Effect of progesterone on the contractile response of isolated pulmonary artery in rabbits.

  title={Effect of progesterone on the contractile response of isolated pulmonary artery in rabbits.},
  author={H F Li and T Z Zheng and W Li and Song-yi Qu and C. L. Zhang},
  journal={Canadian journal of physiology and pharmacology},
  volume={79 6},
The purpose of this study was to assess the direct effect of progesterone on rabbit pulmonary arteries and to examine the mechanism of its action. Rings of pulmonary artery from male rabbits were suspended in organ baths containing Krebs solution, and isometric tension was measured. The response to progesterone was investigated in arterial rings contracted with noradrenaline (NA), KCl, and CaCl2. The effects of endothelium, nitric oxide (NO), prostaglandins, cyclic GMP (cGMP), and the… 
Effect of progesterone on nitric oxide/cyclic guanosine monophosphate signaling and contraction in gastric smooth muscle cells.
Investigation of the effect of progesterone on the nitric oxide (NO)/cyclic guanosine monophosphate (cGMP) pathway and muscle contraction in the stomach suggests that progestersone promotes muscle cell relaxation inThe stomach potentially via the NO/ cGMP pathway.
Non-genomic vasorelaxant effects of 17β-estradiol and progesterone in rat aorta are mediated by L-type Ca2+ current inhibition
The vasorelaxant effects of βES and PRG are due to the inhibition of LTCC, and the K+ channels are not involved in the effects.
The influence of sex hormones on pulmonary vascular reactivity: possible vasodilator therapies for the treatment of pulmonary hypertension.
Interestingly testosterone has been shown to be a vasodilator in both the coronary and pulmonary circulation with a mechanism of action involving calcium channel blockade of the vascular smooth muscle and without endothelial involvement, lending support to the notion that testosterone could be a potential treatment for patients with PAH as vasodILator therapy remains the mainstay of treatment.
Role of mPRα (PAQR7) in progesterone-induced Ca2+ decrease in human vascular smooth muscle cells.
The results suggest that progesterone induces VSMC relaxation by reducing cellular calcium levels through mPRα-induced alterations in multiple signaling pathways.
Estrogens and Development of Pulmonary Hypertension: Interaction of Estradiol Metabolism and Pulmonary Vascular Disease
  • S. Tofovic
  • Biology
    Journal of cardiovascular pharmacology
  • 2010
The effects of estrogens and their metabolites on pulmonary vascular pathobiology and the development of experimental PAH are focused on and potential explanation for the estrogen paradox in PAH is offered.
Estrogen metabolism in pulmonary arterial hypertension
Evidence is provided that the estrogen metabolic axis is dysregulated in female mice that over-express the human serotonin transporter gene and this may underlie their PAH phenotype and this was inhibited by a scavenger of reactive oxygen species.
The Role of Sex in the Pathophysiology of Pulmonary Hypertension.
Several lines of evidence point towards estrogen being pathogenic in the pulmonary circulation, and thus increasing the risk of females developing PAH, and downstream metabolites such as 16α-hydroxyestrone are upregulated in several forms of experimental pulmonary hypertension (PH).