Primary open-angle glaucoma (POAG) is a leading cause of irreversible and preventable blindness and ocular hypertension is the strongest known risk factor. With current classes of drugs, management of the disease focuses on lowering intraocular pressure (IOP). Despite of their use to modify the course of the disease, none of the current medications for POAG is able to reduce the IOP by more than 25%–30%. Also, some glaucoma patients show disease progression despite of the therapeutics. This paper examines the new described physiological targets for reducing the IOP. The main cause of elevated IOP in POAG is thought to be an increased outflow resistance via the pressure-dependent trabecular outflow system, so there is a crescent interest in increasing trabecular meshwork outflow by extracellular matrix remodeling and/or by modulation of contractility/TM cytoskeleton disruption. Modulation of new agents that act mainly on trabecular meshwork outflow may be the future hypotensive treatment for glaucoma patients. There are also other agents in which modulation may decrease aqueous humour production or increase uveoscleral outflow by different mechanisms from those drugs available for glaucoma treatment. Recently, a role for the ghrelin-GHSR system in the pathophysiology modulation of the anterior segment, particularly regarding glaucoma, has been proposed.

Load regulation of pressure fall was analyzed in regionally stunned left ventricles (LV) of anesthetized dogs. Stunning delayed and slowed pressure fall. When partial aortic occlusions elevated systolic pressure by 12.5 +/- 0.4 mmHg, the rate of pressure fall remained unchanged at baseline but slowed after stunning. This different response after stunning could be attributed entirely to decreased contractility and decreased development of peak isovolumetric pressure. Total aortic occlusions were then performed at various timings during ejection. With early occlusions and isovolumetric heartbeats, systolic pressure was lower after stunning, but pressure fall slowed to the same extent. With midocclusions the stunned LV developed relatively more systolic pressure, and pressure fall slowed more. This suggested a delayed transition from contraction to relaxation. With late occlusions pressure fall did not slow as with earlier occlusions, but initial pressure fall accelerated both at baseline and after stunning. The data suggested that load dependence was preserved with stunning and that, even if myocardial inactivation might be delayed, this delay did not contribute to the observed slowing of pressure fall.

There is an ER crucial to embryogenesis in cardiomyocytes besides SR. Certain stimuli may induce reactivation of the transcription pattern present during embryogenesis, leading to overexpression of calreticulin in the heart, altering numerous signaling pathways and subsequently inducing pathology. Normalization of these transcriptional disorders holds promise in the treatment of multiple cardiac diseases.

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