>According to Hale, Ventolin is a bronchodilator and isn't that a smooth
>muscle relaxant?  I took terbutiline (same type of drug) for premature
>labor and still had a premature and very quick delivery, as well as very
>stong and sometimes quite painful milk-ejection reflexes, along with an
>abundant milk supply (although, I was no longer on the meds).
>
>I just checked the USPDI, "Drug Information for the Health Care
>Professional"  which says bronchodilators act "primarily as a
>beta-adrenergic stimulant to relax the uterine muscle, thereby
>inhibiting uterine contractions."  So, it does not appear to have
>hormonal effects.

If ventolin and terbutaline both relax smooth muscle, wouldn't that also
apply to the myoepithelial cells of the alveoli?  The implications of
what you are saying is that oxytocin is not affected, the receptors are
not affected, but the smooth muscle *is* affected, rendering it
unresponsive.  In other words, is it possible that ventolin relaxes the
myoepithelium and therefore blocks let down?

On the other hand, ventolin inhalers work more locally, as opposed to
oral ventolin; I would expect less interference from the inhaler if the
above is true.  Can someone out there more knowledgeable comment?

It might also be enlightening if we can list some of the meds that we do
know seem to inhibit MER and discuss what they appear to act on.  The
first that comes to my mind is cigarettes-- they are known to inhibit let
down, and therefore the milk supply.  What does the nicotine do exactly?

-Lisa