Hypertension is a collective term for intraocular pressure above 21 mmHg and can be seen in various causes such as traumatic anterior chamber hemorrhage, orbital edema, postoperative viscoelastic residue, endophthalmitis, glucocorticoid use, pupillary block, and idiopathic, among others. Ocular hypertension (OHT) is a specific concept first proposed by Drance in 1962, and Perkins et al. in 1966 proposed that OHT requires the following conditions to be met simultaneously: 1. pressure flattening IOP measurement of one or both eyes, with at least 2 times higher than 21 mmHg; 2. visual field examination without glaucomatous visual field defects 3, the optic disc and retinal nerve fiber layer is normal; 4, the atrial angle is open and there is no history of atrial angle closure; 5, other eye diseases that can cause IOP elevation are excluded. Thus, hypertension should chronically meet the above 5 criteria, without other manifestations of primary open angle glaucoma (POAG) and without known causes of IOP elevation. The term has been controversial, with Hitchings et al. arguing that the definition “neither indicates whether the patient will develop glaucoma in the future nor whether it is an early stage of glaucoma”. Some advocate the term “suspected glaucoma” to express the uncertainty of the patient’s diagnosis and prognosis. Therefore, the definitive diagnosis of hypertension is a long-term process to exclude the diagnosis of glaucoma, and it is not possible to rely on a single IOP index to diagnose hypertension, but requires a combination of central corneal thickness, corneal curvature, IOP fluctuations, retinal nerve fiber layer (RNFL) thickness, morphology of the optic nerve papillae and visual function (visual field). The combined analysis requires long-term follow-up and multiple repetitions to clarify. Hyperopthalmia is not a disease per se, but a term used to describe a group of individuals. When IOP exceeds the limits of what the tissues of the own eye can tolerate, it will lead to impaired visual function. The level of elevated intraocular pressure and the tolerance of the optic nerve to pressure damage are closely related to the onset and progression of glaucomatous optic nerve atrophy and visual field defects. There are currently two predominant theories to explain high IOP glaucomatous damage: vascular dysfunction causing optic nerve ischemia, and mechanical compression of the optic nerve axons by the sieve plate. In addition to these two mechanisms causing axoplasmic flow blockage, other possible mechanisms leading to glaucomatous optic neuropathy include neurotoxic damage caused by excessive glutamate release from the retina, neurotrophic factor deprivation, oxidative toxicity caused by changes in nitric oxide synthase activity, immune-mediated neurological damage, and oxidative stress. The exact role and significance of the combined effect of elevated IOP and other factors in the progression of optic nerve damage and progressive cell death in glaucoma is still under investigation. Nonetheless, IOP is the only factor that can be successfully controlled artificially in clinical practice, and the classification and management of patients according to IOP has been used in the selection of treatment options for hypertension in order to prevent glaucoma damage from occurring.