BARORECEPTOR CONTROL OF THE CUTANEOUS ACTIVE VASODILATOR SYSTEM

We sought to identify whether reductions in cutaneous active vasodilat ion during simulated orthostasis could be assigned solely to cardiopul monary or to carotid baroreflexes by unloading cardiopulmonary barorec eptors with low levels of lower body negative pressure (LBNP or unload ing carotid baroreceptors with external pressure applied over the caro tid sinus area [carotid pressure (CP)]. Skin blood flow was measured a t a site at which adrenergic function was blocked via bretylium tosyla te iontophoresis and at an unblocked site. During LBNP of -5 and -10 m mHg in hyperthermia, neither heart rate (HR) nor cutaneous vascular co nductance (CVC) at either site changed (P > 0.05 for both), whereas fo rearm 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 +/- 8.3 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 me an arterial pressure were elevated during CP in both thermal condition s (both P < 0.05). These results suggest that neither selective low le vels of cardiopulmonary baroreceptor unloading nor selective carotid b aroreceptor unloading can account for the inhibition of cutaneous acti ve vasodilator activity seen with simulated orthostasis.