The Investing Fascia-Carotid Sheath Mechanical Coupling Mechanism in Cervicogenic Hypertension: A Positive Feedback Vicious Cycle Hypothesis Based on Six-System Integration and a Global Theory Hierarchical Framework

The core dilemma—that the global hypertension control rate remains below 20%—does not stem from the ineffectiveness of existing drugs, but rather from a long-overlooked upstream issue: we have been asking why the RAAS sustains hypertension, yet we have never systematically addressed a more fundamental question—what initially triggers RAAS activation? This paper offers one answer: the answer lies not in the blood, but in the physical tension of a single fascial layer in the neck. This paper proposes a four-layer causal chain framework: (1) the physical trigger layer—genetic and acquired factors synergistically drive fibrotic thickening of the posterior cervical investing fascia, and the shortened thickened fascia disrupts the anterior-posterior tension balance of the neck, forcing the head into forward translation, with the two forming a bidirectional causal loop; (2) the mechanical transmission layer—once the investing fascia loses its elastic buffering capacity, abnormal shear stresses generated by daily head-neck micromovements are rigidly conducted through the three-layer network of the deep cervical fascia to the carotid sheath, an anatomical hub; (3) six systems are simultaneously affected—the abnormal stress synchronously impacts the arteries (baroreceptor microenvironment), veins (impaired intracranial venous return), lymphatics (immune-metabolic waste retention), glymphatic system (impaired central Ang II clearance), sympathetic nerves (overactivation), and vagus nerve (reduced parasympathetic tone) within and adjacent to the sheath; and (4) the positive feedback closure—abnormal signals from five peripheral pathways converge on the nucleus tractus solitarius, driving sympathetic storm and blood pressure elevation, while elevated Ang II drives further fascial fibrosis via the AT1R-YAP pathway, and impaired glymphatic clearance causes cerebral Ang II retention, jointly forming three unbreakable driver arms together with the GPR146-PIEZO1 molecular accelerator. This framework repositions the classical RAAS theory as the "second layer—the humoral amplification mechanism"—rather than placing it as a competing parallel theory. This hypothesis proposes quantitative diagnostic criteria for cervicogenic hypertension (investing fascia SWE value >35 kPa, reduced baroreflex sensitivity, and forward head posture) and seven testable quantitative predictions, with its applicable population explicitly restricted to the cervicogenic hypertension subtype, excluding organic, non-cervicogenic, and other secondary hypertensions. This hierarchical perspective offers a new dimension for precision phenotyping of hypertension and mechanism-guided individualized therapy.