title: Central attenuation of aortic baroreceptor reflex in prehypertensive DOCA-salt-loaded rats.
abstract: To determine whether the arterial baroreceptor reflex can act to oppose the development of hypertension, deoxycorticosterone acetate (DOCA)-salt hypertension was produced in sinoaortic-denervated and sham-operated rats. Systolic blood pressure measured by tail cuff started to increase in both sinoaortic-denervated and sham-operated rats 7 days after DOCA treatment, and the hypertension developed identically in both denervated and sham-operated rats. These findings suggest that the baroreceptor reflex cannot act against the development of hypertension. To determine whether the baroreceptor reflex is attenuated before the development of hypertension, bradycardiac and sympathoinhibitory responses to i.v. injections of norepinephrine were examined. Bradycardic and sympathoinhibitory responses were significantly smaller in DOCA-salt-treated rats in both prehypertensive (5th day after DOCA-salt treatment) and hypertensive stages (21st day after treatment). In urethane-anesthetized DOCA-loaded and control rats on the 5th day after treatment, aortic depressor nerve stimulation elicited frequency-dependent depressor and bradycardic responses accompanied by inhibition of sympathetic nerve activity in both DOCA-loaded and control rats. However, those responses were significantly smaller in DOCA-loaded rats than in control rats. These results suggest that the central component of the baroreceptor reflex mediated by the aortic depressor nerve is impaired before hypertension develops and that this impairment may contribute to the development of hypertension in DOCA-salt-treated rats.
authors.affiliation: Second Department of Internal Medicine, Kyoto Prefectural University of Medicine, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Nakamura
authors.forename: K
authors.initials: K
authors.lastname: Takeda
authors.forename: T
authors.initials: T
authors.lastname: Nakata
authors.forename: J
authors.initials: J
authors.lastname: Hayashi
authors.forename: S
authors.initials: S
authors.lastname: Kawasaki
authors.forename: L C
authors.initials: LC
authors.lastname: Lee
authors.forename: S
authors.initials: S
authors.lastname: Sasaki
authors.forename: M
authors.initials: M
authors.lastname: Nakagawa
authors.forename: H
authors.initials: H
authors.lastname: Ijichi
mesh_terms: D000818:Animals; D001011:Aorta / Q000294:innervation*; D001794:Blood Pressure; D001921:Brain / Q000502:physiology*; D002320:Cardiovascular Physiological Phenomena; D002319:Cardiovascular System / Q000187:drug effects; D003900:Desoxycorticosterone / Q000494:pharmacology*; D004558:Electric Stimulation; D006339:Heart Rate; D006973:Hypertension / Q000139:chemically induced*; D008297:Male; D009433:Neural Inhibition; D009638:Norepinephrine / Q000494:pharmacology; D011311:Pressoreceptors / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D012018:Reflex / Q000502:physiology*; D012965:Sodium Chloride / Q000494:pharmacology*; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000502:physiology
chemical_list: D003900:Desoxycorticosterone; D012965:Sodium Chloride; D009638:Norepinephrine