Pain sensitivity is typically reduced in individuals with higher blood pressure although the nature of this relationship is poorly understood. Relatedly, the ingestion of sweet tasting solutions has been shown to reduce pain, possibly by an opioid mediated mechanism. The objective of the present research was to investigate the effects of blood pressure and sweet taste on pain sensitivity in healthy adults. The first aim was to test whether blood pressure interacts with sweet taste to affect pain sensitivity. The second aim was to test whether endogenous opioids mediate the effects of sweet taste and blood pressure on pain. In Study One, participants held sweet, bitter and plain water solutions in their mouths during exposure to a painful cold pressor test. Replicating previous research, individuals with higher blood pressure were found to have generally higher pain tolerance than those with lower blood pressure. Sweet taste was associated with an increase in pain tolerance but only in individuals with lower range blood pressure, increasing their tolerance to the level of those with higher blood pressure. In Study Two, participants held sweet solution, plain water or nothing in their mouths during cold pressors on two days. To test the involvement of endogenous opioids, participants were administered an opioid antagonist on one of the test days. Participants with higher resting blood pressure again showed increased tolerance and reduced unpleasantness ratings of the pain tasks, as well as dampened mood reactivity to the testing. In these individuals, the opioid antagonist reduced their pain tolerance and partially reversed their lower mood reactivity. As in Study One, sweet taste increased pain tolerance in participants with lower but not higher blood pressure, but this was unaffected by opioid blockade. Taken together these results suggest some overlap between non-opioid mechanisms of sweet taste and blood pressure related analgesia. These results are also consistent with work suggesting that endogenous opioid activity may play a role in the reduced pain sensitivity, and perhaps mood reactivity, of individuals with higher blood pressure and that multiple processes are involved in blood pressure-related hypoalgesia.

This thesis studied the role of spinal nitric oxide (NO) in carrageenan-induced dermal hyperalgesia in the rat hindpaw by means of intrathecal (i.t.) administration of various NO synthase (NOS) inhibitors. A spinal role for NO in carrageenan-induced thermal hyperalgesia was confirmed by dose-dependently reducing the hyperalgesia with a non-selective NOS inhibitor. Next, it was determined that a relatively selective neuronal NOS (nNOS) inhibitor and two relatively selective inducible NOS (iNOS) inhibitors were able to reduce carrageenan-induced thermal hyperalgesia. Finally, early administration of either an nNOS or an iNOS inhibitor had no significant effect on carrageenan-induced thermal hyperalgesia. However, late administration of an iNOS, but not an nNOS inhibitor, significantly reduced the thermal hyperalgesia. We therefore suggest that iNOS contributes to only the late stages of carrageenan-induced thermal hyperalgesia, while nNOS likely plays a role throughout the entire time course of the injury.

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Liu, Xiaodong. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 135-155). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

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