Sweet taste and blood pressure-related analgesia.

To test the prediction that sweet taste modifies responses to cold induced pain, 72 young adults held sweet, bitter and water solutions in their mouths, in counterbalanced order, before and during a cold pain stimulus. To test whether or not blood pressure interacts with sweet taste analgesia, measurements of resting blood pressure were also obtained. A significant main effect of taste on pain tolerance was observed, as well as a significant interaction between resting mean arterial pressure (MAP) and taste on tolerance. Sweet taste was associated with a prolongation of tolerance compared to the bitter and water conditions. When participants were split along the median for MAP, sweet taste was associated with an 18.1% increase in pain tolerance compared with water for those with lower MAP. No significant impact of taste on pain sensitivity was observed among participants with higher MAP. Groupwise comparisons revealed a significant difference in pain tolerance between participants with higher and lower MAP in the water condition but not in the sweet condition, replicating previous findings of a reduced sensitivity to pain among those with higher blood pressure. The analgesic effects of sweet tasting solutions seen previously in human infants and children may also be present in adults. Individuals with higher blood pressure may not be as sensitive to the presumably opioid-mediated analgesic effects of sweet taste, perhaps due to opioid dysregulation.

Effects of cardiopulmonary baroreceptor activation on pain may be moderated by risk for hypertension.

Cardiopulmonary baroreceptor stimulation may modulate pain, though the literature is much smaller than research showing that sinoaortic baroreceptor stimulation can buffer pain. To examine the possibility that risk for established high blood pressure may moderate the effects of cardiopulmonary baroreceptor stimulation on pain, 22 borderline hypertensive and 18 normotensive men participated in a laboratory experiment. Group differences in blood pressure were documented by 24-h ambulatory blood pressure recording. Ratings of the intensity of acute heat pain were influenced by both group membership and leg position. Passive elevation of the legs, a technique that stimulates cardiopulmonary baroreceptors, reduced ratings of heat pain though only among borderline hypertensives. Alteration of pain sensitivity may reflect the development of the hypertensive process.

Effects of opioid blockade on the modulation of pain and mood by sweet taste and blood pressure in young adults.

Increased blood pressure and sweet taste are often associated with decreased pain sensitivity. Animal research suggests that endogenous opioids are involved in both these relationships. Fifty-eight healthy young adults (36 male, 22 female) participated in two sessions receiving a placebo tablet or 50mg of naltrexone on counterbalanced days. On each day, three cold-pressor tests were administered while the participant held a sweet solution, water, or nothing in their mouth when their hand was in the water. 2 Drug x 3 Solution x 2 Gender x Pre-Drug Resting Blood Pressure general linear models (GLM) were conducted separately for systolic (SBP) and diastolic (DBP) pressure. Consistent with previous research, significant main effects of SBP were observed in GLMs of pain tolerance and pain unpleasantness ratings. A main effect of solution on tolerance was seen in the GLM with DBP, which was qualified by an interaction of solution by blood pressure. Sweet taste increased pain tolerance among those with lower DBP across drug conditions. This suggests some overlap between mechanisms of sweet taste and blood pressure analgesia, without implicating opioid activity in sweet taste analgesia. However, the GLM of tolerance also produced a significant drug by DBP interaction suggesting that blood pressure-related analgesia is at least partially opioid-mediated. Also participants with higher DBP showed dampened mood reactivity to the experiment, which was partially reversible by naltrexone. These results are consistent with findings suggesting that endogenous opioid activity may contribute to generally reduced pain sensitivity, and perhaps mood reactivity, in those with higher BP.