Evaluation of forearm vascular resistance during orthostatic stress: Velocity is proportional to flow and size doesn’t matter

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.

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Enhanced vasodilation to acetylcholine in athletes is associated with lower plasma cholesterol

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1996.270.6.h2008 ◽

1996 ◽

Vol 270 (6) ◽

pp. H2008-H2013 ◽

Cited By ~ 18

Author(s):

B. A. Kingwell ◽

B. Tran ◽

J. D. Cameron ◽

G. L. Jennings ◽

A. M. Dart

Keyword(s):

Sodium Nitroprusside ◽

Vascular Resistance ◽

Repeated Measures ◽

Vascular Reactivity ◽

Plasma Cholesterol ◽

Total Cholesterol Level ◽

Venous Occlusion ◽

Ang Ii ◽

Elevated Cholesterol ◽

Forearm Vascular Resistance

We investigated a change in vascular reactivity as a potential adaptive mechanism to chronic exercise. The study consisted of 2 separate protocols with 10 male athletes and 10 age-matched sedentary male control subjects participating in each. Protocol 1 investigated forearm blood flow responses to intra-arterial infusions of acetylcholine and sodium nitroprusside by use of venous occlusion plethysmography. Protocol 2 used identical techniques to study responses to norepinephrine, angiotensin II (ANG II), and NG-monomethyl-L-arginine (L-NMMA). The percent reduction in forearm vascular resistance to acetylcholine was significantly greater in the athletic compared with the sedentary group (multivariate analysis of variance for repeated measures, P = 0.03). Covariance analysis suggested that the lower total cholesterol level of the athletic group (P = 0.03) may contribute to their enhanced responsiveness to acetylcholine. There were no differences between athletic and sedentary groups in the forearm vascular resistance responses to norepinephrine, ANG II, sodium nitroprusside, or L-NMMA. These data support the hypothesis that long-term endurance training is associated with enhanced endothelium-dependent dilator reserve due to altered lipoprotein levels in athletes. This finding may have therapeutic application in conditions of elevated cholesterol and impaired vasodilator capacity including hypertension, hypercholesterolemia, atherosclerosis, and cardiac failure.

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Effects of water immersion on forearm vascular resistance in normotensive subjects

Journal of Hypertension ◽

10.1097/00004872-199312050-00068 ◽

1993 ◽

Vol 11 (5) ◽

pp. S178???S179 ◽

Cited By ~ 1

Author(s):

Giuseppe Regolisti ◽

Pietro Coghi ◽

Giacomo Bruschi ◽

Guido Orlandini ◽

Aderville Cabassi ◽

...

Keyword(s):

Vascular Resistance ◽

Water Immersion ◽

Normotensive Subjects ◽

Forearm Vascular Resistance

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Reflex sympathetic activation in humans is accompanied by inhibition of gastric HCO3- secretion

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1988.255.6.g752 ◽

1988 ◽

Vol 255 (6) ◽

pp. G752-G758 ◽

Cited By ~ 2

Author(s):

H. Sjovall ◽

H. Forssell ◽

J. Haggendal ◽

L. Olbe

Keyword(s):

Heart Rate ◽

Vascular Resistance ◽

Pulse Pressure ◽

Negative Pressure ◽

Sympathetic Activity ◽

Plasma Catecholamine ◽

Series Of Experiments ◽

Plasma Catecholamine Concentrations ◽

Peripheral Sympathetic Activity ◽

Forearm Vascular Resistance

The study was performed to determine whether the sympathetic nervous system contributes to the reflex control of gastric HCO3- secretion in humans. Gastric HCO3- secretion was registered by a computerized technique based on measurements of pH and PCO2 in gastric effluent. To minimize formation of CO2 in the stomach, subjects were pretreated with the H2-receptor blocker ranitidine. Compensations were made for HCO3- of nongastric origin. As indicators of cardiovascular sympathetic activity, we measured heart rate, forearm vascular resistance, and plasma catecholamine concentrations. In one series of experiments, peripheral sympathetic activity was enhanced by the application of a negative pressure around the lower part of the body (lower body negative pressure, LBNP), at a rate sufficient to induce a slight decrease in systemic arterial pressure. In another series of experiments, peripheral sympathetic activity was inhibited by elevation of the legs, a procedure that simulates volume loading by redistributing blood volume toward the central circulation. LBNP at -20 mmHg decreased systolic pressure and pulse pressure and significantly increased heart rate, forearm vascular resistance, and plasma catecholamine levels. All these effects were observed in the first 15-min period of LBNP and were well maintained throughout the 45-min observation period. LBNP also inhibited basal gastric HCO3- secretion rate in seven of eight individuals, but this response was slower in onset with a latency of at least 15 min. Elevation of the legs increased pulse pressure and decreased forearm vascular resistance. Catecholamines were not measured in these experiments. Gastric HCO3- secretion tended to increase, but the magnitude of the response was highly variable.(ABSTRACT TRUNCATED AT 250 WORDS)

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Adenosine contributes to hypoxia-induced forearm vasodilation in humans

Journal of Applied Physiology ◽

10.1152/jappl.1999.87.6.2218 ◽

1999 ◽

Vol 87 (6) ◽

pp. 2218-2224 ◽

Cited By ~ 66

Author(s):

Urs A. Leuenberger ◽

Kris Gray ◽

Michael D. Herr

Keyword(s):

Blood Flow ◽

Vascular Resistance ◽

Brachial Artery ◽

Adenosine Receptors ◽

Forearm Blood Flow ◽

Minute Ventilation ◽

Acute Hypoxia ◽

Normal Subjects ◽

Local Release ◽

Forearm Vascular Resistance

In humans, hypoxia leads to increased sympathetic neural outflow to skeletal muscle. However, blood flow increases in the forearm. The mechanism of hypoxia-induced vasodilation is unknown. To test whether hypoxia-induced vasodilation is cholinergically mediated or is due to local release of adenosine, normal subjects were studied before and during acute hypoxia (inspired O210.5%; ∼20 min). In experiment I, aminophylline (50–200 μg ⋅ min−1 ⋅ 100 ml forearm tissue−1) was infused into the brachial artery to block adenosine receptors ( n = 9). In experiment II, cholinergic vasodilation was blocked by atropine (0.4 mg over 4 min) infused into the brachial artery ( n = 8). The responses of forearm blood flow (plethysmography) and forearm vascular resistance to hypoxia in the infused and opposite (control) forearms were compared. During hypoxia (arterial O2 saturation 77 ± 2%), minute ventilation and heart rate increased while arterial pressure remained unchanged; forearm blood flow rose by 35 ± 6% in the control forearm but only by 5 ± 8% in the aminophylline-treated forearm ( P < 0.02). Accordingly, forearm vascular resistance decreased by 29 ± 5% in the control forearm but only by 9 ± 6% in the aminophylline-treated forearm ( P < 0.02). Atropine did not attenuate forearm vasodilation during hypoxia. These data suggest that adenosine contributes to hypoxia-induced vasodilation, whereas cholinergic vasodilation does not play a role.

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Contribution of potassium to exercise-induced vasodilation in humans

Journal of Applied Physiology ◽

10.1152/jappl.1994.77.6.2552 ◽

1994 ◽

Vol 77 (6) ◽

pp. 2552-2557 ◽

Cited By ~ 16

Author(s):

J. R. Wilson ◽

S. C. Kapoor ◽

G. G. Krishna

Keyword(s):

Skeletal Muscle ◽

Vascular Resistance ◽

Plasma Potassium ◽

Normal Subjects ◽

Bicycle Exercise ◽

Potassium Release ◽

Forearm Exercise ◽

Exercise Induced ◽

Arteriolar Vasodilation ◽

Forearm Vascular Resistance

It has been postulated that skeletal muscle release of potassium contributes to exercise-induced vasodilation of skeletal muscle arterioles. To determine whether potassium produces muscle arteriolar vasodilation in humans, we measured plethysmographic forearm blood flow and brachial venous potassium concentrations during brachial arterial infusion of potassium (0.6, 3, 6, 15, and 30 mueq.min-1.100 ml forearm volume-1) in nine normal subjects. Infusion of potassium decreased forearm vascular resistance, with an increase in brachial venous potassium of 1 meq/l decreasing forearm vascular tone by 25–30%. We then measured plasma potassium concentrations during forearm and upright bicycle exercise in 15 normal subjects. Forearm exercise at 0.6 W decreased forearm vascular resistance by 83%, whereas brachial venous potassium increased by only 0.5 +/- 0.2 meq/l (both P < 0.05). Maximal bicycle exercise increased systemic potassium concentrations by 1.2 +/- 0.2 meq/l. These findings indicate that potassium produces muscle arteriolar vasodilation in humans and therefore supports the hypothesis that potassium release from exercising muscle contributes to exercise-induced vasodilation. The relatively small change in venous potassium noted during forearm exercise despite marked forearm vasodilation suggests that local potassium release is only a small contributor to exercise-induced vasodilation. However, potassium release during maximal exercise may have significant vasodilatory effects on arterioles both in exercising and nonexercising tissues.

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Endothelium-derived nitric oxide mediates hypoxic vasodilation of resistance vessels in humans

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1996.271.3.h1182 ◽

1996 ◽

Vol 271 (3) ◽

pp. H1182-H1185 ◽

Cited By ~ 33

Author(s):

M. L. Blitzer ◽

S. D. Lee ◽

M. A. Creager

Keyword(s):

Nitric Oxide ◽

Blood Flow ◽

Nitric Oxide Synthase ◽

Vascular Resistance ◽

Forearm Blood Flow ◽

Vasodilator Response ◽

Healthy Humans ◽

Resistance Vessels ◽

Oxide Synthase ◽

Forearm Vascular Resistance

Endothelium-derived nitric oxide (EDNO) contributes to basal systemic vascular resistance under normoxic conditions. The purpose of this investigation was to determine whether EDNO contributes to the regulation of limb vascular resistance during hypoxia in healthy humans. Forearm blood flow was assessed by venous occlusion plethysmography. Hypoxia was induced by delivering a mixture of N2 and O2 via a gas blender adjusted to reduce the PO2 to 50 mmHg. During hypoxia, forearm blood flow increased from 2.4 +/- 0.2 to 3.0 +/- 0.3 ml.100 ml-1.min-1 (P < 0.001), and forearm vascular resistance decreased from 38 +/- 3 to 29 +/- 3 units (P < 0.001). The nitric oxide synthase inhibitor NG-monomethyl-L-arginine (L-NMMA, 2,000 micrograms/min intra-arterially) was administered to eight subjects. The percent increase in forearm vascular resistance after administration of L-NMMA was greater during hypoxia than normoxia (67 +/- 14 vs. 39 +/- 15%, P < 0.05). L-NMMA reduced the forearm vasodilator response to hypoxia from 27 +/- 3 to 11 +/- 5% (P = 0.01). To exclude the possibility that this attenuated response to hypoxia was a consequence of vasoconstriction and not specific for nitric oxide synthase inhibition, six subjects received intra-arterial phenylephrine. Phenylephrine did not affect the vasodilator response to hypoxia (17 +/- 3 vs. 21 +/- 6%, P = NS). It is concluded that EDNO contributes to hypoxia-induced vasodilation in the forearm resistance vessels in healthy humans.

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Role of Vascular Adaptation in Determining Systolic Blood Pressure in Young Adults

Journal of the American Heart Association ◽

10.1161/jaha.119.014375 ◽

2020 ◽

Vol 9 (7) ◽

Cited By ~ 1

Author(s):

Shikai Yu ◽

Jessica E. Middlemiss ◽

Chiara Nardin ◽

Stacey S. Hickson ◽

Karen L. Miles ◽

...

Keyword(s):

Blood Pressure ◽

Young Adults ◽

Systolic Blood Pressure ◽

Vascular Resistance ◽

Impaired Ability ◽

Vessel Structure ◽

Underlying Mechanisms ◽

Different Levels ◽

Forearm Vascular Resistance

Background Two individuals can have a similar pulse pressure ( PP ) but different levels of systolic blood pressure ( SBP ), although the underlying mechanisms have not been described. We hypothesized that, for a given level of PP , differences in SBP relate to peripheral vascular resistance ( PVR ); and we tested this hypothesis in a large cohort of healthy young adults. Methods and Results Demographic, biochemical, and hemodynamic data from 3103 subjects were available for the current analyses. In both men and women, for a given level of PP , higher SBP was associated with significantly higher body weight, body mass index, heart rate, and PVR ( P <0.05 versus those with lower BP for all comparisons). Moreover, stratifying individuals by quartiles of PP and PVR revealed a stepwise increase in SBP from the lowest to highest quartile for each variable, with the highest SBP occurring in those in the highest quartile of both PP and PVR ( P <0.001 for overall trend for both sexes). PVR was also increased with increasing tertile of minimum forearm vascular resistance, in both men ( P =0.002) and women ( P =0.03). Conclusions Increased PVR , mediated in part through altered resistance vessel structure, strongly associates with the elevation of SBP for a given level of PP in young adults. An impaired ability to adapt PVR appropriately to a given level of PP may be an important mechanism underlying elevated SBP in young adults.

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Local vasoconstriction in spinal cord-injured and able-bodied individuals

Journal of Applied Physiology ◽

10.1152/japplphysiol.00053.2007 ◽

2007 ◽

Vol 103 (3) ◽

pp. 1070-1077 ◽

Cited By ~ 12

Author(s):

M. Kooijman ◽

M. de Hoog ◽

G. A. Rongen ◽

H. J. M. van Kuppevelt ◽

P. Smits ◽

...

Keyword(s):

Spinal Cord ◽

Blood Flow ◽

Vascular Resistance ◽

Venous Occlusion ◽

Myogenic Response ◽

Cuff Inflation ◽

Limb Blood Flow ◽

Percent Increase ◽

Spinal Cord Injured ◽

Forearm Vascular Resistance

Local vasoconstriction plays an important role in maintaining blood pressure in spinal cord-injured individuals (SCI). We aimed to unravel the mechanisms of local vasoconstriction [venoarteriolar reflex (VAR) and myogenic response] using both limb dependency and cuff inflation in SCI and compare these with control subjects. Limb blood flow was measured in 11 male SCI (age: 24–55 yr old) and 9 male controls (age: 23–56 yr old) using venous occlusion plethysmography in forearm and calf during three levels of 1) limb dependency, and 2) cuff inflation. During limb dependency, vasoconstriction relies on both the VAR and the myogenic response. During cuff inflation, the decrease in blood flow is caused by the VAR and by a decrease in arteriovenous pressure difference, whereas the myogenic response does not play a role. At the highest level of leg dependency, the percent increase in calf vascular resistance (mean arterial pressure/calf blood flow) was more pronounced in SCI than in controls (SCI 186 ± 53%; controls 51 ± 17%; P = 0.032). In contrast, during cuff inflation, no differences were found between SCI and controls (SCI 17 ± 17%; controls 14 ± 10%). Percent changes in forearm vascular resistance in response to either forearm dependency or forearm cuff inflation were equal in both groups. Thus local vasoconstriction during dependency of the paralyzed leg in SCI is enhanced. The contribution of the VAR to local vasoconstriction does not differ between the groups, since no differences between groups existed for cuff inflation. Therefore, the augmented local vasoconstriction in SCI during leg dependency relies, most likely, on the myogenic response.

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