Why the study?
Does central administration of Angiotensin II attenuate baroreflex responses in normotensive and spontaneously hypertensive rats?
Does central administration of Angiotensin II attenuate baroreflex responses in normotensive and spontaneously hypertensive rats?
Central Angiotensin II attenuates baroreflex responses independently of vasopressin, contributing to central baroreflex resetting in spontaneously hypertensive rats.
Central Ang II baroreflex attenuation in rats merits human studies; leaves open its contribution to clinical hypertension.
To determine whether angiotensin II (A II) can modify baroreflex centrally and contribute to the central resetting of baroreflex in spontaneously hypertensive rats (SHRs), the aortic depressor nerve (ADN) was electrically stimulated following intracerebroventricular (ICV) administration of A II and/or A II analog in urethane-anesthetized normotensive Wistar rats (WKYs) and SHRs. Electric stimulation of the ADN elicited frequency-dependent depressor, bradycardic, and sympatho-inhibitory responses. Angiotensin II, administered ICV, dose-dependently attenuated these responses induced by ADN stimulation in normotensive rats. We found, however, these attenuations could be abolished by ICV pretreatment with A II analog. Vasopressin (ICV) did not change any responses to ADN stimulation. The vasopressor and sympatho-inhibitory responses to ADN stimulation were significantly less in SHRs when compared with those in WKYs: In SHRs, A II analog completely cancelled the A II-attenuated responses to ADN stimulation. These findings suggest that A II can centrally attenuate baroreflex, which might be independent from vasopressin, and in the brain A II can contribute to the central resetting of baroreflex in SHRs.
No takes yet. Share an insight, caveat, or question.
Hayashi et al. (1988) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: