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(Hypertension. 2003;42:974.)
© 2003 American Heart Association, Inc.
Scientific Contributions |
From Circulatory Control Laboratory, Department of Physiology, University of Auckland, Auckland, New Zealand.
Correspondence to Dr Simon C. Malpas, Circulatory Control Laboratory, Department of Physiology, University of Auckland Medical School, Private Bag 92019, Auckland, New Zealand. E-mail s.malpas{at}auckland.ac.nz
Although the vascular action of endothelium-derived nitric oxide in modulating arterial pressure is well established, nitric oxide can also act as a neurotransmitter in the central nervous system. In addition, there is evidence for an interaction between nitric oxide and baroreceptor afferent processing; thus, nitric oxide may regulate blood pressure through central modulation of arterial baroreflexes. To test this possible interaction of nitric oxide and baroreflexes in the long-term regulation of blood pressure, we measured arterial pressure and heart rate responses to nitric oxide blockade by using L-NAME (50 mg/kg per day in drinking water) over 7 days in baroreceptor intact and sinoaortic denervated conscious rabbits. In the baroreceptor intact animals, blockade of nitric oxide leads to a significant increase in mean arterial pressure (from 75±2 to 84±3 mm Hg) and decrease in heart rate (from 233±8 to 195±8 bpm) that was sustained over the 7 days of nitric oxide blockade. In the sinoaortic denervated animals, blockade of nitric oxide initially led to a similar increase in arterial pressure (82±3 mm Hg on the second day), but in all sinoaortic denervated animals this increase was not sustained and recovered back to preL-NAME levels. This finding indicates that baroreflexes play an important role in the long-term control of blood pressure, and, second, that one mediator of this control is nitric oxide.
Key Words: baroreflex sympathetic nervous system blood pressure hypertension, chronic nitric oxide
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