We sought to identify whether reductions in cutaneous active vasodilation during simulated orthostasis could be assigned solely to cardiopulmonary or to carotid baroreflexes by unloading cardiopulmonary baroreceptors with low levels of lower body negative pressure (LBNP) or unloading carotid baroreceptors with external pressure applied over the carotid sinus area [carotid pressure (CP)]. Skin blood flow was measured at a site at which adrenergic function was blocked via bretylium tosylate iontophoresis and at an unblocked site. During LBNP of -5 and -10 mmHg in hyperthermia, neither heart rate (HR) nor cutaneous vascular conductance (CVC) at either site changed (P > 0.05 for both), whereas forearm vascular conductance (FVC) was reduced (-5 mmHg: from 21.6 +/- 4.8 to 19.8 +/- 4.1 FVC units, P = 0.05; -10 mmHg: from 22.3 +/- 4.0 to 19.3 +/- 3.7 FVC units, P = 0.002). LBNP of -30 mmHg in hyperthermia reduced CVC at both sites (untreated: from 51.9 +/- 5.7 to 43.2 +/- 5.1% maximum, P = 0.02; bretylium tosylate: from 60.9 +/- 5.4 to 53.2 +/- 4.4% maximum, P = 0.02), reduced FVC (from 23.2 +/- 3.6 to 18.1 +/- 3.3 FVC units; P = 0.002), and increased HR (from 83 +/- 4 to 101 +/- 3 beats/min; P = 0.003). Pulsatile CP (45 mmHg) did not affect FVC or CVC during normothermia or hyperthermia (P > 0.05). However, HR and mean arterial pressure were elevated during CP in both thermal conditions (both P < 0.05). These results suggest that neither selective low levels of cardiopulmonary baroreceptor unloading nor selective carotid baroreceptor unloading can account for the inhibition of cutaneous active vasodilator activity seen with simulated orthostasis.