Previously, we showed that the cutaneous active vasodilator system can be modulated by baroreceptor unloading with 40 mmHg lower body negative pressure (LBNP). Could arterial baroreceptor unloading have caused this response? The purpose of the present study was to test whether carotid baroreceptors are capable of modulating active cutaneous vasodilation. To address this question, carotid baroreceptors were unloaded by 45 mmHg pulsatile neck pressure while forearm skin blood flow was monitored by laser-Doppler flowmetry (LDF) at a 0.6 cm site at which adrenergic vasoconstrictor function was blocked via bretylium tosylate (BT) iontophoresis and at an unblocked site. Each 3 min trial was conducted in normothermia (NT) and hyperthermia (HT). Cutaneous vascular conductance (CVC) was estimated from the ratio of LDF and mean arterial pressure (MAP) and expressed as a percentage of maximal CVC at that site (%CVCmax). Carotid baroreceptor unloading did not significantly change CVC at either site in NT (untreated: 20±4 to 22±5 %CVCmax; BT-treated: 24±4 to 24±4 %CVCmax) or HT (untreated: 77±6 to 75±6 %CVCmax: BT-treated: 63±5 to 65±6 %CVCmax). During both thermal conditions significant elevations in heart rate (NT: 66±6 to 70±5 bpm; HT: 87±7 to 95±6 bpm) and MAP (NT: 90±3 to 99±4 mmHg; HT: 78±4 to 89±4 mmHg) were observed by carotid unloading, demonstrating that a carotid baroreflex had been evoked. These results suggest that reductions in CVC during 40 mmHg LBNP cannot be attributed to only carotid baroreceptor unloading.
|Original language||English (US)|
|State||Published - Dec 1 1996|
ASJC Scopus subject areas
- Molecular Biology