Interplay between noise-induced sensorineural hearing loss and hypertension: pathophysiological mechanisms and therapeutic prospects

Abstract

More than 5% of the global population suffers from disabling hearing loss, primarily sensorineural hearing loss (SNHL). SNHL is often caused by factors such as vascular disorders, viral infections, ototoxic drugs, systemic inflammation, age-related labyrinthine membrane degeneration, and noise-induced hearing loss (NIHL). NIHL, in particular, leads to changes in blood-labyrinth-barrier (BLB) physiology, increased permeability, and various health issues, including cardiovascular disease, hypertension, diabetes, neurological disorders, and adverse reproductive outcomes. Recent advances in neuromodulation and vector-based approaches offer hope for overcoming biological barriers such as the BLB in the development of innovative treatments. Computational methods, including molecular docking, molecular dynamics simulations, QSAR/QSPR analysis with machine/deep learning algorithms, and network pharmacology, hold potential for identifying drug candidates and optimizing their interactions with BLB transporters, such as the glutamate transporter. This paper provides an overview of NIHL, focusing on its pathophysiology; its impact on membrane transporters, ion channels, and BLB structures; and associated symptoms, comorbidities, and emerging therapeutic approaches. Recent advancements in neuromodulation and vector-based strategies show great promise in overcoming biological barriers such as BLB, facilitating the development of innovative treatment options. The primary aim of this review is to examine NIHL in detail and explore its underlying mechanisms, physiological effects, and cutting-edge therapeutic strategies for its effective management and prevention.

Keywords: blood-labyrinth barrier; hypertension; network pharmacology; noise-induced hearing loss; sensorineural hearing loss; taVNS; vagus nerve stimulation.

Figure 1

Structure and blood supply of the cochlea. The spiral modiolar artery supplies the OoC of the modiolus and forms the capillaries of the spiral ligament and stria vascularis in the cochlear lateral wall. SMA, spiral modular artery; SL, spiral ligament; SV, stria vascularis; OoC, organ of Corti; ScV, scala vestibuli; SM, scala media; ST, scala tympani; RM, Reissner membrane; LA, labyrinthinth artery.

Figure 2

Cross section of one cochlear turn and rough structure of the stria vascularis, SV. Structural and functional damage to the SV mediated by noise trauma, specifically to the endothelial blood–labyrinth barrier (BLB), causes hearing loss, but the underlying mechanisms remain mostly unclear.

Figure 3

SNHL—functional contribution of the blood-labyrinth-barrier. Pathogens leading to SNHL include vascular disorders, viral infections, noise trauma, ototoxic drug exposure, and age-related degeneration of the labyrinthine membrane.

Figure 4

Auditory and nonauditory effects of noise overexposure. Noise occurs in everyday life and can lead to both auditory and nonauditory adverse health effects, including hearing loss, tinnitus, neuropsychiatric effects, and cognitive impairment, and can be secondary to triggered circuit conditions, such as cardiovascular and neurodegenerative disease and hypertension.

Figure 5

Stress response elicited by elevated noise. Pathways of elevated noise action lead to hypertension through mental stress, autonomic nervous system changes in sympathetic imbalance, anxiety, and neurohormonal mechanisms. The elevated risk factor is noise exposure because of a primary rudimentary stress reaction, which is mediated either by activation of the sympathetic nervous system or the hypothalamic–pituitary–adrenal (HPA) axis, resulting in fight/flight response, anxiety, and hypertension.

Figure 6

Transcutaneous vagus nerve stimulation targeting the auricular branch of the vagus nerve: taVNS. Noninvasive taVNS delivery systems rely on the cutaneous distribution of vagal fibers at the external ear (auricular branch of the vagus nerve) (Butt et al., 2020), as detailed in the insert. The red circles in the main image and the clamps in the insert represent the best anatomical sites for active left tragus stimulation by the taVNS device, and the blue circles and clamps represent the sham control stimulation sites.