Inhibitory Effect of Sex Steroids on Guinea-Pig Airway Smooth Muscle Contractions

Perusquı́a, Mercedes; Hernández, Roberto; Montaño, Luis M.; Villalón, Carlos M.; Campos, Marı́a G.

doi:10.1016/s0742-8413(97)00029-7

Cited by 43 publications

(17 citation statements)

References 29 publications

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“…The progressive increase in PEF after 14-16 weeks of gestation is in concordance with previously reported bronchodilatation occurring during pregnancy. 28 The physiological mechanisms of bronchodilatation in pregnancy remain unclear, but pregnancy-induced reduction in pulmonary vagal efferent activity, 29 and progesterone-mediated alteration in airway smooth muscle tone, [30][31][32] may separately or in combination be responsible.…”

Section: Discussionmentioning

confidence: 99%

Changes in pulmonary function during pregnancy: a longitudinal cohort study

Grindheim

Toska

et al. 2011

BJOG

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Objective To record any physiological changes in lung function during healthy pregnancies, and evaluate the influence of parity, pregestational overweight, and excessive weight gain.Design Longitudinal cohort study.Setting Antenatal clinic at Oslo University Hospital.Population One hundred healthy white women with singleton pregnancies.Methods The women were studied with repeated measures of lung function using spirometry at a gestational age of 14-16, 22-24, 30-32, and 36 weeks, and at 6 months postpartum.Main outcome measures Forced vital capacity (FVC), forced expiratory volume in 1 second (FEV1), and peak expiratory flow (PEF), also expressed as a percentage of predicted values according to age and height: i.e. FVC%, FEV1%, and PEF%.Results Both FVC and FVC% increased significantly after 14-16 weeks of gestation (P = 0.001), as was the case for both PEF and PEF% (P < 0.001). FVC, FVC%, PEF, and PEF% in early and mid-pregnancy were significantly lower compared with the postpartum value (all P < 0.05). Nulliparous women had an overall 4.4% lower value of FVC% than parous women (P = 0.039). There were no differences in FVC, FEV1, or PEF dependent upon pregestational overweight or excessive weight gain.Conclusions Forced vital capacity (FVC) increases significantly after 14-16 weeks of gestation. The FVC% is significantly higher in parous compared with primigravida women, suggesting that the changes in FVC occurring during pregnancy persist postpartum. PEF increases significantly during healthy pregnancies, and should be interpreted cautiously in pregnant women with impaired lung function.

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Section: Discussionmentioning

confidence: 99%

Changes in pulmonary function during pregnancy: a longitudinal cohort study

Grindheim

Toska

et al. 2011

BJOG

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“…However, these concentrations may be reached in pregnancy or in women taking hormone replacement therapy, and therefore the vascular responses can be pharmacologically relevant. In addition to vascular smooth muscle, progesterone has been reported to directly relax airway smooth muscle (Perusquia et al 1997). In all cases this inhibitory action of progesterone appears not to be mediated by the classical steroid hormone receptor mechanisms involving genomic expression.…”

Section: Discussionmentioning

confidence: 99%

“…The result agrees with, and extends, results obtained by others (Crews & Khalil 1999), showing that progesterone inhibits 45 Ca in¯ux into coronary artery smooth muscle. Progesterone has also been shown to inhibit calcium in¯ux into airway smooth muscle (Perusquia et al 1997) and to inhibit calcium currents in intestinal smooth muscle cells (Bielefeldt et al 1996). Many reports indicate that diOE erent agents could regulate Ca 2 + -channel currents in smooth muscle cells.…”

Section: Discussionmentioning

confidence: 99%

Rapid inhibition of the contraction of rat tail artery by progesterone is mediated by inhibition of calcium currents

Zhang

Benishin

Pang

2002

Journal of Pharmacy and Pharmacology

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Progesterone induced rapid relaxation of KCl-contracted tail artery helical strips from rats. The effect was dose dependent, with an IC50 (inhibitory concentration which produces 50% of the maximal response) of 8.9 microM progesterone. The actions of progesterone were not blocked by bicuculline, indicating that in this tissue the non-genomic actions of progesterone were not mediated via a gamma-aminobutyric acid (GABA)-A receptor. Fura-2 was used to measure intracellular calcium levels ([Ca(2+)](i)) in isolated vascular smooth muscle cells (VSMC). Incubation of cultured VSMC for 15 min with progesterone (10 microM) resulted in an inhibition of the KCl-induced [Ca(2+)](i )increase. The whole-cell patch-clamp technique was used to examine Ca(2+)-channel currents in the membrane of isolated VSMC. Progesterone suppressed the L-type Ca(2+)-channel currents in cells held at a potential of -40 mV. The effects of progesterone were quickly reversed by washout in all three experimental protocols suggesting that these effects on vascular tissues are non-genomic. The correlation of the effects on all these preparations, their time course and reversibility suggested that the rapid relaxation of the rat tail artery induced by progesterone is mediated at least in part by inhibition of L-type calcium channels, leading to inhibition of calcium responses in the VSMC of this tissue.

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“…This effect is more potent than testosterone, but not as comparable to E 2 (Foster et al, 1983). Other studies show that via inhibition of calcium entry, progesterone and 5β-pregnenalone abolish agonist-induced contraction in guinea pig trachea (Perusquia et al, 1997). On the other hand, Hellings et al showed that progesterone exacerbates AHR in ovalbumin-sensitized male mice (Hellings et al, 2003), although there are no reports on PR expression per se .…”

Section: Contribution Of Sex Steroids To Airway Structure and Funcmentioning

confidence: 98%

Sex steroid signaling: Implications for lung diseases

Sathish

Martin

Prakash

2015

Pharmacology & Therapeutics

136

134

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There is increasing recognition that the sex hormones (estrogen, progesterone, and testosterone) have biological and pathophysiological actions in peripheral, non-reproductive organs, including the lung. Clinically, sex differences in the incidence, morbidity and mortality of lung diseases such as asthma, chronic obstructive pulmonary disease (COPD), pulmonary fibrosis, lung cancer and pulmonary hypertension have been noted, although intrinsic sex differences vs. the roles of sex steroids are still not well-understood. Accordingly, it becomes important to ask the following questions: 1) Which sex steroids are involved? 2) How do they affect different components of the lung under normal circumstances? 3) How does sex steroid signaling change in or contribute to lung disease, and in this regard, are sex steroids detrimental or beneficial? As our understanding of sex steroid signaling in the lung improves, it is important to consider whether such information can be used to develop new therapeutic strategies to target lung diseases, perhaps in both sexes or in a sex-specific manner. In this review, we focus on the basics of sex steroid signaling, and the current state of knowledge regarding how they influence structure and function of specific lung components across the life span and in the context of some important lung diseases. We then summarize the potential for sex steroids as useful biomarkers and therapeutic targets in these lung diseases as a basis for future translational research in the area of gender and individualized medicine.

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Inhibitory Effect of Sex Steroids on Guinea-Pig Airway Smooth Muscle Contractions

Cited by 43 publications

References 29 publications

Changes in pulmonary function during pregnancy: a longitudinal cohort study

Changes in pulmonary function during pregnancy: a longitudinal cohort study

Rapid inhibition of the contraction of rat tail artery by progesterone is mediated by inhibition of calcium currents

Sex steroid signaling: Implications for lung diseases

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