title: Essential hypertension--is erroneous receptor output to blame?
abstract: Hypertension is a chronic medical condition in which systemic arterial blood pressure is elevated. About 80-90% of diagnosed hypertension is considered essential (idiopathic), which means there is no obvious cause of the increase in blood pressure. My hypothesis states that part of idiopathic hypertension results from erroneous information that the brain receives from receptors involved in the regulation of arterial blood pressure, i.e. if, despite high systemic blood pressure, the brain receives false "low-arterial pressure input" from cardiovascular receptors. As a result the brain centres which control blood pressure reset and produce an inappropriate output to the effectors (heart, blood vessels, kidneys and glands). The information errors may result from: (i) structural and/or functional impairment of cardiovascular receptors, (ii) changes in cardiovascular receptors activity, which are caused by other factors than changes in blood pressure, and (iii) impaired transmission in afferent fibres. I assume that in contrast to the lack of input from damaged or denervated cardiovascular receptors, an erroneous input will impair the control of arterial blood pressure. This will apply especially to false input which imitates "low-arterial pressure input". Higher priority of "low-arterial pressure input" over "high-arterial pressure input" or none input may be explained by the evolutionary adaptation, i.e. low blood pressure, mostly due to haemorrhage, used to be a more common condition than high blood pressure and constitute a major threat to humans.
authors.affiliation: Department of Experimental and Clinical Physiology, Medical University of Warsaw, Krakowskie Przedmiescie 26/28, 00-927 Warsaw, Poland.
authors.forename: Marcin
authors.initials: M
authors.lastname: Ufnal
mesh_terms: D000344:Afferent Pathways / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology*; D001921:Brain / Q000502:physiology*; D006801:Humans; D006973:Hypertension / Q000209:etiology*; D008954:Models, Biological; D011311:Pressoreceptors / Q000503:physiopathology*