scholarly journals Hyperinsulinemia blunts sympathetic vasoconstriction: A possible role of β-adrenergic activation

2021 ◽  
Author(s):  
Jaqueline K. Limberg ◽  
Rogerio Nogueira Soares ◽  
Gavin Power ◽  
Jennifer L. Harper ◽  
James A. Smith ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Cold Pressor Test ◽  
Peripheral Resistance ◽  
Cold Pressor ◽  
Insulin Stimulation ◽  
Sympathetic Vasoconstriction ◽  
Sympathetic Nervous ◽  
Isolated Arteries ◽  
Adrenergic Activation

Herein we report in a sample of healthy young men (n=14) and women (n=12) that hyperinsulinemia induces time-dependent decreases in total peripheral resistance and its contribution to the maintenance of blood pressure. In the same participants, we observe profound vasodilatory effects of insulin in the lower limb despite concomitant activation of the sympathetic nervous system. We hypothesized this prominent peripheral vasodilation is possibly due to an ability of the leg vasculature to escape sympathetic vasoconstriction during systemic insulin stimulation. Consistent with this notion, we demonstrate in a subset of healthy men (n=9) and women (n=7) that systemic infusion of insulin blunts sympathetically-mediated leg vasoconstriction evoked by a cold pressor test, a well-established sympathoexcitatory stimulus. Further substantiating this observation, we show in mouse aortic rings that insulin exposure suppresses epinephrine and norepinephrine-induced vasoconstriction. Notably, we found that such insulin-suppressing effects on catecholamine-induced constriction are diminished following β-adrenergic receptor blockade. In accordance, we also reveal that insulin augments β-adrenergic-mediated vasodilation in isolated arteries. Collectively, these findings support the idea that sympathetic vasoconstriction can be attenuated during systemic hyperinsulinemia in the leg vasculature of both men and women and that this phenomenon may be in part mediated by potentiation of β-adrenergic vasodilation neutralizing α-adrenergic vasoconstriction.

The Arg16/Gly β2-adrenergic receptor polymorphism is associated with altered cardiovascular responses to isometric exercise

2004 ◽  
Vol 16 (3) ◽  
pp. 323-328 ◽  
Author(s):  
John H. Eisenach ◽  
Antonio M. McGuire ◽  
Rachel M. Schwingler ◽  
Stephen T. Turner ◽  
Michael J. Joyner
Keyword(s):  
Adrenergic Receptor ◽  
Pressor Response ◽  
Isometric Exercise ◽  
Cold Pressor Test ◽  
Peripheral Resistance ◽  
Cold Pressor ◽  
Cardiovascular Responses ◽  
Amino Acid Position ◽  
Gene Encoding ◽  
Time Interaction

A polymorphism in the gene encoding the β2-adrenergic receptor (arginine or glycine at amino acid position 16) is associated with altered vasodilator responses to β2-agonists, which may modulate the pressor response to endogenous catecholamines during stress. To test the hypothesis that the Arg16/Gly polymorphism is associated with differences in acute pressor responses to sympathoexcitation, we measured mean arterial pressure (MAP, Finapres) and heart rate (HR, ECG) during mental stress (MS), cold pressor test (CPT), and handgrip (HG) to fatigue in 31 healthy, nonobese, normotensive adults (mean age ± SE: 31 ± 1; 16 females). Subjects were homozygous for Gly16 ( n = 16) or Arg16 ( n = 15). Both groups had similar baseline MAP (Arg16, 86 ± 3 mmHg; Gly16, 89 ± 2 mmHg; P = 0.4) and HR (Arg16, 68 ± 2 beats/min; Gly16, 65 ± 3 beats/min; P = 0.3). For MS and CPT, MAP and HR did not differ between genotype groups. Handgrip also produced similar increases in MAP; however, the change in HR was greater in the Gly16 homozygotes ( PANOVA = 0.001, genotype-by-time interaction). During HG, peak HR at fatigue was 100 ± 4 beats/min for Gly16 (54% increase from rest) vs. 93 ± 3 beats/min for Arg16 (37% increase). We conclude that the cardiovascular responses to MS and CPT do not differ between Gly16 and Arg16 homozygotes. However, the greater HR response to exercise in the Gly16 homozygotes may serve to maintain the pressor response (increased cardiac output) in the face of augmented peripheral vasodilation (decreased total peripheral resistance) in this group.

Hemodynamic and neural mechanisms of acute neurogenic hypertension in the rat

1984 ◽  
Vol 247 (6) ◽  
pp. H991-H998 ◽  
Author(s):  
A. H. Werber ◽  
W. J. Bryan ◽  
G. D. Fink
Keyword(s):  
Peripheral Resistance ◽  
Neural Mechanisms ◽  
Acute Hypertension ◽  
Neurogenic Hypertension ◽  
Sympathetic Vasoconstriction ◽  
Induced Hypertension ◽  
Before And After ◽  
Autonomic Blockade ◽  
Sympathetic Nervous

Experiments were performed to test the hypothesis that acute hypertension caused by aortic baroreceptor deafferentation (ABD) is the result of sympathetic vasoconstriction. Cardiac output (CO), mean arterial pressure (MAP), and total peripheral resistance (TPR) were measured before and after ABD in anesthetized and conscious rats. The role of the sympathetic nervous system in acute ABD-induced hypertension was evaluated by examining the ability of adrenalectomy, adrenal demedullation, guanethidine or combined adrenal demedullation, and guanethidine pretreatment to prevent, and total autonomic blockade to reverse, ABD-induced hypertension. CO did not change significantly after ABD at any time, whereas MAP and TPR increased significantly (P less than 0.05). Only combined adrenal demedullation and guanethidine pretreatment prevented ABD-induced hypertension, and autonomic blockade normalized MAP in ABD rats. Normalization of blood pressure was the result of a decreased TPR. It is concluded that acute ABD-induced hypertension results from vasoconstriction caused by neurally released and/or circulating catecholamines.

scholarly journals The expanding role of the cold pressor test: a brief history

2021 ◽  
Author(s):  
Guillaume Lamotte ◽  
Christopher J. Boes ◽  
Phillip A. Low ◽  
Elizabeth A. Coon
Keyword(s):  
Cold Pressor Test ◽  
Cold Pressor ◽  
Pressor Test

scholarly journals Blunted cardiovascular responses to exercise in Parkinson’s disease patients: role of the muscle metaboreflex

2018 ◽  
Vol 120 (4) ◽  
pp. 1516-1524 ◽  
Author(s):  
Jeann L. Sabino-Carvalho ◽  
André L. Teixeira ◽  
Milena Samora ◽  
Maurício Daher ◽  
Lauro C. Vianna
Keyword(s):  
Blood Pressure ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cold Pressor Test ◽  
Peripheral Resistance ◽  
Cold Pressor ◽  
Cardiovascular Responses ◽  
Group Differences ◽  
Muscle Metaboreflex ◽  
Pressor Test

Patients with Parkinson’s disease (PD) exhibit attenuated cardiovascular responses to exercise. The underlying mechanisms that are potentially contributing to these impairments are not fully understood. Therefore, we sought to test the hypothesis that patients with PD exhibit blunted cardiovascular responses to isolated muscle metaboreflex activation following exercise. For this, mean blood pressure, cardiac output, and total peripheral resistance were measured using finger photoplethysmography and the Modelflow method in 11 patients with PD [66 ± 2 yr; Hoehn and Yahr score: 2 ± 1 a.u.; time since diagnosis: 7 ± 1 yr; means ± SD) and 9 age-matched controls (66 ± 3 yr). Measurements were obtained at rest, during isometric handgrip exercise performed at 40% maximal voluntary contraction, and during postexercise ischemia. Also, a cold pressor test was assessed to confirm that blunted cardiovascular responses were specific to exercise and not representative of generalized sympathetic responsiveness. Changes in mean blood pressure were attenuated in patients with PD during handgrip (PD: ∆25 ± 2 mmHg vs. controls: ∆31 ± 3 mmHg; P < 0.05), and these group differences remained during postexercise ischemia (∆17 ± 1 mmHg vs. ∆26 ± 1 mmHg, respectively; P < 0.01). Additionally, changes in total peripheral resistance were attenuated during exercise and postexercise ischemia, indicating blunted reflex vasoconstriction in patients with PD. Responses to cold pressor test did not differ between groups, suggesting no group differences in generalized sympathetic responsiveness. Our results support the concept that attenuated cardiovascular responses to exercise observed in patients with PD are, at least in part, explained by an altered skeletal muscle metaboreflex. NEW & NOTEWORTHY Patients with Parkinson’s disease (PD) presented blunted cardiovascular responses to exercise. We showed that cardiovascular response evoked by the metabolic component of the exercise pressor reflex is blunted in patients with PD. Furthermore, patients with PD presented similar pressor response during the cold pressor test compared with age-matched controls. Altogether, our results support the hypothesis that attenuated cardiovascular responses to exercise observed in patients with PD are mediate by an altered skeletal muscle metaboreflex.

The role of adrenal medullary catecholamine release in the response to a cold pressor test

1983 ◽  
Vol 17 (4) ◽  
pp. 189-191 ◽  
Author(s):  
M. F CUMMINGS ◽  
P. M STEELE ◽  
L. J M MAHAR ◽  
D. B FREWIN ◽  
W J. RUSSELL
Keyword(s):  
Cold Pressor Test ◽  
Cold Pressor ◽  
Catecholamine Release ◽  
Pressor Test

scholarly journals Exercise hyperemia and vasoconstrictor responses in humans with cystic fibrosis

2005 ◽  
Vol 99 (5) ◽  
pp. 1866-1871 ◽  
Author(s):  
William G. Schrage ◽  
Brad W. Wilkins ◽  
Vicki L. Dean ◽  
John P. Scott ◽  
Nancy K. Henry ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cystic Fibrosis ◽  
Blood Flow ◽  
Forearm Blood Flow ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Pressor Test ◽  
Sympathetic Vasoconstriction ◽  
Exercise Hyperemia ◽  
Forearm Exercise

ATP released from circulating erythrocytes is a potential signal regulating muscle blood flow during exercise (exercise hyperemia), and intravascular ATP appears to blunt sympathetic vasoconstriction during exercise. Erythrocytes from patients with cystic fibrosis (CF) do not release ATP. The goal of the present study was to determine whether increases in forearm blood flow during exercise are blunted in CF patients and whether CF patients exhibit greater vasoconstrictor responsiveness during exercise. Nine control subjects and 10 CF patients who were free of other disease complications (∼96% O2 saturation) performed incremental rhythmic forearm exercise at 5, 10, and 15% of maximum handgrip strength for 21 min (7 min at each workload). We used a cold pressor test to evoke sympathetic vasoconstriction under resting conditions and at each exercise workload. As a control, subjects performed a second exercise bout without the cold pressor test. Continuous brachial artery blood velocity was monitored beat-to-beat, and vessel diameter was assessed by Doppler ultrasound. Artery diameter, as well as blood pressure, heart rate, and O2 saturation, was measured at steady-state exercise and at 1 min into the cold pressor stimulus. Blood pressure and heart rate responses to the forearm exercise and each cold pressor test were similar in both groups ( P > 0.05). Contrary to our hypothesis, forearm blood flow ( P = 0.91) and forearm vascular conductance ( P = 0.82) were similar at rest and at each level of exercise between CF patients and controls. Additionally, there was no difference in the degree of sympathetic vasoconstriction between groups at rest and at each level of exercise ( P = 0.22). Our results suggest that ATP released from the deformation of erythrocytes is not an obligatory signal for exercise hyperemia in human skeletal muscle.

Cold pressor test protocol to evaluate cardiac autonomic function

2006 ◽  
Vol 31 (3) ◽  
pp. 235-243 ◽  
Author(s):  
Jennifer L Wirch ◽  
Larry A Wolfe ◽  
Tracey L Weissgerber ◽  
Gregory A.L Davies
Keyword(s):  
Nervous System ◽  
Autonomic Function ◽  
Parasympathetic Nervous System ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Cardiac Autonomic Function ◽  
Pressor Test ◽  
Lateral Decubitus ◽  
Sympathetic Nervous ◽  
Frequency Power

The primary objective of this study was to develop a cold pressor test (CPT) protocol to evaluate cardiac autonomic function. Secondary objectives were to assess CPT protocol reliability and to examine gender differences in response to orthostatic stress and the CPT. Healthy, normotensive men and women (n = 12 per group) completed 2 trials on different days in the left lateral decubitus and standing postures and during a 6 min CPT (hand immersion while seated). Measurements included R-R interval, blood pressure, ventilatory responses, spontaneous baroreflex sensitivity, and heart rate variability indices. During the CPT, blood pressure and the sympathetic nervous system (SNS) indicator increased significantly and low-frequency power, high-frequency power (normalized for tidal volume), and the parasympathetic nervous system (PNS) indicator decreased significantly. Standing caused significant increases in the SNS indicator and decreases in the R-R interval in both genders. The PNS indicator was higher in women than in men in the left lateral decubitus posture. The 6 min hand-immersion CPT provoked cardiac sympathetic activation and parasympathetic withdrawal; however, it is best suited to studies with a repeated measures design, as analysis of reliability suggests that responses are highly variable between individuals. Performing the CPT in the left lateral decubitus position may prevent vasovagal responses.Key words: cold pressor test, sympathetic nervous system, parasympathetic nervous system, gender, posture.

Preeclampsia is not associated with elevated muscle sympathetic reactivity.

2020 ◽  
Author(s):  
Laura Marcela Reyes ◽  
Charlotte W. Usselman ◽  
Rshmi Khurana ◽  
Radha S. Chari ◽  
Michael K. Stickland ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pregnant Women ◽  
Gestational Age ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Tonic Activity ◽  
Sympathetic Nervous ◽  
Peripheral Chemoreflex

Objective: To determine whether increased chemoreflex tonic activity is associated with augmented muscle sympathetic nervous sys activity (MSNA) in women diagnosed with preeclampsia. Methods: Women with preeclampsia (n=19; 32±5 years old, 31±3 weeks gestation) were matched by age and gestational age with pregnant women (controls, n=38, 32±4 years old, 31±4 weeks gestation; 2:1 ratio). MSNA (n=9 preeclampsia) was assessed during baseline, peripheral chemoreflex de-activation (hyperoxia) and a cold pressor test (CPT). Baroreflex gain, diastolic blood pressure at which there is a 50% likelihood of MSNA occurring (T50) and plasma noradrenaline concentrations were measured. Results: Baseline mean arterial pressure (MAP: 106±11 vs. 87±10 mmHg, p<0.0001), noradrenaline concentrations (498±152 pg/mL vs. 326±147, p=0.001) and T50 (79±7 vs. 71±9 mmHg, p=0.02) were greater in women with preeclampsia compared to controls. However, baseline MSNA (burst incidence [BI]: 41±16 vs. 45±13 bursts/100hb, p=0.4) was not different between groups. Responses to hyperoxia (ΔBI -5±7 vs. -1±8 bursts/100hb, p=0.1; ΔMAP -1±3 vs. -2±3 mmHg, p=0.7) and CPT (ΔBI 15±7 vs. 12±11 bursts/100hb, p=0.6; ΔMAP 10±4 vs. 12±11 mmHg, p=0.6) were not different between groups. Conclusion: Our findings question the assumption that increased MSNA contributes to hypertension in women with preeclampsia. The chemoreflex does not appear to contribute to an increase in MSNA in women with preeclampsia.

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