Effects of estrogen and progesterone on carotid body neural output responsiveness to hypoxia

Hannhart, B.; Pickett, Cheryl A.; Moore, Lorna G.

doi:10.1152/jappl.1990.68.5.1909

Cited by 124 publications

(82 citation statements)

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“…The rise in V E was greater than that which can be accounted for by increased CO 2 production, as demonstrated by the fall in PET CO 2 . We showed previously that about two-thirds of the V E rise can be attributed to elevated progesterone and estrogen hormones which act, in turn, to raise carotid body chemosensory sensitivity to hypoxia (20,22), central translation, and thus respiratory drive (11,12). The present study was consistent with these observations insofar as the women with the highest HVR had the highest alveolar V E (lowest PET CO 2 ).…”

Section: Discussionsupporting

confidence: 92%

Determinants of blood oxygenation during pregnancy in Andean and European residents of high altitude

Vargas

Julian

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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High altitude decreases birth weight, but this effect is diminished in long vs. short-resident, high-altitude populations. We asked whether women from long vs. short-resident, high-altitude populations had higher arterial oxygenation levels by comparing 42 Andean and 26 European residents of La Paz, Bolivia (3,600 m), serially during pregnancy (weeks 20, 30, and 36) and again 4 mo postpartum. Pregnancy raised hypoxic ventilatory sensitivity threefold, resting ventilation (V E), and arterial O2 saturation (SaO 2 ) in both groups. Ancestry, as identified using 81 genetic markers, correlated with respiratory pattern, such that greater Andean ancestry was associated with higher respiratory frequency and lower tidal volume. Pregnancy increased total blood and plasma volume ϳ40% in both groups without changing red blood cell mass relative to body weight; hence, hemoglobin fell. The hemoglobin decline was compensated for by the rise in V E and SaO 2 with the result that arterial O2 content (Ca O 2 ) was maintained near nonpregnant levels in both groups. Birth weights were similar for all Andean and European babies, but after adjusting for variation in gestational age, maternal height and parity, Andeans weighed 209 g more than Europeans. Babies with heavier birth weights and greater ponderal indices were born to Andean women with higher V E during pregnancy. We concluded that while maternal V E and arterial oxygenation were important, some factor other than higher Ca O 2 was responsible for protecting Andeans from altitude-associated reductions in fetal growth.hypoxia; ventilation; ventilatory control; infant birth weight; fetal growth; genetics of birth weight; human adaptation; respiratory pattern RESIDENCE AT HIGH ALTITUDE (Ͼ8,000 ft, 2,500 m) exerts among the most powerful effects on birth weight with values falling, on average, 121 g per 1,000 m in Colorado high-altitude (Ͼ2,500 m, 8,000 ft) residents (15). This effect is due primarily to a slowing of fetal growth, not shortened gestation, and is greater than the effects of parity, the number of prenatal visits, or moderate maternal smoking on birth weight. Existing data indicate that the birth weight fall is not due to socioeconomic or other known risk factors (6, 15), but rather to the effects of hypoxia itself.Some 140 million persons live at high altitude, making them the largest single group at risk of low birth weight (16). While birth weight declines in all populations studied to date, the magnitude of fall varies, being least in long-and greatest in short-resident groups. For example, across a 2,700 -4,700 m (8,900 -15,500 ft) altitude range, birth weight decreases three times as much in Han ("Chinese") compared with Tibetans (24). In La Paz, Bolivia, at 3,600 m (11,880 ft), women of indigenous (Aymára or Quechua) ancestry give birth to heavier weight infants than European women, regardless of whether the data are adjusted for differences in maternal body size, nutrition, or the mother's own altitude of birth and development (9).On the basis of our previo...

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Section: Discussionsupporting

confidence: 92%

Determinants of blood oxygenation during pregnancy in Andean and European residents of high altitude

Vargas

Julian

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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“…This sex difference is mostly mediated by endogenous ovarian steroids, which act both on the central nervous system (7,8) and on peripheral chemoreceptors to increase ventilatory output (17,23,26,49). Alternatively, estradiol decreases erythropoietin synthesis under hypoxic exposure (35), which may also contribute to lower hematological response during chronic hypoxia in females.…”

Section: Interaction Between Sex and Long-term Consequences Of Neonatmentioning

confidence: 99%

Impaired acclimatization to chronic hypoxia in adult male and female rats following neonatal hypoxia

Lumbroso¹,

Joseph²

2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Lumbroso D, Joseph V. Impaired acclimatization to chronic hypoxia in adult male and female rats following neonatal hypoxia. Am J Physiol Regul Integr Comp Physiol 297: R421-R427, 2009. First published June 3, 2009 doi:10.1152/ajpregu.00068.2009.-We tested the hypothesis that neonatal exposure to hypoxia alters acclimatization to chronic hypoxia later in life. Rat pups were exposed to normobaric hypoxia (12% O2; nHx group) in a sealed chamber, or to normoxia (21% O2; nNx group) from the day before birth to postnatal day 10. The animals were then raised in normal conditions until reaching 12 wk of age. At this age, we assessed ventilatory and hematological acclimatization to chronic hypoxia by exposing male and female nHx and nNx rats for 2 wk to 10% O2. Minute ventilation, metabolic rate, hypoxic ventilatory response, hematocrit, and hemoglobin levels were measured both before and after acclimatization. We also quantified right ventricular hypertrophy as an index of pulmonary hypertension both before and after acclimatization. There was a significant effect of neonatal hypoxia that decreases ventilatory response (relative to metabolic rate, V E/V CO2) to acute hypoxia before acclimatization in males but not in females. nHx rats had an impaired acclimatization to chronic hypoxia characterized by altered respiratory pattern and elevated hematocrit and hemoglobin levels after acclimatization, in both males and females. Right ventricular hypertrophy was present before and after acclimatization in nHx rats, indicating that neonatal hypoxia results in pulmonary hypertension in adults. We conclude that neonatal hypoxia impairs acclimatization to chronic hypoxia in adults and may be a factor contributing to the establishment of chronic mountain sickness in humans living at high altitude.hypoxic ventilatory acclimatization; neonatal hypoxia; chronic mountain sickness

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“…Previous reports have also suggested that endogenous and exogenous increases in progesterone markedly increase both the V E and carotid body neural output response to hypoxia (10,11,22,33). These effects appear to be intrinsic to the carotid body (i.e., peripheral chemoreflex) (10,11) and potentiated by increased plasma estrogen concentrations (10).…”

mentioning

confidence: 91%

“…In addition, progesterone administered alone, or in combination with estrogen, to men (5,15,29,35) and ovariohysterectomized women (28) significantly increases the sensitivity of the central ventilatory chemoreflex response to CO 2 . However, the effects of exogenous progesterone and estrogen on the central chemoreflex threshold for CO 2 are unclear, as some (13,15,23,28,29) but not all (5,10,35) studies have reported a significant decrease.…”

mentioning

confidence: 99%

Effects of human pregnancy on the ventilatory chemoreflex response to carbon dioxide

Jensen¹,

Wolfe²,

Slatkovska³

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

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This study examined the effects of human pregnancy on the central chemoreflex control of breathing. Subjects were two groups ( n = 11) of pregnant subjects (PG, gestational age, 36.5 ± 0.4 wk) and nonpregnant control subjects (CG), equated for mean age, body height, prepregnant body mass, parity, and aerobic fitness. All subjects performed a hyperoxic CO2 rebreathing procedure, which includes prior hyperventilation and maintenance of iso-oxia. Resting blood gases and plasma progesterone and estradiol concentrations were measured. During rebreathing trials, end-tidal Pco2 increased, whereas end-tidal Po2 was maintained at a constant hyperoxic level. The point at which ventilation (V̇e) began to rise as end-tidal Pco2 increased was identified as the central chemoreflex ventilatory recruitment threshold for CO2 (VRTco2). V̇e levels below (basal V̇e) and above (central chemoreflex sensitivity) the VRTco2 were determined. The VRTco2 was significantly lower in the PG vs. CG (40.5 ± 0.8 vs. 45.8 ± 1.6 Torr), and both basal V̇e (14.8 ± 1.1 vs. 9.3 ± 1.6 l/min) and central chemoreflex sensitivity (5.07 ± 0.74 vs. 3.16 ± 0.29 l·min−1·Torr−1) were significantly higher in the PG vs. CG. Pooled data from the two groups showed significant correlations for resting arterial Pco2 with basal V̇e, central chemoreflex sensitivity, and the VRTco2. The VRTco2 was also correlated with progesterone and estradiol concentrations. These data support the hypothesis that pregnancy decreases the threshold and increases the sensitivity of the central chemoreflex response to CO2. These changes may be due to the effects of gestational hormones on chemoreflex and/or nonchemoreflex drives to breathe.

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Effects of estrogen and progesterone on carotid body neural output responsiveness to hypoxia

Cited by 124 publications

References 0 publications

Determinants of blood oxygenation during pregnancy in Andean and European residents of high altitude

Determinants of blood oxygenation during pregnancy in Andean and European residents of high altitude

Impaired acclimatization to chronic hypoxia in adult male and female rats following neonatal hypoxia

Effects of human pregnancy on the ventilatory chemoreflex response to carbon dioxide

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