Cyclosporine-induced hypertension is associated with sympathetic neural activation, which may be accentuated by the cardiac denervation that results from heart transplantation.

Microneurographic measurements of muscle sympathetic nerve activity (SNA) have suggested that, during static exercise, central command is much less important than skeletal muscle afferents in causing sympathetic neural activation. The possibility remains, however, that the sympathetic discharge produced by central commandis targeted mainly to tissues other than skeletal muscle. To examine this possibility, we recorded SNA with microelectrodes placed selectively in skin, as well as in muscle, nerve fascicles of the peroneal nerve during static handgrip maneuvers designed to separate the effects of central command from those of muscle afferents. To study the relative effects of cutaneous sympathetic activation on sudomotor versus vasomotor function, we simultaneously estimated changes in skin blood flow (laser Doppler velocimetry) and in sudomotor (electrodermal) activation in the region of skin innervated by the impaled nerve fascicle. Two minutes of static handgrip at 10%, 20%, and 30% of maximal voluntary contraction caused large and intensity-dependent increases in skin SNA. These increases in SNAimmediately preceded the onset of muscle tension, accelerated progressively during sustained handgrip, and resolved promptly with the cessation of motor effort. The handgrip-induced increases in skin SNA were not maintained when handgrip was followed by arrest of the forearm circulation, a maneuver that maintains the stimulation of chemically sensitive muscle afferents while eliminating theinfluences of central command and mechanically sensitive muscle afferents. During normothermia, static handgrip at 30% maximal voluntary contraction caused sustained increases in skin SNA (+400±83%, mean±SEM, p <0.05) and in electrodermal activity (+276±56%, p <0.05) but only transient increases in estimated skin vascular resistance (+ 11+2%, p<0.05). When skin temperature was increased or decreased to a new stable baseline level, subsequent increases in skin SNA during handgrip were accompanied by sustained but directionally opposite changes in estimated skin vascular resistance, with exercise-induced vasodilation during hyperthermia but exercise-induced vasoconstriction during hypothermia. From these observations, we conclude the following: 1) static exercise markedly increases sympathetic outflow to skin as well as to skeletal muscle; 2) the increases in skin SNA, unlike muscle SNA, appear to be caused mainly by central command rather than by muscle afferent reflexes; and 3) this cutaneous sympathetic activation appears to be targeted both to sweat glands and to vascular smooth muscle, with the relative targeting being temperature dependent. These findings provide neurophysiological evidencein humans to support the hypothesis that central command can be a potent stimulus to sympathetic outflow, and they emphasize the marked heterogeneity in the regulation of regional sympathetic discharge during exercise by central neural and peripheral reflex mechanisms. (Circulation Research 1991;69:228-238) A ctivation of the sympathetic ...

These results indicate a healthy worker effect among hairdressers diagnosed with eczema. Ammonium persulfate and p-phenylenediamine remain frequent sensitizers in hairdressers with contact dermatitis. Cysteamine hydrochloride and chloroacetamide should be included in future surveillance studies.

1. Haemodynamic studies in humans have concluded that the cutaneous circulation is regulated by cardiopulmonary baroreceptors. In contrast, neurophysiological studies have indicated that skin sympathetic outflow, unlike muscle sympathetic outflow, is unaffected by perturbations in baroreceptor activity. 2. Thus, in an attempt to resolve this discrepancy, both muscle and skin sympathetic nerve activity was recorded during unloading of mainly cardiopulmonary afferents with non-hypotensive lower body negative pressure (LBNP) performed in both normothermic and hyperthermic conditions. The function of the sympathetic activity was studied by estimations of skin blood flow (laser Doppler velocimetry), of calf blood flow (plethysmography) and of sudomotor activity (electrodermal responses). 3. A level of LBNP that caused robust increases in sympathetic outflow and vascular resistance in the skeletal muscle of the lower leg had no effect on sympathetic activity and vascular resistance in the skin of the same region in the same subjects. Both at normothermia and during hyperthermia LBNP decreased electrodermal activity. Experiments performed during sham LBNP and with skin temperature kept constant suggest that the electrodermal response was due to a decrease in skin temperature produced by the LBNP. 4. In conclusion, these findings challenge the concept that the cutaneous circulation participates importantly in the peripheral circulatory adjustments to unloading of cardiopulmonary afferents during orthostatic stress in humans. During nonhypotensive LBNP, the skeletal muscle constriction in the calf.

The cutaneous circulation is thought to participate in the neurocirculatory adjustments during orthostatic stress, but the underlying mechanisms mediating such reflex cutaneous vasoconstriction are poorly understood. The aim of this study was to assess the relative importance of baroreceptor (cardiopulmonary and arterial) and positional (vestibular, exercise, veno-arteriolar and myogenic) reflexes in triggering cutaneous vasoconstriction during upright posture. First, hypotensive lower body negative pressure (LBNP) was compared with actual postural changes to assess the relative contributions of baroreceptor reflexes and positional reflexes. Then changes in body position were compared with changes in limb position in the absence or presence of proximal (axillary) or distal (local cutaneous) nerve blocks, to assess the relative contributions of vestibular, exercise, veno-arteriolar and myogenic reflexes. Skin sympathetic nerve activity was determined by microneurography, and skin blood flow was determined by laser Doppler velocimetry. LBNP of -50 mm Hg cardiopulmonary + arterial baroreceptors) had no effect on skin sympathetic nerve activity or skin vascular resistance. In contrast, an upright posture with the arms dependent (baroreceptor + vestibular + exercise + veno-arteriolar reflexes) caused a two- to threefold increase in skin vascular resistance. In the supine position passive movement of the arm into a dependent position to activate veno-arteriolar reflexes alone evoked an increase in skin vascular resistance which approximated the response to normal upright posture. Blocking central sympathetic nerve impulses by application of an axillary blockade did not influence the cutaneous vasoconstrictor response to an upright posture or changes in limb position. In contrast, application of a distal nerve block by local cutaneous surface anaesthesia completely blocked vasoconstrictor responses evoked by these manoeuvres. In conclusion, these experiments in human subjects identify a primary role for veno-arteriolar reflexes in triggering vasoconstriction in the cutaneous circulation during upright posture.