**Background:** Hypertension affects approximately 1 billion adults globally and is associated with 9 million annual fatalities. Anxiety disorders have a global prevalence of approximately 7.3% and account for 3.3% of the global disease burden. The comorbidity of hypertension and anxiety is common, with a meta-analysis reporting an incidence of approximately 38%. Patients with comorbid hypertension and anxiety have lower treatment compliance, lower quality of life, and higher healthcare costs. This narrative review aims to summarize the common risk factors and potential mechanisms underlying the comorbidity of hypertension and anxiety.
**Methods:** This is a narrative review that synthesizes existing literature on the epidemiology, risk factors, and mechanistic pathways linking hypertension and anxiety. The authors discuss individual risk factors (age, sex), lifestyle factors (smoking, alcohol abuse, obesity), and environmental exposures (lead, traffic noise). Mechanistic sections cover interleukin-6 (IL-6), interleukin-17 (IL-17), reactive oxygen species (ROS), and gut microbiota dysbiosis.
**Key Results:** The review identifies several key findings: (1) Age is a significant risk factor—hypertension prevalence is 26% in people aged 20–44 versus 78% in those over 65. (2) Women are twice as likely as men to experience anxiety, and hormonal changes (e.g., estrogen loss during menopause) increase susceptibility to both conditions. (3) Smoking more than 20 cigarettes per day is strongly linked to elevated anxiety risk. (4) Obesity causes 65%–75% of primary hypertension cases. (5) Anxiety disorders were more prevalent in hypertensive patients (37.9%) than in the general population (12.4%). Mechanistically, elevated IL-6 levels are found in both hypertension (via angiotensin II-mediated pathways) and anxiety disorders. IL-17 reduces nitric oxide production and promotes arterial stiffness, contributing to hypertension, while also reducing brain-derived neurotrophic factor (BDNF) and glial fibrillary acidic protein (GFAP) expression, which are linked to anxiety. ROS contribute to hypertension through endothelial dysfunction, eNOS uncoupling, activation of PARP1-TRPM2 and TXNIP-NLRP3 pathways, and isoketal formation. ROS promote anxiety by suppressing BDNF-synapsin I/CREB signaling, inducing ERK1/2 hyperphosphorylation, and activating NF-κB-COX2-mPGES-1 pathways. Gut dysbiosis contributes to both conditions through reduced short-chain fatty acids (SCFAs), increased trimethylamine N-oxide (TMAO), vitamin D deficiency, and reduced 5-hydroxytryptamine (5-HT) secretion. SCFA deficiency increases intestinal permeability and proinflammatory cytokines, while TMAO induces hypertension via the TMAO-AVP-AQP-2 axis and promotes anxiety by inhibiting MsrA and activating microglia.
**Clinical Implications:** The high comorbidity rate and negative impact on treatment outcomes underscore the need for integrated screening and management of hypertension and anxiety. Healthcare systems should implement interventions to improve screening, diagnosis, and timely treatment. The shared mechanisms—IL-6, IL-17, ROS, and gut dysbiosis—represent potential therapeutic targets. Lifestyle optimization (smoking cessation, reducing alcohol intake, weight management) and environmental modifications (reducing lead and traffic noise exposure) remain cornerstone preventive strategies. The authors also suggest that autophagy may be a future therapeutic target, though direct evidence is lacking.