Response from Authors
Pirodda et al's discussion on the pathogenesis of Meniere's symptom is noteworthy because a recent animal study demonstrated that peripheral vestibular receptors may respond to acute decreases in blood pressure (Choi et al, Citation2008) and another animal study showed that vestibular stimulation induces a release of vasopressin (Horii et al, Citation2004). It is therefore highly possible that an abrupt decrease in blood pressure could transmit ‘misleading’ information to the local receptors, thus inducing an abnormal release of vasopressin. In fact, some patients with Meniere's disease show facial pallor, diaphoresis, and hypotension; however few patients with Meniere's disease suffer from syncope-like symptom with hypotension during attacks. Previous studies have demonstrated that systematic hypotension and autonomic disorder are predisposed to Meniere's disease, however they do not appear to be its cause. Our previous paper showed an elevation in plasma vasopressin levels without any change in plasma osmolarity in most Meniere's disease patients in the acute phase (Aoki et al, Citation2010). Acute sensorineural hearing loss such as sudden deafness may be possibly related to an abrupt decrease in blood pressure in selected cases, however I question its application of the hypothesis to Meniere's disease and elevation of vasopressin during acute Meniere's attacks for the above-mentioned reason. As Pirodda et al described in the letter, we also suggest that abnormal release of vasopressin may be induced by a disturbance of the inner ear osmoregulatory mechanisms via labyrinthine volume receptors in Meniere's disease. However further studies are required to elucidate this mechanism.