Role of sympathetic nerves in the vascular effects of local temperature in human forearm skin

Pèrgola, Pablo E.; Kellogg, Dean L.; Johnson, John M.; Kosiba, Wojciech A.; Solomon, Dale

doi:10.1152/ajpheart.1993.265.3.h785

Cited by 155 publications

(219 citation statements)

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“…In a recent epidemiological study carried out in a representative urban Swiss population (age: 20 -40 yr) it could be shown that ϳ30% of women exhibit a VS, in contrast to only 7% of men, and that the relative risk of DIS in these subjects is doubled (34 and Kräuchi K, Fontana P, Vollenweider S, von Arb M, Dubler B, Orgül S, Flammer J, Zemp-Stutz E, unpublished observations). This large survey confirmed our previous findings in a small sample of women with VS and normal tension glaucoma who exhibited significantly prolonged sleep-onset latency (SOL) compared with controls (51,53). Therefore, prolonged SOL in these subjects could be associated with their impaired capacity for distal vasodilatation and heat loss before habitual bedtime (34).…”

supporting

confidence: 87%

Chronobiological characterization of women with primary vasospastic syndrome: body heat loss capacity in relation to sleep initiation and phase of entrainment

Vollenweider

Wirz‐Justice²,

Orgül³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Women with primary vasospastic syndrome (VS), but otherwise healthy, exhibit a functional disorder of vascular regulation (main symptom: cold extremities) and often suffer from difficulties initiating sleep (DIS). Diverse studies have shown a close association between distal vasodilatation before lights off and a rapid onset of sleep. Therefore, we hypothesized that DIS in women with VS could be due to a reduced heat loss capacity in the evening, i.e., subjects are physiologically not ready for sleep. The aim of the study was to elucidate whether women having both VS and DIS (WVD) or not (controls) show different circadian characteristics (e.g., phase delay of the circadian thermoregulatory system with respect to the sleep-wake cycle). Healthy young women ( n = 9 WVD and n = 9 control) completed a 40-h constant routine protocol (adjusted to habitual bedtime) before and after an 8-h sleep episode. Skin temperatures [off-line calculated as distal-proximal skin temperature gradient (DPG)] and core body temperature (CBT; rectal) were continuously recorded. Half-hourly saliva samples were collected for melatonin assay and subjective sleepiness was assessed on the Karolinska Sleepiness Scale (KSS). Compared with control, WVD showed no differences in habitual bed times, but a 1-h circadian phase delay of dim light-melatonin onset (hours after lights on: WVD 14.6 ± 0.3 h; control 13.5 ± 0.2 h; P = 0.01). Similar phase shifts were observed in CBT, DPG, and KSS ratings. In conclusion, WVD exhibit a phase delay of the endogenous circadian system with respect to their habitual sleep-wake cycle, which could be a cause of DIS.

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supporting

confidence: 87%

Chronobiological characterization of women with primary vasospastic syndrome: body heat loss capacity in relation to sleep initiation and phase of entrainment

Vollenweider

Wirz‐Justice²,

Orgül³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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“…This resulted in higher CVC values at untreated sites in T2DM patients, suggesting decreased resting sympathetic vasoconstrictor tone in the patient group (13,16). However, vasoconstrictor responses to body cooling were similar to controls, suggesting that the response of the system to thermal stimuli was not changed.…”

Section: Discussionmentioning

confidence: 91%

Delayed threshold for active cutaneous vasodilation in patients with Type 2 diabetes mellitus

Wick¹,

Roberts

Basu³

et al. 2006

Journal of Applied Physiology

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Delayed threshold for active cutaneous vasodilation in patients with Type 2 diabetes mellitus. J Appl Physiol 100: 637-641, 2006. First published October 6, 2005 doi:10.1152/japplphysiol.00943.2005.-Epidemiological evidence suggests decreased heat tolerance in patients with Type 2 diabetes mellitus (T2DM), but it is not known whether the mechanisms involved in thermoregulatory control of skin blood flow are altered in these patients. We tested the hypothesis that individuals with T2DM have a delayed internal temperature threshold for active cutaneous vasodilation during whole body heating compared with healthy control subjects. We measured skin blood flow using laser-Doppler flowmetry (LDF), internal temperature (T or) via sublingual thermocouple, and mean arterial pressure via Finometer at baseline and during whole body heating in 9 T2DM patients and 10 control subjects of similar age, height, and weight. At one LDF site, sympathetic noradrenergic neurotransmission was blocked by local pretreatment with bretylium tosylate (BT) to isolate the cutaneous active vasodilator system. Whole body heating was conducted using a water-perfused suit. There were no differences in preheating T or between groups (P Ͼ 0.10). Patients with T2DM exhibited an increased internal temperature threshold for the onset of vasodilation at both untreated and BT-treated sites. At BT-treated sites, T or thresholds were 36.28 Ϯ 0.07°C in controls and 36.55 Ϯ 0.05°C in T2DM patients (P Ͻ 0.05), indicating delayed onset of active vasodilation in patients. Sensitivity of vasodilation was variable in both groups, with no consistent difference between groups (P Ͼ 0.05). We conclude that altered control of active cutaneous vasodilation may contribute to impaired thermoregulation in patients with T2DM. temperature regulation; sweating; metabolic disorders IN RECENT YEARS, THE INCIDENCE of Type 2 diabetes mellitus (T2DM) has reached epidemic proportions in the United States and other developed countries (24), leading to increasing interest in mechanisms of metabolic, cardiovascular, and neurological dysfunction in this disease. Importantly, dysfunction in some or all of these areas can lead to significant impairment in mechanisms of thermoregulation, which itself can cause increased morbidity and mortality in patients with T2DM. Epidemiological data indicate that individuals with diabetes are at significantly higher risk for heat illness during heat waves compared with the general population (19,20). Although physiological/pathophysiological mechanisms are not well understood, some existing data are consistent with the potential for impaired thermoregulation. For example, diabetic patients with length-dependent peripheral neuropathy exhibit impaired sweating in affected areas (7,14). Furthermore, individuals with diabetes have been shown to have decreased vasodilator responsiveness to pharmacological stimuli in vascular beds, including the skin (3,11,21,22). Such peripheral impairments could lead to a decrease in the ability of the cutaneous vascu...

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“…Postsynaptic ␣ 2 -adrenergic receptors have an enhanced affinity for norepinephrine, perhaps mediated through translocation of ␣ 2C -receptors to the membrane through a Rho kinase mechanism, and there is an increased ␣ 1 -receptor reserve, these effects countering negative effects of cooling on norepinephrine synthesis and release and on contractile function (2,4,6,29,41). Previous studies in our laboratory show that presynaptic blockade of sympathetic vasoconstrictor nerves with bretylium, applied to the intact skin iontophoretically, reverses the initial vasoconstrictor response to local cooling to one of vasodilation (31) and reverses the inhibition by local cooling of reflex cutaneous vasodilation (30). The implication is that local skin cooling may enhance or stimulate transmitter release from sympathetic vasoconstrictor nerve endings in the skin.…”

mentioning

confidence: 82%

Sympathetic, sensory, and nonneuronal contributions to the cutaneous vasoconstrictor response to local cooling

Johnson¹,

Yen²,

Zhao³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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Sympathetic, sensory, and nonneuronal contributions to the cutaneous vasoconstrictor response to local cooling. Am J Physiol Heart Circ Physiol 288: H1573-H1579, 2005. First published December 2, 2004; doi:10.1152/ajpheart.00849.2004.-Previous work indicates that sympathetic nerves participate in the vascular responses to direct cooling of the skin in humans. We evaluated this hypothesis further in a four-part series by measuring changes in cutaneous vascular conductance (CVC) from forearm skin locally cooled from 34 to 29°C for 30 min. In part 1, bretylium tosylate reversed the initial vasoconstriction (Ϫ14 Ϯ 6.6% control CVC, first 5 min) to one of vasodilation (ϩ19.7 Ϯ 7.7%) but did not affect the response at 30 min (Ϫ30.6 Ϯ 9% control, Ϫ38.9 Ϯ 6.9% bretylium; both P Ͻ 0.05, P Ͼ 0.05 between treatments). In part 2, yohimbine and propranolol (YP) also reversed the initial vasoconstriction (Ϫ14.3 Ϯ 4.2% control) to vasodilation (ϩ26.3 Ϯ 12.1% YP), without a significant effect on the 30-min response (Ϫ26.7 Ϯ 6.1% YP, Ϫ43.2 Ϯ 6.5% control; both P Ͻ 0.05, P Ͼ 0.05 between sites). In part 3, the NPY Y1 receptor antagonist BIBP 3226 had no significant effect on either phase of vasoconstriction (P Ͼ 0.05 between sites both times). In part 4, sensory nerve blockade by anesthetic cream (Emla) also reversed the initial vasoconstriction (Ϫ20.1 Ϯ 6.4% control) to one of vasodilation (ϩ213.4 Ϯ 87.0% Emla), whereas the final levels did not differ significantly (Ϫ37.7 Ϯ 10.1% control, Ϫ37.2 Ϯ 8.7% Emla; both P Ͻ 0.05, P Ͼ 0.05 between treatments). These results indicate that local cooling causes cold-sensitive afferents to activate sympathetic nerves to release norepinephrine, leading to a local cutaneous vasoconstriction that masks a nonneurogenic vasodilation. Later, a vasoconstriction develops with or without functional sensory or sympathetic nerves.human; peripheral circulation; local control of blood flow; skin circulation; microdialysis; iontophoresis; neuropeptide Y; norepinephrine; axon reflex THE CONTROL OF SKIN BLOOD FLOW in humans involves several mechanisms. Reflex control occurs through a vasoconstrictor pathway and through an independent active vasodilator system (18, 33). These systems are both known to be sympathetic in origin. In the case of the vasoconstrictor system, the transmitters appear to be norepinephrine and one or more cotransmitters (26 -27, 36, 37, 39 -40). The active vasodilator mechanism is less well defined but appears to be cholinergic and also to involve a cotransmitter, perhaps vasoactive intestinal polypeptide (3, 21).Local thermal control of skin blood flow has also been the subject of considerable attention. Direct local warming of the skin leads to a vasodilation that involves nitric oxide and sensory nerves (20,25,38). With respect to direct local cooling, several lines of evidence point to an involvement of the sympathetic vasoconstrictor system in the reduction of skin blood flow. Postsynaptic ␣ 2 -adrenergic receptors have an enhanced affinity for norepinephrine, perhaps mediated th...

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Role of sympathetic nerves in the vascular effects of local temperature in human forearm skin

Cited by 155 publications

References 0 publications

Chronobiological characterization of women with primary vasospastic syndrome: body heat loss capacity in relation to sleep initiation and phase of entrainment

Chronobiological characterization of women with primary vasospastic syndrome: body heat loss capacity in relation to sleep initiation and phase of entrainment

Delayed threshold for active cutaneous vasodilation in patients with Type 2 diabetes mellitus

Sympathetic, sensory, and nonneuronal contributions to the cutaneous vasoconstrictor response to local cooling

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