scholarly journals Forearm vasodilator responses to environmental stress and reactive hyperaemia are impaired in young South Asian men

2018 ◽  
Vol 118 (5) ◽  
pp. 979-988 ◽  
Author(s):  
Natalie G. Ormshaw ◽  
Rehan T. Junejo ◽  
Janice M. Marshall
Keyword(s):  
Forearm Blood Flow ◽  
South Asians ◽  
Arterial Occlusion ◽  
Environmental Stressors ◽  
Reactive Hyperaemia ◽  
Intra Class Correlation ◽  
Arterial Blood ◽  
Pressor Responses ◽  
Asian Men ◽  
Forearm Vascular Conductance

Abstract Purpose Prevalence of cardiovascular disease (CVD) is greater in South Asians (SAs) than White Europeans (WEs). Endothelial dysfunction and blunted forearm vasodilatation to environmental stressors have been implicated in CVD. We investigated whether these features are present in young SA men. Methods In 15 SA and 16 WE men (19–23 years), we compared changes in forearm blood flow, arterial blood pressure (ABP), forearm vascular conductance (FVC), heart rate, and electrodermal resistance (EDR; sweating) following release of arterial occlusion (reactive hyperaemia endothelium-dependent) and 5 single sounds at 5–10 min intervals (stressors). Results All were normotensive. Peak reactive hyperaemia was smaller in SAs than WEs (FVC increase: 0.36 ± 0.038 vs 0.44 ± 0.038 units; P < 0.05). Furthermore, in WEs, mean FVC increased at 5, 15, and 20 s of each sound (vasodilatation), but increased at 5 s only in SAs, decreasing by 20 s (vasoconstriction). This reflected a smaller proportion of SAs showing forearm vasodilatation at 15 s (5/15 SAs vs 11/16 WEs: P < 0.01), the remainder showing vasoconstriction. Concomitantly, WEs showed greater bradycardia and EDR changes. Intra-class correlation analyses showed that all responses were highly reproducible over five sounds in both WEs and SAs. Moreover, sound-evoked changes in ABP and FVC were negatively correlated in each ethnicity (P < 0.01). However, WEs showed preponderance of forearm vasodilatation and depressor responses; SAs showed preponderance of vasoconstriction and pressor responses. Conclusions Endothelium-dependent vasodilatation is blunted in young SA men. This could explain their impaired forearm vasodilatation and greater pressor responses to repeated environmental stressors, so predisposing SAs to hypertension and CVD.

Potentiation of the exercise pressor reflex by muscle ischemia

1989 ◽  
Vol 66 (3) ◽  
pp. 1046-1053 ◽  
Author(s):  
C. L. Stebbins ◽  
J. C. Longhurst
Keyword(s):  
Blood Flow ◽  
Pressor Response ◽  
Muscle Blood Flow ◽  
Arterial Occlusion ◽  
Acid Base Balance ◽  
Active Muscle ◽  
Arterial Blood ◽  
Muscle Ischemia ◽  
Pressor Responses ◽  
Static Contraction

The reflex responses to static contraction are augmented by ischemia. The metabolic “error signals” that are responsible for these observed responses are unknown. Therefore this study was designed to test the hypothesis that static contraction-induced pressor responses, which are enhanced during muscle ischemia, are the result of alterations in muscle oxygenation, acid-base balance, and K+. Thus, in 36 cats, the pressor response, active muscle blood flow, and muscle venous pH, PCO2, PO2, lactate, and K+ were compared during light and intense static contractions with and without arterial occlusion. During light contraction (15–16% of maximal), active muscle blood flow increased without and decreased with arterial occlusion (+35 +/- 12 vs. -60 +/- 11%). Arterial occlusion augmented these pressor responses by 132 +/- 25%. Without arterial occlusion, changes (P less than 0.05) were seen in PO2, O2 content, PCO2, and K+. Lactate and pH were unchanged. With arterial occlusion, changes in muscle PCO2 were augmented and significant changes were seen in pH and lactate. During intense static contraction (67–69% of maximal), muscle blood flow decreased without arterial occlusion (-39 +/- 9%) and decreased further during occlusion (-81 +/- 6%). Arterial occlusion augmented the pressor responses by 39 +/- 12%. All metabolic variables increased during contraction without arterial occlusion, but occlusion failed to augment any of these changes. These data suggest that light static ischemic contractions cause increases in muscle PCO2 and lactate and decreases in pH that may signal compensatory reflex-induced changes in arterial blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Absence of compensatory vasodilation with perfusion pressure challenge in exercise: evidence for and implications of the noncompensator phenotype

2018 ◽  
Vol 124 (2) ◽  
pp. 374-387 ◽  
Author(s):  
Robert F. Bentley ◽  
Jeremy J. Walsh ◽  
Patrick J. Drouin ◽  
Aleksandra Velickovic ◽  
Sarah J. Kitner ◽  
...  
Keyword(s):  
Blood Flow ◽  
Oxygen Delivery ◽  
Exercise Tolerance ◽  
Forearm Blood Flow ◽  
Perfusion Pressure ◽  
Pressor Response ◽  
Muscle Blood Flow ◽  
Interindividual Differences ◽  
Arterial Blood ◽  
Pressor Responses

Compromising oxygen delivery (O2D) during exercise requires compensatory vasodilatory and/or pressor responses to protect O2D:demand matching. The purpose of the study was to determine whether compensatory vasodilation is absent in some healthy young individuals in the face of a sudden reduction in exercising forearm perfusion pressure and whether this affects the exercise pressor response. Twenty-one healthy young men (21.6 ± 2.0 yr) completed rhythmic forearm exercise at a work rate equivalent to 70% of their own maximal exercise vasodilation. During steady-state exercise, the exercising arm was rapidly adjusted from below to above heart level, resulting in a reduction in forearm perfusion pressure of −30.7 ± 0.9 mmHg. Forearm blood flow (ml/min; brachial artery Doppler and echo ultrasound), mean arterial blood pressure (mmHg; finger photoplethysmography), and exercising forearm venous effluent (antecubital vein catheter) measurements revealed distinct compensatory vasodilatory differences. Thirteen individuals responded with compensatory vasodilation (509 ± 128 vs. 632 ± 136 ml·min−1·100 mmHg−1; P < 0.001), while eight individuals did not (663 ± 165 vs. 667 ± 167 ml·min−1·100 mmHg−1; P = 0.6). Compensatory pressor responses between groups were not different (5.5 ± 5.5 and 9.7 ± 9.5 mmHg; P = 0.2). Forearm blood flow, O2D, and oxygen consumption were all protected in compensators (all P > 0.05) but not in noncompensators, who therefore suffered compromises to exercise performance (6 ± 14 vs. −36 ± 29 N; P = 0.004). Phenotypic differences were not explained by potassium or nitric oxide bioavailability. In conclusion, both compensator and noncompensator vasodilator phenotype responses to a sudden compromise to exercising muscle blood flow are evident. Interindividual differences in the mechanisms governing O2D:demand matching should be considered as factors influencing exercise tolerance. NEW & NOTEWORTHY In healthy young individuals, compromising submaximally exercising muscle perfusion appears to evoke compensatory vasodilation to defend oxygen delivery. Here we report the absence of compensatory vasodilation in 8 of 21 such individuals, despite their vasodilatory capacity and increases in perfusion with increasing exercise intensity being indistinguishable from compensators. The absence of compensation impaired exercise tolerance. These findings suggest that interindividual differences in oxygen delivery:demand matching efficacy affect exercise tolerance and depend on the nature of a delivery:demand matching challenge.

Targeting angiotensin type-2 receptors located on pressor neurons in the nucleus of the solitary tract to relieve hypertension in mice

2021 ◽  
Author(s):  
Mazher Mohammed ◽  
Dominique N Johnson ◽  
Lei A Wang ◽  
Scott W Harden ◽  
Wanhui Sheng ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Gaba Release ◽  
Access Point ◽  
Central Administration ◽  
Solitary Tract ◽  
Arterial Blood ◽  
Pressor Responses ◽  
Pressure Lowering ◽  
Angiotensin Type

Abstract Aims These studies evaluate whether angiotensin type-2 receptors (AT2Rs) that are expressed on γ-aminobutyric acid (GABA) neurons in the nucleus of the solitary tract (NTS) represent a novel endogenous blood pressure-lowering mechanism. Methods and results Experiments combined advanced genetic and neuroanatomical techniques, pharmacology, electrophysiology, and optogenetics in mice to define the structure and cardiovascular-related function of NTS neurons that contain AT2R. Using mice with Cre-recombinase directed to the AT2R gene, we discovered that optogenetic stimulation of AT2R-expressing neurons in the NTS increases GABA release and blood pressure. To evaluate the role of the receptor, per se, in cardiovascular regulation, we chronically delivered C21, a selective AT2R agonist, into the brains of normotensive mice and found that central AT2R activation reduces GABA-related gene expression and blunts the pressor responses induced by optogenetic excitation of NTS AT2R neurons. Next, using in situ hybridization, we found that the levels of Agtr2 mRNAs in GABAergic NTS neurons rise during experimentally induced hypertension, and we hypothesized that this increased expression may be exploited to ameliorate the disease. Consistent with this, final experiments revealed that central administration of C21 attenuates hypertension, an effect that is abolished in mice lacking AT2R in GABAergic NTS neurons. Conclusion These studies unveil novel hindbrain circuits that maintain arterial blood pressure, and reveal a specific population of AT2R that can be engaged to alleviate hypertension. The implication is that these discrete receptors may serve as an access point for activating an endogenous depressor circuit.

Forearm and finger blood flow responses to passive body tilts

1979 ◽  
Vol 46 (2) ◽  
pp. 288-292 ◽  
Author(s):  
Y. A. Mengesha ◽  
G. H. Bell
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Pulse Rate ◽  
Forearm Blood Flow ◽  
Body Tilt ◽  
Finger Blood Flow ◽  
Arterial Blood ◽  
Forearm Vascular Resistance

Ten to fifteen healthy subjects, ages 18--30 yr, were used to assess the correlation of forearm blood flow with graded passive body tilts and vascular resistance and also to discern the relative effects of body tilts on finger blood flow. In the head-up tilts forearm blood flow and arterial blood pressure fell progressively, whereas forearm vascular resistance and pulse rate increased. In the head-down tilts the forearm blood flow and the arterial blood pressure increased, whereas the forearm vascular resistance and pulse rate decreased. These changes were found to be significantly correlated with the different tilt angles and with one another. In a preliminary study it was found that infrared heating of the carpometacarpal region produced finger vasodilatation similar to the forearm vasodilatation observed by Crockford and Hellon (6). However, unlike forearm blood flow, finger blood flow showed no appreciable response to either the head-up or head-down tilts. This indicates that the sympathetic tone and the volume of blood in the finger are not appreciably altered by this test procedure at least 1 min after the body tilt is assumed.

Histamine-induced pulmonary edema distal to pulmonary arterial occlusion

1985 ◽  
Vol 58 (4) ◽  
pp. 1092-1098 ◽  
Author(s):  
M. D. Walkenstein ◽  
B. T. Peterson ◽  
J. E. Gerber ◽  
R. W. Hyde
Keyword(s):  
Pulmonary Edema ◽  
Pulmonary Circulation ◽  
Arterial Occlusion ◽  
Arterial Blood Flow ◽  
Water Volume ◽  
Lung Water ◽  
Arterial Blood ◽  
Perfused Lung ◽  
Pulmonary Arterial ◽  
The Right

Histological studies provide evidence that the bronchial veins are a site of leakage in histamine-induced pulmonary edema, but the physiological importance of this finding is not known. To determine if a lung perfused by only the bronchial arteries could develop pulmonary edema, we infused histamine for 2 h in anesthetized sheep with no pulmonary arterial blood flow to the right lung. In control sheep the postmortem extravascular lung water volume (EVLW) in both the right (occluded) and left (perfused) lung was 3.7 +/- 0.4 ml X g dry lung wt-1. Following histamine infusion, EVLW increased to 4.4 +/- 0.7 ml X g dry lung wt-1 in the right (occluded) lung (P less than 0.01) and to 5.3 +/- 1.0 ml X g dry wt-1 in the left (perfused) lung (P less than 0.01). Biopsies from the right (occluded) lungs scored for the presence of edema showed a significantly higher score in the lungs that received histamine (P less than 0.02). Some leakage from the pulmonary circulation of the right lung, perfused via anastomoses from the bronchial circulation, cannot be excluded but should be modest considering the low pressures in the pulmonary circulation following occlusion of the right pulmonary artery. These data show that perfusion via the pulmonary arteries is not a requirement for the production of histamine-induced pulmonary edema.

scholarly journals Bradykinin Contributes to Sympathetic and Pressor Responses Evoked by Activation of Skeletal Muscle Afferents P2X in Heart Failure

2016 ◽  
Vol 39 (6) ◽  
pp. 2101-2109 ◽  
Author(s):  
Jihong Xing ◽  
Jianhua Li
Keyword(s):  
Heart Failure ◽  
Nervous Activity ◽  
Muscle Afferents ◽  
Receptor Expression ◽  
Sympathetic Nervous Activity ◽  
Published Data ◽  
Drg Neurons ◽  
Arterial Blood ◽  
Pressor Responses ◽  
Muscle Afferent

Background/Aims: Published data suggest that purinergic P2X receptors of muscle afferent nerves contribute to the enhanced sympathetic nervous activity (SNA) and blood pressure (BP) responses during static exercise in heart failure (HF). In this study, we examined engagement of bradykinin (BK) in regulating responses of SNA and BP evoked by P2X stimulation in rats with HF. We further examined cellular mechanisms responsible for BK. We hypothesized that BK potentiates P2X currents of muscle dorsal root ganglion (DRG) neurons, and this effect is greater in HF due to upregulation of BK kinin B2 and P2X3 receptor. As a result, BK amplifies muscle afferents P2X-mediated SNA and BP responses. Methods: Renal SNA and BP responses were recorded in control rats and rats with HF. Western Blot analysis and patch-clamp methods were employed to examine the receptor expression and function of DRG neurons involved in the effects of BK. Results: BK injected into the arterial blood supply of the hindlimb muscles heightened the reflex SNA and BP responses induced by P2X activation with α,β-methylene ATP to a greater degree in HF rats. In addition, HF upregulated the protein expression of kinin B2 and P2X3 in DRG and the prior application of BK increased the magnitude of α,β-methylene ATP-induced currents in muscle DRG neurons from HF rats. Conclusion: BK plays a facilitating role in modulating muscle afferent P2X-engaged reflex sympathetic and pressor responses. In HF, P2X responsivness is augmented due to increases in expression of kinin B2 and P2X3 receptors and P2X current activity.

scholarly journals Assessment of Post-Occlusive Reactive Hyperaemia in the Evaluation of Endothelial Function in Patients with Lower Extremity Artery Disease

2017 ◽  
Vol 63 (3) ◽  
pp. 129-132 ◽  
Author(s):  
Cosmin Carasca ◽  
Annamaria Magdas ◽  
Ioan Tilea ◽  
Alexandru Incze
Keyword(s):  
Endothelial Function ◽  
Challenge Test ◽  
Ankle Brachial Index ◽  
Arterial Occlusion ◽  
Control Group ◽  
Reactive Hyperaemia ◽  
Peripheral Perfusion ◽  
Surgical Revascularisation ◽  
Healthy Control ◽  
Artery Disease

Abstract Background: The aim was to assess endothelial function with photoplethysmography (PPG), by post-occlusive reactive hyperaemia (PORH) combined with alprostadil challenge test in patients with peripheral artery disease (PAD). Methods: Forty-nine PAD patients stage II-III Fontaine (39 male, 10 female, mean age 68.45±5.86 years) and a control group of 49 healthy individuals (24 male, 25 female; mean age 25.1±3.8 for a young subgroup; 71.0±0.16 years for an elderly subgroup) were included. Ankle-brachial index (ABI) was assessed at baseline, peripheral perfusion (PP) and PORH were assessed at baseline and after the 30 minutes administration of parenteral alprostadil. Results: After 3 minutes of arterial occlusion, peripheral perfusion increased from 0.69±0.94 mV/V to 2.27±2.42 mV/V (p<0.0001). After alprostadil challenge, peripheral perfusion increased from 0.84±1.24 mV/V to 4.52±3.52 mV/V (p<0.0001). In controls PP was 2.4±1.7 mV/V versus 3.8±1.5 mV/V, p<0.0001. Conclusion: In patients with PAD, an increase in PORH after alprostadil challenge due to the release of nitric oxide (NO), provides information on the endothelial function and could reflect the presence of collaterals. In the healthy control group, the increase in PORH could reflect the integrity of main arterial branch. In PAD patients with an increase in PORH, conservative therapy should be preferred over surgical revascularisation.

Ascending pathways mediating somatoautonomic reflexes in exercising dogs

1987 ◽  
Vol 62 (3) ◽  
pp. 1186-1191 ◽  
Author(s):  
J. W. Kozelka ◽  
G. W. Christy ◽  
R. D. Wurster
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Surgical Techniques ◽  
Arterial Occlusion ◽  
Cardiovascular Responses ◽  
Spinal Pathways ◽  
Arterial Blood ◽  
Bilateral Carotid ◽  
Dorsolateral Funiculus ◽  
Carotid Arterial

The ascending spinal pathways mediating somatocardiovascular reflexes during exercise were studied in unanesthetized dogs by placing lesions in the lumbar spinal cord. After training to run on a treadmill with hindlimbs only, 20 dogs were anesthetized and instrumented using sterile surgical techniques. To chronically record heart rate and arterial blood pressure, the aorta was cannulated via the omocervical artery. To test the intactness of descending spinal sympathetic pathways, reflex pressor responses to baroreceptor hypotension were produced by bilateral carotid arterial occlusion using pneumatic vessel occluders placed around the common carotid arteries. To generate transient ischemic exercise (120 s), a pneumatic occluder was placed around the left iliac artery. Eight to 10 days after instrumentation, blood pressure and heart rate were monitored at rest and during hindlimb running with and without simultaneous iliac arterial occlusion. The modest pressor response and tachycardia elicited by hindlimb exercise were markedly augmented by simultaneous hindlimb ischemia (i.e., iliac arterial occlusion). Lesion placement in the dorsolateral sulcus area and the dorsolateral funiculus at L2 significantly reduced the blood pressure and heart rate responses to simultaneous exercise occlusion. The cardiovascular responses to nonischemic exercise and bilateral carotid arterial occlusion were not altered by such spinal sections. It is concluded that in the dog the ascending spinal pathways mediating cardiovascular responses to ischemic exercise are located in the lateral funiculus, including the dorsolateral sulcus area and dorsolateral funiculus.

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