Effect of Temperature on Alpha-Adrenoceptor Affinity and Contractility of Rabbit Ear Blood Vessels

Roberts, Michel F.; Chilgren, John D.; Zygmunt, Andrew C.

doi:10.1159/000158767

Cited by 17 publications

(14 citation statements)

References 10 publications

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“…The physiological effects of local cooling have been established elsewhere [27][28][29][30][31][32][33][34][35][36][37][38][39]. It is generally known that the response to moderate local cooling is normally characterised by a decrease in skin blood flow, an increase of blood pressure, and a fall in HR.…”

Section: Discussionmentioning

confidence: 99%

“…At the cooling site (direct response of skin vessels) cold decreases the amount of norepinephrine released from nerve-endings [31], reduces the enzymatic breakdown of norepinephrine within the vessel wall [32], decreases smooth muscle contractility, diminishes the affinity of alpha1 adrenoceptors for norepinephrine [33][34][35], and stimulates the mobilization of alpha2c adrenoceptors from the Golgi apparatus to the vascular smooth muscle plasma membrane [36][37][38]. In contrast, at the site remote from the cooling (indirect response) the response mediated by the sympathetic vasomotor reflexes prevails [39].…”

Section: Introductionmentioning

confidence: 99%

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Microcirculation response to local cooling in patients with Huntington’s disease

et al. 2011

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Altered autonomic nervous system (ANS) functioning in early stages of Huntington's disease (HD) has been suggested, presumably due to distorted high-order autonomic control. ANS functioning in the early stages of HD was further investigated. Laser-Doppler (LD) flux in the skin of the fingertips, heart rate (HR), HR variability, systolic and diastolic blood pressure were measured during rest and during a 6 min cooling of one hand at 15°C. Data of 15 presymptomatic gene mutation carriers (PHD), 15 early symptomatic HD patients (EHD), and two groups of 15 age- and sex-matched controls were compared. The area under the low frequency (LF) and high frequency (HF) bands of the HR variability spectrum were calculated. An augmented reduction of cutaneous LD flux was found in response to the direct cooling in the PHD group (37.5 ± 8.5% of resting value) compared to the PHD controls (67.27 ± 8.4%) (p < 0.05). In addition, the PHD group had higher (LF/(LF + HF) index of primary sympathetic modulation of the HR at rest (53.6 ± 3.3) compared to the EHD patients (39.7 ± 4.2) (p < 0.05). In the EHD group, a significantly smaller change of HR during cooling (100.26 ± 1.2%) was found compared to the EHD controls (95.9 ± 1.0%) (p < 0.05). The results are in line with the hypothesis that ANS dysfunction occurs even in PHD subjects. Further, they support the hypothesis that dysfunction of the high-order autonomic centres are involved in HD.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Microcirculation response to local cooling in patients with Huntington’s disease

et al. 2011

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“…Less consistent are the effects of heating on vasoconstrictor responsiveness in isolated vessels of animals. For example, in isolated dog saphenous veins and isolated rabbit ear veins and arteries, vasoconstrictor responsiveness to ␣-adrenergic agents was reduced when the vessels were heated (2,20,30,31). On the other hand, in isolated rat mesenteric arteries, others have shown no effect of Fig.…”

Section: Discussionmentioning

confidence: 99%

Phenylephrine-induced elevations in arterial blood pressure are attenuated in heat-stressed humans

Cui

Wilson

Crandall

2002

American Journal of Physiology-Regulatory, Integrative and Comp

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To test the hypothesis that phenylephrine-induced elevations in blood pressure are attenuated in heat-stressed humans, blood pressure was elevated via steady-state infusion of three doses of phenylephrine HCl in 10 healthy subjects in both normothermic and heat stress conditions. Whole body heating significantly increased sublingual temperature by ϳ0.5°C, muscle sympathetic nerve activity (MSNA), heart rate, and cardiac output and decreased total peripheral vascular resistance (TPR; all P Ͻ 0.005) but did not change mean arterial blood pressure (MAP; P Ͼ 0.05). At the highest dose of phenylephrine, the increase in MAP and TPR from predrug baselines was significantly attenuated during the heat stress [⌬MAP 8.4 Ϯ 1.2 mmHg; ⌬TPR 0.96 Ϯ 0.85 peripheral resistance units (PRU)] compared with normothermia (⌬MAP 15.4 Ϯ 1.4 mmHg, ⌬TPR 7.13 Ϯ 1.18 PRU; all P Ͻ 0.001). The sensitivity of baroreflex control of MSNA and heart rate, expressed as the slope of the relationship between MSNA and diastolic blood pressure, as well as the slope of the relationship between heart rate and systolic blood pressure, respectively, was similar between thermal conditions (each P Ͼ 0.05). These data suggest that phenylephrine-induced elevations in MAP are attenuated in heat-stressed humans without affecting baroreflex control of MSNA or heart rate. baroreflex sensitivity; vasoconstrictor agents; muscle sympathetic nerve activity; heart rate; whole body heating EXPOSURE OF HUMANS to hyperthermic conditions leads to increases in skin blood flow, splanchnic and renal vascular resistances, heart rate, and cardiac output, while decreasing total peripheral resistance (TPR; Refs. 10, 21). These combined responses result in little or no change in mean arterial blood pressure (MAP), accompanied with pronounced decreases in central venous filling pressure (5,17,23).Humans become more susceptible to fainting during orthostatic stress and gravitation acceleration when combined with heat stress (1,14,34). A possible mechanism leading to heat-induced reductions in orthostatic tolerance is impaired baroreflex responsiveness.However, we and others have shown that whole body heating does not alter the maximal gain of baroreflex control of heart rate during carotid baroreceptor perturbations (4, 35) or during acute changes in arterial blood pressure (7,36). Moreover, the gain expressing the relationship between blood pressure and muscle sympathetic nerve activity (MSNA) was unaffected by whole body heating (7). In contrast, we reported that whole body heating impairs carotid baroreflex regulation of blood pressure (4), as well as reduces the transfer function gain of the relationship between spontaneous blood pressure and heart rate within the high-frequency range (6). Thus the effects of whole body heating on baroreflex function in humans may depend on the baroreceptor population assessed and/or the method of assessing baroreflex function.Sympathetic neural outflow plays a pivotal role in blood pressure control via baroreflexes. Sympathetic adrenergic nerves...

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“…Several additional factors associated with exercise, such as a decrease in pH (53), an increase in circulating norepinephrine, an increase in body temperature (49) during and after exercise, and vasodilator prostaglandins (56), may also contribute to the attenuated vasoconstrictor responses to PE in the postexercise condition. However, results from this study suggest that NO is the major mediator responsible for postexercise ␣ 1 -adrenergic receptor hyporesponsiveness.…”

Section: Discussionmentioning

confidence: 99%

Postexercise α-adrenergic receptor hyporesponsiveness in hypertensive rats is due to nitric oxide

Rao

Collins

DiCarlo

2002

American Journal of Physiology-Regulatory, Integrative and Comp

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.-We tested the hypothesis that a single bout of dynamic exercise produces a postexercise hypotension (PEH) and ␣ 1-adrenergic receptor hyporesponsiveness in spontaneously hypertensive rats (SHR). The postexercise ␣1-adrenergic receptor hyporesponsiveness is due to an enhanced buffering of vasoconstriction by nitric oxide. Male (n ϭ 8) and female (n ϭ 5) SHR were instrumented with a Doppler ultrasonic flow probe around the femoral artery. Distal to the flow probe, a microrenathane catheter was inserted into a branch of the femoral artery for the infusion of the ␣ 1-adrenergic receptor agonist phenylephrine (PE). A microrenathane catheter was inserted into the descending aorta via the left common carotid artery for measurements of arterial pressure (AP) and heart rate. Dose-response curves to PE (3.8 ϫ 10 Ϫ3 Ϫ 1.98 ϫ 10 Ϫ2 g/kHz) were generated before and after a single bout of dynamic exercise. Postexercise AP was reduced in male (13 Ϯ 3 mmHg) and female SHR (18 Ϯ 7 mmHg). Postexercise vasoconstrictor responses to PE were reduced in males due to an enhanced influence of nitric oxide. However, in females, postexercise vasoconstrictor responses to PE were not altered. Results suggest that nitric oxidemediated ␣1-adrenergic receptor hyporesponsiveness contributes to PEH in male but not female SHR. vascular function; gender; arterial pressure; adrenergic receptors FIFTY MILLION AMERICANS HAVE hypertension or are taking antihypertensive medications (30). The morbidity and mortality associated with cardiovascular disease increase exponentially with increasing levels of arterial pressure (AP) (18). Thus interventions designed to lower AP are being vigorously investigated (13, 51). It is well documented that a single bout of dynamic exercise reduces postexercise AP for several hours (11,20,31). Thus acute exercise may be a safe therapeutic approach for lowering AP in hypertensive individuals.The mechanisms mediating postexercise hypotension (PEH) remain the focus of numerous investigative efforts (7,22,35,55). It is generally accepted that PEH is most often associated with elevations in cardiac output (CO) as well as reductions in peripheral vascular resistance (22,24,35) and sympathetic nerve activity (SNA) (16,22,24,35). The postexercise reduction in peripheral vascular resistance may be due to the reduction in SNA as well as a decreased vascular responsiveness to ␣-adrenergic receptor activation. This is suggested because recent evidence has shown that a single bout of dynamic exercise significantly attenuates the vasoconstrictor response to phenylephrine (PE) in an isolated aortic ring preparation (29) and in the intact conscious normotensive rabbit (28) and rat (45). Furthermore, Halliwill and colleagues (22) reported that sympathetic activity is reduced and the transduction of sympathetic activity into vascular resistance is attenuated after dynamic exercise. These data suggest that the ability of the vasculature to respond to a change in SNA or a sustained catecholamine increase after exercise is significantly re...

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Effect of Temperature on Alpha-Adrenoceptor Affinity and Contractility of Rabbit Ear Blood Vessels

Cited by 17 publications

References 10 publications

Microcirculation response to local cooling in patients with Huntington’s disease

Microcirculation response to local cooling in patients with Huntington’s disease

Phenylephrine-induced elevations in arterial blood pressure are attenuated in heat-stressed humans

Postexercise α-adrenergic receptor hyporesponsiveness in hypertensive rats is due to nitric oxide

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