Thank you for your interest and comments about our study. In regards to your first question, I am not aware of a NO-COX relationship in skeletal muscle arterioles, although it certainly could exist. The key to that question would be to look to a tissue where both NO and COX are involved in arteriolar regulation. For example, our laboratory has shown in the spinotrapezius muscle that cyclooxygenase products are not involved in arteriolar flow dependent dilation, but NO is involved. Conversely, cyclooxygenase products appear to play a greater role in cremaster muscle arteriolar regulation and NO plays a smaller one. However, isolated arterioles from the gracilis muscle have been shown by Koller et al (1994) to be dependent on both NO and COX products for flow-induced dilation and this may be the tissue of interest in regards to your question.
Your second question regarding a suppression of endogenous vasodilatory prostaglandins with high dietary salt is also quite interesting. If this occurred, one would expect an augmentation of the myogenic response. In fact, work by Hill et al (1990) has shown that cyclooxygenase inhibition augments arteriolar myogenic behavior in the cremaster muscle. Therefore, if high dietary salt has a suppressing effect on COX products in the cremaster, one could expect an augmentation in arteriolar myogenic responsiveness. And this would most certainly would be an interesting hypothesis to explore! Thanks for your question!