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Sympathetic activity during hypobaric hypoxic condition would increase while parasympathetic action would decrease. Parasympathetic activity via the vegus nerve would decrease its affects on the AV and SA nodes because of the increase in sympathetic activity. Cyclic AMP from the increase in sympathetic activity blocks Ach from binding muscarinic receptors on the nerves. This blocking of Ach would slow G protein from keeping leak K channels being open and for the G Protein to slow its closing of T-type Ca channels. Increase in sympathetic activity leads to norepinephrine and epinephrine being released. They bind to B1 receptors that activate Gs to activate Adenylate cyclase to activate cAMP that causes pro Kinase to open funny channles and t-type Ca channles causing depolerization.

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Q: How do sympathetic and parasympathetic activity control heart rate during hypobaric hypoxic conditions What is the basic mechanism of action?
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