[Sympathetic hyperactivity in hypertension].
It has been suggested that sympathetic hyperactivity is found in patients with metabolic syndrome (MS) by measuring turnover rate of catecholamines and/or muscle sympathetic nerve firing rate. Increased leptin associated with MS stimulates sympathetic outflow from the hypothalamus, which may be one of causes of sympathetic hyperactivity. Insulin increased in association with insulin resistant in MS increases sodium reabsorption in the kidney leading to sodium retention. Increased intra-cranial sodium ions are known to augment sympathetic nervous system activity via stimulation of epithelial sodium channels, mineralocorticoid receptors, the renin-angiotensin-aldosterone system and endogenous digitalislike factors in the brain. This mechanism may be true in patients with essential hypertension, particularly in those who are sensitive to sodium loading.
Takahashi
Hakuo
H
Department of Clinical Sciences Laboratory Medicine, Kansai Medical University.
D001921:Brain / Q000378:metabolism; D002395:Catecholamines / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000209:etiology*; D007333:Insulin Resistance; D007668:Kidney / Q000378:metabolism; D020738:Leptin / Q000502:physiology; D024821:Metabolic Syndrome / Q000378:metabolism / Q000503:physiopathology; D018161:Receptors, Mineralocorticoid / Q000378:metabolism; D012084:Renin-Angiotensin System / Q000502:physiology; D012964:Sodium / Q000378:metabolism; D015222:Sodium Channels / Q000378:metabolism; D013564:Sympathetic Nervous System / Q000503:physiopathology*
D002395:Catecholamines; D020738:Leptin; D018161:Receptors, Mineralocorticoid; D015222:Sodium Channels; D012964:Sodium