Autonomic degeneration and altered blood pressure control in humans.
The study of patients with partial or total defects of their sympathetic nerves can help clarify the role of the sympathetic nervous system in blood pressure control. Denervation supersensitivity of both beta and alpha receptors develops in humans and is proportional to the degree of sympathetic withdrawal. Although alterations in beta-receptor sensitivity are familiar responses to beta agonists or antagonists, patients with decreased norepinephrine (NE) levels appear to develop alpha-receptor supersensitivity of greater hemodynamic importance. When beta supersensitivity is marked, there may be a pressor response to beta blockade even when circulating levels of NE and epinephrine are very low. Indomethacin blocks prostaglandin synthesis and causes an increase in blood pressure in patients with partial autonomic neuropathies. The drug increases blood pressure by enhancing alpha- and diminishing beta-receptor sensitivity to NE, so it is effective only in patients who have some residual NE release.
D001342:Autonomic Nervous System Diseases / Q000503:physiopathology*; D001794:Blood Pressure / Q000187:drug effects; D006801:Humans; D009410:Nerve Degeneration; D009638:Norepinephrine / Q000502:physiology; D011453:Prostaglandins / Q000502:physiology; D011943:Receptors, Adrenergic, beta / Q000502:physiology; D012791:Shy-Drager Syndrome / Q000503:physiopathology; D013564:Sympathetic Nervous System / Q000503:physiopathology
D011453:Prostaglandins; D011943:Receptors, Adrenergic, beta; D009638:Norepinephrine