Hypertension and pain: A state-based framework for cardiovascular-nociceptive coupling.

Experimental and epidemiological studies suggest that blood pressure (BP)-pain associations vary across normotension, hypertension, and chronic pain, but the mechanisms underlying these differences remain unclear. In pain-free individuals, higher resting BP is often associated with lower experimental pain sensitivity. Similar hypoalgesia is reported in some normotensive individuals with familial hypertension risk and in established hypertension, suggesting that reduced pain sensitivity is unlikely to be attributable to elevated BP alone. Acute baroreceptor activation can inhibit nociceptive reflexes and pain ratings, and current evidence points to contributions from baroreflex, autonomic, opioid, sensory, vascular, and renin-angiotensin pathways in BP-related hypoalgesia across groups. In chronic pain, the inverse BP-pain association is often weaker, absent, or reversed for selected pain facilitation measures. Prospective epidemiological studies suggest that chronic pain may be associated with increased later hypertension risk, although these observational findings do not establish causality. This review organizes the literature into four states: familial hypertension risk without sustained hypertension, inverse BP-pain associations in normotensive individuals, hypoalgesia in established hypertension, and attenuated or reversed BP-pain associations in chronic pain. Longitudinal studies are needed to determine whether these patterns reflect distinct phenotypes, transitional processes, overlapping mechanisms, or study-context differences.