Hypertension-associated hypoalgesia is widely recognized in
acute pain conditions. In
chronic pain states, however, the relationship between blood pressure and
pain sensitivity is still ill-defined, with different authors reporting negative, positive, or even no relationship at all. This work addresses this issue, using complete
Freund's adjuvant (CFA)-induced monoarthritis in different models of
hypertension: Spontaneous (spontaneously hypertensive rats, SHR), induced by infusion of
angiotensin II (ANG) or
1,3-dipropyl-8-sulfophenylxanthine (
DPSPX, an
adenosine receptors' antagonist), and renal artery
ligation (RAL). Nociceptive responses associated with monoarthritis were evaluated by different behavioral tests (von Frey, ankle-bend and CatWalk) and by quantification of Fos expression at the dorsal horn upon noxious stimulation. In all
hypertension models, higher von Frey thresholds and lower Fos expression were detected in hypertensive rats with chronic inflammatory
pain, as compared to normotensive monoarthritic rats. In SHR and
DPSPX, but not ANG or RAL models, hypertensive animals displayed lower
inflammation than normotensives. Ankle-bend and CatWalk results indicated lower
pain sensitivity in hypertensive rats only in SHR and
DPSPX models. The present study shows the importance of using multiple models of
hypertension, and evaluating
pain responses by various methods, to better understand the complexity of the interactions between
pain and cardiovascular regulatory systems.
PERSPECTIVE: This study used different models of
hypertension to investigate whether
chronic pain alters the normal integration of cardiovascular and
pain regulatory systems. A complete understanding of the mechanisms underlying the complex interactions between these systems may disclose future therapeutic approaches to treat
hypertension/
chronic pain comorbidity states.