title: Central alpha-adrenergic control of blood pressure. Effects of clonidine withdrawal.
abstract: Studies were undertaken to investigate the role of the CNS in withdrawal hypertension caused by abrupt cessation of long-term clonidine treatment. The studies were conducted on male wistar rats receiving clonidine, 100 micrograms/kg subcutaneously twice daily for seven days. Withdrawal hypertension occurred 16 to 18 hours following the last injection of clonidine. Pressor responses to posterior hypothalamic stimulation were significantly potentiated in the rats undergoing clonidine withdrawal, and the depressor response to a single injection of 10 micrograms of clonidine into the lateral cerebral ventricle was significantly attenuated in these animals. Studies on pithed rats demonstrated that destruction of the CNS eliminated the withdrawal hypertension. These data suggest that alpha-adrenoreceptors in the nucleus tractus solitarius play an important role in the normal maintenance of blood pressure, and a decrease in sensitivity of these receptors could result in the development of a hypertensive state.
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D003000:Clonidine / Q000009:adverse effects*; D004558:Electric Stimulation; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000139:chemically induced*; D007034:Hypothalamus, Posterior / Q000502:physiology; D008297:Male; D008526:Medulla Oblongata / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D011941:Receptors, Adrenergic / Q000502:physiology*; D011942:Receptors, Adrenergic, alpha / Q000502:physiology*; D013375:Substance Withdrawal Syndrome / Q000503:physiopathology*
chemical_list: D011941:Receptors, Adrenergic; D011942:Receptors, Adrenergic, alpha; D003000:Clonidine