Baroreflex control of regional vascular resistances during simulated orthostatism

Orthostatic stress or moderate hypovolemia was simulated in 10 healthy volunteers by the lower body negative pressure technique (LBNP at -10, -20 and -40 mm Hg). LBNP induced a progressive and parallel decrease in central venous pressure and cardiac output but mean arterial pressure remained unchanged regardless of the LBNP level. Heart rate and pulse pressure were only significantly increased and decreased at LBNP -40 mm Hg, respectively, indicating that cardiopulmonary baroreflexes were selectively deactivated up to LBNP -20 mm Hg, whereas both cardiopulmonary and arterial baroreflexes were deactivated at LBNP -40 mm Hg. The LBNP-induced increase in total peripheral resistance was heterogeneously distributed within the body. Forearm vasoconstriction occurred at low levels of LBNP and was exclusively related to an increase in sympathetic tone. Splanchnic vasoconstriction also occurred at low levels of LBNP, but was related to activation in sympathetic and renin-angiotensin systems. Renal vasoconstriction occurred mainly at high levels of LBNP (-40 mm Hg), but glomerular filtration rate and filtration fraction increased at low levels of LBNP (-10 mm Hg). Thus, if renal vascular resistance is not of major importance for the control of blood pressure during orthostatism or moderate hypovolemia, neurohumoral mechanisms triggered through deactivation of cardiopulmonary receptors play a key role in the maintenance of intrarenal homeostasis associated with reduction in cardiac filling pressure.