The defense reaction: a common denominator of coronary risk and blood pressure in neurogenic hypertension?
In addition to high blood pressure, patients with hypertension often have insulin resistance, dyslipidemia and increased sympathetic tone. An increased sympathetic tone can negatively affect glucose utilization through three distinct mechanisms; a direct beta-adrenoreceptor-mediated insulin resistance, through conversion to more insulin resistant fast twitch fibers and through alpha-adrenergic vasoconstriction which may decrease the delivery of insulin and glucose to the skeletal muscle cells. The insulin resistance in turn may be responsible for the observed dyslipidemia in hypertension. The sympathetic overactivity in hypertension reflects a chronic activation of defense/vigilance reaction. The increase of cardiac output, blood pressure and insulin resistance in the course of the defense reaction are viewed as an appropriate preparatory response to facilitate muscular exercise (through higher cardiac output and increased pressure) and preserve (through insulin resistance) the optimal supply of glucose to the brain. The defense reaction may have been useful in evolution and may have offered survival advantage. In modern times with prolonged life expectancy the previously useful response (in evolutionary terms) contributes to a faster and deleterious wear and tear of the cardiovascular system.
Julius
S
S
Department of Internal Medicine, University of Michigan Medical School, Ann Arbor 48109-0356, USA.
D001143:Arousal / Q000502:physiology; D001161:Arteriosclerosis / Q000209:etiology / Q000503:physiopathology / Q000523:psychology; D001794:Blood Pressure / Q000502:physiology; D002318:Cardiovascular Diseases / Q000209:etiology / Q000503:physiopathology / Q000523:psychology; D002319:Cardiovascular System / Q000503:physiopathology; D003674:Defense Mechanisms; D006801:Humans; D006973:Hypertension / Q000209:etiology* / Q000503:physiopathology / Q000523:psychology*; D012307:Risk Factors; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D014661:Vasoconstriction / Q000502:physiology