So I read a journal article entitled "Maternal hypoxia and caffeine exposure depress fetal CV function during primary organogenesis" (Momoi, et al., 2012) and in essence the article speaks of the period of time in embryological development when the cardiovascular system is developing as being the time when the fetus is most susceptible to epigenetic events, and how adenosine and its A2 receptor have a role in dilating coronary arteries in hypoxic conditions. It later goes on to say that since caffeine is an adenosine A2 receptor antagonist, mothers who consume caffeine regularly create a suboptimal environment for the fetus - this is referred to in the article as IUGR (intrauterine growth restriction).

My question is: Are there any effects (or do you believe there could be effects) of this inhibition occurring during development that affect the fetus later in life? As in, do you think there would be adult phenotypic changes of any kind due to the regular inhibition of a receptor during development?

I thought about this for a while and all that was apparent to me is that if the mother was both consuming caffeine and hypoxic, then the fetus could experience myocardial damage because its coronary arteries wouldn't be receiving the signal to dilate and the heart might be "starved" of the proper oxygenation. But even so, the receptor would still be present in the adult. Do you think there could be a decrease in transcription of a receptor that is continuously blocked (you don't need to address this in your answer -- notice that I'm asking for an opinion, which you can choose to give or withhold)?

FYI: I'm writing a review on how maternal prenatal health contributes to the epigenetic profile of offspring and I'm actually focusing more on the epigenetic contributions to the adult hypertensive phenotype. I stumbled upon the CV/adenosine article and was curious about whether there could be any long-term changes, so I asked all you wise folk. It has been observed that mothers fed a low-protein diet give birth to children with reduced nephron count and glomerular hypertrophy -- my goal is to understand what the current state of knowledge of this mechanism is. So if you have any ideas about anything here, or you've got an awesome resource related to this material, I'd really appreciate hearing about it.


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