This paper presents a review of experimental and clinical research on the contribution of hypertension to cochlear hearing loss. Hypertension is one of the crucial risk factors underlying pathophysiological processes taking place in the cochlea. Several mechanisms explaining these processes have been described, mainly in animal models, such as the disturbance of the inner ear potassium recycling process due to the detrimental action of natriuretic hormone, and the decrease in the cochlear oxygen partial pressure. Current evidence linking hypertension to sensorineural high-frequency cochlear hearing loss in humans may be confounded by other concomitant diseases or risk factors such as age, coronary artery disease, diabetes, obesity, hyperlipidemia, smoking and noise exposure. Therefore, further research in this field is clearly needed.

Objectives: Arterial hypertension negatively influences the peripheral auditory system, causing sensorineural hearing loss. Much less is known about the detrimental effects of hypertension on the central auditory functions. Methods: We tested 32 arterial hypertension patients and 32 age and sex-matched healthy volunteers with the expanded tonal audiometry (0.125–12.5 kHz), distortion product otoacoustic emissions (0.75–8 kHz), horizontal minimum audible angle test for eight azimuths with binaural stimulation and the random gap detection test. Results: Peripheral hearing of the hypertensive patients was impaired in comparison with the controls within all audiometric frequencies (0.125–12.5 kHz) and within specific groups of frequencies. Distortion product otoacoustic emission results were significantly lower for frequencies 4 (P = 0.04) and 6 kHz (P < 0.001). The sound localization ability in the horizontal minimum audible angle test was significantly worse in the hypertensive patients in the 0°, 45°, 90°, 135°, and 270° azimuth when the interaural pure tone average (0.5–1–2 kHz) was set less than 20 dB hearing level (P < 0.05), and in the 0°, 90°, 225°, and 270°azimuth when the binaural pure tone average (0.5–1–2 kHz) was set 20 dB or less hearing level (P < 0.05). Gap detection thresholds in the random gap detection test did not differ between the two groups. Conclusion: Arterial hypertension is independently related to the damage of the peripheral part of the auditory system resulting in high-frequency hearing loss. Hypertensive disturbances of central auditory processing are more discrete and concern the spatial hearing resolution.

Ischemic stroke causes mobilization of various groups of progenitor cells from bone marrow to bloodstream and this correlates with the neurological status of stroke patients. The goal of our study was to identify the activity of chosen progenitor/stem cells in the peripheral blood of acute ischemic stroke patients in the first 7 days after the incident, through associations between the levels of the cells and clinical features of the patients. Thirty-three acute ischemic stroke patients and 15 non-stroke control subjects had their venous blood collected repeatedly in order to assess the levels of the CD45–CD34 + CD271+, the CD45–CD34 + CXCR4+, the CD45–CD34 + CXCR7+, and the CD45–CD34 + CD133+ stem/progenitor cells by means of flow cytometry. The patients underwent repeated neurological and clinical assessments, pulse wave velocity (PWV) assessment on day 5, and MRI on day 1 and 5 ± 2. The levels of the CD45–CD34 + CXCR7+ and the CD45–CD34 + CD271+ cells were lower in the stroke patients compared with the control subjects. Only the CD45–CD34 + CD271+ cells correlated positively with lesion volume in the second MRI. The levels of the CD45–CD34 + CD133+ cells on day 2 correlated negatively with PWV and NIHSS score on day 9. The patients whose PWV was above 10 m/s had significantly higher levels of the CD45–CD34 + CXCR4+ and the CD45–CD34 + CXCR7+ cells on day 1 than those with PWV below 10 m/s. This study discovers possible activity of the CD45–CD34 + CD271+ progenitor/stem cells during the first 7 days after ischemic stroke, suggests associations of the CD45–CD34 + CD133+ cells with the neurological status of stroke patients, and some activity of the CD45–CD34 + CD133+, the CD45–CD34 + CXCR4+, and the CD45–CD34 + CXCR7+ progenitor/stem cells in the process of arterial remodeling.