title: Regulation of blood pressure with calcium-dependent dopamine synthesizing system in the brain and its related phenomena.
abstract: The effects of calcium on blood pressure regulation remain controversial. Although the mechanism by which calcium increases blood pressure when it is given intravenously and acutely has been elucidated, that by which calcium reduces blood pressure when it is supplemented chronically and slightly through daily diet is unclear. From a number of animal experiments concerning the effects of calcium on blood pressure, we believe that calcium ions have two separate roles in the regulation of blood pressure through both central and peripheral systems: (1) calcium ions reduce blood pressure through a central, calcium/calmodulin-dependent dopamine-synthesizing system and (2) calcium ions increase blood pressure through an intracellular, calcium-dependent mechanism in the peripheral vasculature. These concepts were applied to elucidate the mechanisms underlying hypertension in spontaneously hypertensive rats (SHR) and changes in blood pressure in other experimental animals, and the following conclusions were reached. The decrease of the serum calcium level in spontaneously hypertensive rats (SHR) causes a decrease in calcium/calmodulin-dependent dopamine synthesis in the brain. The subsequent low level of brain dopamine induces hypertension. The increase in susceptibility to epileptic convulsions and the occurrence of hypertension in epileptic mice (El mice) may be linked through a lowering of calcium-dependent dopamine synthesis in the brain, and epilepsy and hypertension may be associated. Exercise leads to increases in calcium-dependent dopamine synthesis in the brain, and the increased dopamine levels induce physiological changes, including a decrease in blood pressure. Cadmium which is not distinguished from calcium by calmodulin, activates calmodulin-dependent functions in the brain, and increased dopamine levels may decrease blood pressure. In this report, our studies are considered in light of reports from many other laboratories.
authors.affiliation: Institute of Medical Science, University of Tsukuba, Japan. dustoo@md.tsukuba.ac.jp
authors.forename: D
authors.initials: D
authors.lastname: Sutoo
authors.forename: K
authors.initials: K
authors.lastname: Akiyama
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D001921:Brain / Q000187:drug effects / Q000502:physiology*; D002104:Cadmium / Q000494:pharmacology; D002118:Calcium / Q000494:pharmacology* / Q000502:physiology*; D002147:Calmodulin / Q000502:physiology; D004298:Dopamine / Q000096:biosynthesis*; D015444:Exercise / Q000502:physiology; D006706:Homeostasis; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D051379:Mice; D051381:Rats; D011918:Rats, Inbred SHR
chemical_list: D002147:Calmodulin; D002104:Cadmium; D002118:Calcium; D004298:Dopamine