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Front Physiol. 2012 Dec 7;3:461. doi: 10.3389/fphys.2012.00461. eCollection 2012.

The arterial baroreflex resets with orthostasis.

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Department of Physiology, The Center for Hypotension, New York Medical College Valhalla, NY, USA ; Department of Pediatrics, The Center for Hypotension, New York Medical College Valhalla, NY, USA.


The arterial baroreflexes, located in the carotid sinus and along the arch of the aorta, are essential for the rapid short term autonomic regulation of blood pressure. In the past, they were believed to be inactivated during exercise because blood pressure, heart rate, and sympathetic activity were radically changed from their resting functional relationships with blood pressure. However, it was discovered that all relationships between carotid sinus pressure and either HR or sympathetic vasoconstriction maintained their curvilinear sigmoidal shape but were reset or shifted so as to best defend BP during exercise. To determine whether resetting also occurs during orthostasis, we examined the arterial baroreflexes measured supine and upright tilt. We studied the relationships between systolic BP and HR (the cardiovagal baroreflex), mean BP, and ventilation (the ventilatory baroreflex) and diastolic BP and sympathetic nerve activity (the sympathetic baroreflex). We accomplished these measurements by using the modified Oxford method in which BP was rapidly varied with bolus injections of sodium nitroprusside followed 1 min later by bolus injections of phenylephrine. Both the cardiovagal and ventilatory baroreflexes were "reset" with no change in gain or response range. In contrast, the sympathetic baroreflex was augmented as well as shifted causing an increase in peripheral resistance that improved the subjects' defense against hypotension. This contrasts with findings during exercise in which peripheral resistance in active skeletal muscle is not increased. This difference is likely selective for exercising muscle and may represent the actions of functional sympatholysis by which exercise metabolites interfere with adrenergic vasoconstriction.


cardiovascular regulation; heart rate; standing; sympathetic nerve activity; ventilation

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