Thyrotropin releasing hormone increases intraocular pressure. Mechanism of action.

Intravenous injections of 1-100 micrograms thyrotropin releasing hormone (TRH) in rabbits elevated intraocular pressure (IOP). The 2-5 mm Hg increase of IOP lasted for less than 2 hr. No change of pupil size was observed. This IOP elevation was not due to a direct effect of TRH on ocular tissues since intravitreal injections of 0.1 and 1 micrograms TRH did not change IOP. Concentrations of thyroid stimulating hormone (TSH), triiodothyronine (T-3), epinephrine (Epi) and norepinephrine (NE) in the plasma were elevated at 30 min after an i.v. injection of 10 micrograms TRH. Plasma levels of prolactin and thyroxine were not changed. Bolus i.v. injections of 0.1-1 micrograms TSH and 0.1-1 micrograms T-3, which would produce an equivalent increase of relevant hormones in the circulation, did not increase IOP. However, similar i.v. injections of 10-100 ng Epi and 100 ng NE caused a 1.5-3 mm Hg IOP elevation for 15-30 min. Thus, the IOP elevation following TRH administration probably is caused by the increase of circulating endogenous catecholamines and not by the stimulation of the TSH-thyroid hormone axis. Heart rate, but not blood pressure, was increased with 10 micrograms TRH. After unilateral transection of the cervical sympathetic trunk, the IOP elevation in the decentralized eye was larger than that in the intact eye. Topical treatment of 0.1% or 1% timolol in the decentralized eye inhibited the IOP elevations in both eyes, but 0.1% prazosin was not effective. Topical 1% atropine and atropine given subcutaneously at 0.6 mg/kg decreased the bilateral IOP elevations. These observations indicate that beta-adrenergic and muscarinic mechanisms, not an alpha-1-adrenergic mechanism, are involved.