I have come across various studies about this, but this is the latest one I believe. http://www.ncbi.nlm.nih.gov/pubmed/25131393 Long-term administration of vasopressin can cause Ménière's disease in mice. Katagiri Y1, Takumida M, Hirakawa K, Anniko M. Author information Abstract CONCLUSION: A new murine model of Ménière's disease has been developed, based on long-term administration of vasopressin. Induction of vestibular dysfunction in the present animal model can cause additional stress, by reducing inner ear blood flow. Latanoprost, a selective agonist for the FP prostanoid receptor, may become a new remedy for Ménière's disease. OBJECTIVE: The purpose of this study was to develop a more suitable animal model, with a closer resemblance to the pathophysiological process in Ménière's disease. METHODS: Adult CBA/J or ICR mice were treated by subcutaneous injection of vasopressin for 5 days up to 8 weeks. Morphological analyses were performed of the cochlea, vestibular end organs and endolymphatic sac. The effect of latanoprost on the development of endolymphatic hydrops was also examined. RESULTS: All experimental animals showed mild to moderate endolymphatic hydrops, increasing in severity as the vasopressin treatment was prolonged. Animals treated with vasopressin for 8 weeks showed severe endolymphatic hydrops with partial loss of outer hair cells and spiral ganglion cells. These animals also had a reversible vestibular dysfunction following intratympanic injection of epinephrine. Latanoprost inhibited the development of endolymphatic hydrops caused by vasopressin. here are 2 older studies but several more studies link the vasopressin and EH http://www.ncbi.nlm.nih.gov/pubmed/7882884 Abstract Ear Nose Throat J. 1994 Dec;73(12):921-5. The relationship between vasopressin and endolymphatic hydrops in the guinea pig. Kitano H1, Takeda T, Pulec JL, Saadat D, Uchida K. Author information Abstract Clinical studies have shown that plasma vasopressin level is significantly elevated in patients with Meniere's disease. Other reports indicated that histamine induced a very quick and high elevation of vasopressin level and caused nystagmus in experimentally produced endolymphatic hydrops. We became interested in further investigating the details of this relationship by studying the effect of experimental endolymphatic hydrops and histamine upon plasma vasopressin level in the guinea pig. The results are as follows: 1) Histamine increased the plasma vasopressin level in normal guinea pigs. 2) There was no statistically significant difference in the plasma vasopressin level between the hydrops model and normal guinea pigs. 3) Histamine increased the plasma vasopressin level more in the hydrops model group than in normals. 4) Plasma vasopressin level was elevated in the vertiginous model caused by inner ear anesthesia. Our results support those of clinical investigators who reported that the plasma vasopressin level was elevated more in the Meniere's disease group than any other equilibrium disorder group. It is possible that vasopressin is in someway involved in the development of endolymphatic hydrops. http://www.ncbi.nlm.nih.gov/pubmed/10675630 Hear Res. 2000 Feb;140(1-2):1-6. Endolymphatic hydrops induced by chronic administration of vasopressin. Takeda T1, Takeda S, Kitano H, Okada T, Kakigi A. Author information Abstract Recently, many lines of evidence have supported the possibilities that vasopressin (VP) is closely linked to the formation of endolymphatic hydrops in Meniere's disease. In the present study, it was examined whether or not the chronic administration of VP might induce endolymphatic hydrops. For this purpose, histological studies and VP radioimmunoassay were independently performed in 20 and 40 guinea pigs, respectively. The degree of hydrops was quantitatively assessed by the increase ratio (IR) of the scala media area in the mid-modiolar sections of the cochlea. The IR was defined by the following equation: 100x(A-B)/B (A: the cross-sectional area of the bulging scala media; B: the no-bulging scala media, enclosed by an idealized straight Reissner's membrane). VP was administered at the rates of 200 microU/kg/min, 400 microU/kg/min and 1000 microU/kg/min for 1 week via the osmotic mini-pump. The IR of the total of the apical, second, third and basal turns (means+/-S.D.s) were 4.4+/-0.7, 10.4+/-1.8, 17.4+/-7.9 (n=10 ears, each) in respective doses of VP. Comparing with that of the control animals (5.2+/-1.7, n=10 ears), the area increased significantly in the VP dosage of 400 and 1000 microU/kg/min (Bonferroni's method, P<0.05). Plasma VP concentrations produced by the VP administration in these dosages were 2.2+/-0.4, 3.5+/-0.8 and 14.0+/-3.9 (n=10, each) pg/ml. Although 3.5 pg/ml is the upper limit of plasma VP concentration in normal human subjects, 14.0 pg/ml was almost the same concentration as those observed in the acute phase of Meniere's disease (Takeda et al., 1995). Therefore, the formation of endolymphatic hydrops in cases of Meniere's disease might be caused by high concentrations of plasma VP.
Interesting read. Is vasopressin naturally occurring in the human body then? This might indicate a connection to things that chronically release abnormal quantities of histamine in the body, like environmental allergies, right?
yes vasopressin occurs normally in the body and yes that links allergies with MM too as you stated, Histamine is an inflammatory chemical that the body releases in the case of an allergic reaction. Which may also help explain why allergy medications are helpful with Meniere's and why allergies are Meniere's triggers.