A.

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We have examined the effect on respiration of the steroid hormone progesterone, administered either intravenously or directly into the medulla oblongata in anesthetized and paralyzed male and female cats. The carotid sinus and vagus nerves were cut, and end-tidal Pco2 and temperature were kept constant with servo-controllers. Phrenic nerve activity was used to quantitate central respiratory activity.Repeated doses of progesterone (from 0.1 to 2.0 ,ug/kg, cumulative) caused a sustained (>45 min) facilitation of phrenic nerve activity in female and male cats; however, the response was much more variable in females. Progesterone injected into the region of nucleus tractus solitarii, a respiratory-related area in the medulla oblongata, also caused a prolonged stimulation of respiration. Progesterone administration at high concentration by both routes also caused a substantial hypotension. Identical i.v. doses of other classes of steroid hormones (17f8-estradiol, testosterone, and cortisol) did not elicit the same respiratory effect. Pretreatment with RU 486, a progesterone-receptor antagonist, blocked the facilitatory effect of progesterone. We conclude that progesterone acts centrally through a steroid receptor-mediated mechanism to facilitate respiration.It has been known since the turn of the century that women hyperventilate during pregnancy (1, 2) and during the luteal phase of the menstrual cycle (3). Because the level of circulating progesterone correlates positively with increased ventilation, progesterone has been proposed as the ventilatory stimulant in these conditions (4)-a contention further supported by studies in which exogenously administered progesterone caused hyperventilation in normal male subjects (5, 6) and in patients with breathing disorders (7-12).Even though many animal species hyperventilate during pregnancy when endogenous progesterone levels are elevated (13-15), most fail to respond in a like manner to exogenously administered progesterone under experimental conditions (5,(15)(16)(17). Such data has been interpreted to mean that progesterone is not the respiratory stimulant during pregnancy and the luteal phase of the menstrual cycle. However, a reasonable explanation exists for this apparent discrepancy. Estrogen levels increase during pregnancy, and estrogen causes induction, or upregulation, of progesterone receptors within certain regions of the brain (18,19 Respiratory feedback from the arterial chemoreceptors and the pulmonary mechanoreceptors was blocked by cutting the carotid sinus and vagus nerves. A dorsal laminectomy was performed in one cat, and the spinal cord was transected at C7/T1 to eliminate input from visceral or somatic receptors. One phrenic nerve root (C5) was exposed, cut distally, desheathed, and placed in a bipolar platinum recording electrode that was built into a small acrylic platform placed in a tissue well adjacent to the nerve. Because the electrode had no fixed external attachments (the electrical wires were flexible and moved freely), it was poss...

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“…In normal males progesterone administration has increased ventilation (Schoene, Pierson, Lackshminaryan, Shrader & Butler, 1980;Skatrud, Dempsey & Kaiser, 1978; Zwillich, Natalino, Sutton & Weil, 1978) and decreased carbon dioxide partial pressure (Goodland, Reynolds, McCoord & Pommerenke, 1953;Schoene et al, 1980;Skatrud et al, 1978;Zwillich et al, 1978). Other effects include increased hypercapnic and hypoxic ventilatory responsiveness (Schoene et al, 1980;Zwillich et al, 1978).…”

Section: Effects In Normal Males and Experimental Animalsmentioning

confidence: 99%

Ventilation during sleep onset

Colrain

Trinder

Fraser

et al. 1987

Journal of Applied Physiology

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There is now considerable evidence which indicates that respiratory activity is different during sleep compared with wakefulness. However, there has been little work on respiratory changes during the transitional period from wakefulness to sleep. The present study was concerned with the quantitative and temporal properties of ventilation during sleep onset. Sleep onsets were studied in five young male adults in a series of single-subject designs in which sleep onsets were replications. The results indicated that during sleep onset the loss of alpha-activity in the electroencephalogram was associated with a substantial, rapid, and highly predictable reduction in ventilation. The change in ventilation was typically due to a reduction in tidal volume and was, in part, secondary to a reduction in metabolic rate. We speculate that the nonmetabolic component may reflect the loss of waking neural drive to respiration, though the present study did not eliminate a variety of other interpretations.

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Respiratory and Electrolyte Effects Induced by Estrogen and Progesterone

Cited by 65 publications

References 19 publications

The Stimulation of Respiration by Progesterone in Ovariectomized Cat Is Mediated by an Estrogen-Dependent Hypothalamic Mechanism Requiring Gene Expression*

The Stimulation of Respiration by Progesterone in Ovariectomized Cat Is Mediated by an Estrogen-Dependent Hypothalamic Mechanism Requiring Gene Expression*

Progesterone stimulates respiration through a central nervous system steroid receptor-mediated mechanism in cat.

Ventilation during sleep onset

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