Inhibition of vascular ATP-sensitive K+channels does not affect reactive hyperemia in human forearm

2003 ◽  
Vol 284 (2) ◽  
pp. H711-H718 ◽  
Author(s):  
H. M. Omar Farouque ◽  
Ian T. Meredith
Keyword(s):  
Blood Flow ◽  
Adaptive Response ◽  
Healthy Subjects ◽  
Forearm Blood Flow ◽  
Reactive Hyperemia ◽  
Venous Occlusion ◽  
Channel Inhibition ◽  
Human Forearm ◽  
Hyperemic Response

The extent to which ATP-sensitive K+ channels contribute to reactive hyperemia in humans is unresolved. We examined the role of ATP-sensitive K+channels in regulating reactive hyperemia induced by 5 min of forearm ischemia. Thirty-one healthy subjects had forearm blood flow measured with venous occlusion plethysmography. Reactive hyperemia could be reproducibly induced ( n = 9). The contribution of vascular ATP-sensitive K+ channels to reactive hyperemia was determined by measuring forearm blood flow before and during brachial artery infusion of glibenclamide, an ATP-sensitive K+ channel inhibitor ( n = 12). To document ATP-sensitive K+ channel inhibition with glibenclamide, coinfusion with diazoxide, an ATP-sensitive K+ channel opener, was undertaken ( n = 10). Glibenclamide did not significantly alter resting forearm blood flow or the initial and sustained phases of reactive hyperemia. However, glibenclamide attenuated the hyperemic response induced by diazoxide. These data suggest that ATP-sensitive K+ channels do not play an important role in controlling forearm reactive hyperemia and that other mechanisms are active in this adaptive response.

scholarly journals Relative contribution of vasodilator prostanoids, NO, and KATP channels to human forearm metabolic vasodilation

2003 ◽  
Vol 284 (6) ◽  
pp. H2405-H2411 ◽  
Author(s):  
H. M. Omar Farouque ◽  
Ian T. Meredith
Keyword(s):  
Blood Flow ◽  
Forearm Blood Flow ◽  
Katp Channels ◽  
Venous Occlusion ◽  
Channel Blockade ◽  
Relative Contribution ◽  
Channel Inhibition ◽  
Human Forearm ◽  
Exercise Induced ◽  
Metabolic Vasodilation

Isolated ATP-sensitive K+(KATP) channel inhibition with glibenclamide does not alter exercise-induced forearm metabolic vasodilation. Whether forearm metabolic vasodilation would be influenced by KATP channel inhibition in the setting of impaired nitric oxide (NO)- and prostanoid-mediated vasodilation is unknown. Thirty-seven healthy subjects were recruited. Forearm blood flow (FBF) was assessed using venous occlusion plethysmography, and functional hyperemic blood flow (FHBF) was induced by isotonic wrist exercise. Infusion of N G-monomethyl-l-arginine(l-NMMA), aspirin, or the combination reduced resting FBF compared with vehicle ( P < 0.05). Addition of glibenclamide to l-NMMA, aspirin, or the combination did not further reduce resting FBF. l-NMMA decreased peak FHBF by 26%, and volume was restored after 5 min ( P < 0.05). Aspirin reduced peak FHBF by 13%, and volume repaid after 5 min ( P < 0.05). Coinfusion of l-NMMA and aspirin reduced peak FHBF by 21% ( P < 0.01), and volume was restored after 5 min ( P < 0.05). Addition of glibenclamide to l-NMMA and aspirin did not further decrease FHBF. Vascular KATP channel blockade with glibenclamide does not affect resting FBF or FHBF in the setting of NO and vasodilator prostanoid inhibition.

Noninvasive measurement of forearm blood flow and oxygen consumption by near-infrared spectroscopy

1994 ◽  
Vol 76 (3) ◽  
pp. 1388-1393 ◽  
Author(s):  
R. A. De Blasi ◽  
M. Ferrari ◽  
A. Natali ◽  
G. Conti ◽  
A. Mega ◽  
...  
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Infrared Spectroscopy ◽  
Near Infrared Spectroscopy ◽  
Healthy Subjects ◽  
Near Infrared ◽  
Forearm Blood Flow ◽  
Vascular Occlusion ◽  
Venous Occlusion ◽  
The Subject

We applied near-infrared spectroscopy (NIRS) for the simultaneous measurement of forearm blood flow (FBF) and oxygen consumption (VO2) in the human by inducing a 50-mmHg venous occlusion. Eleven healthy subjects were studied both at rest and after hand exercise during vascular occlusion. FBF was also measured by strain-gauge plethysmography. FBF measured by NIRS was 1.9 +/- 0.8 ml.100 ml-1.min-1 at rest and 8.2 +/- 2.9 ml.100 ml-1.min-1 after hand exercise. These values showed a correlation (r = 0.94) with those obtained by the plethysmography. VO2 values were 4.6 +/- 1.3 microM O2 x 100 ml-1.min-1 at rest and 24.9 +/- 11.2 microM O2 x 100 ml-1.min-1 after hand exercise. The scatter of the FBF and VO2 values showed a good correlation between the two variables (r = 0.93). The results demonstrate that NIRS provides the particular advantage of obtaining the contemporary evaluation of blood flow and VO2, allowing correlation of these two variables by a single maneuver without discomfort for the subject.

scholarly journals Parathyroid Hormone's Acute Effect on Vasodilatory Function

2010 ◽  
Vol 3 ◽  
pp. CMED.S4650 ◽  
Author(s):  
P. Farahnak ◽  
L. Lind ◽  
K. Mattala ◽  
I-L. Nilsson
Keyword(s):  
Cardiovascular Disease ◽  
Blood Flow ◽  
Healthy Subjects ◽  
Forearm Blood Flow ◽  
Acute Effect ◽  
Venous Occlusion ◽  
Arterial Infusion ◽  
Resistance Vessels ◽  
Vasodilatory Function ◽  
Pth Level

Parathyroid hormone (PTH) seems to affect the risk of cardiovascular disease. The aim of the present study was to investigate PTH's acute effect on endothelial vasodilatory function in forearm resistance vessels. Ten healthy subjects underwent forearm venous occlusion plethysmography. We measured forearm blood flow at baseline and at a stable, locally increased PTH level after intra-arterial infusion of metacholine and nitroprusside. The contralateral arm served as a control. Ionized calcium (Ca++) and PTH values were normal in all subjects at baseline (1.26 ± 0.02 mM/L, 3.6 ± 1.2 pM/L). After 30 minutes of PTH infusion, the PTH level increased in the active arm (13.8 ± 4.0 pM/L P < 0.01), while the Ca++ level was unchanged (1.25 ± 0.04; mM/L). Both the PTH and the Ca++ level in the contralateral arm remained unchanged, which indicates no systemic influence. The endothelial-dependent vasodilation was inversely correlated to the Ca++ level at baseline (r = −0.75, P < 0.05) and after PTH infusion (r = −0.68, P < 0.05). The vasodilatory function was not affected during PTH-infusion.

Role of Nitric Oxide towards Vasodilator Effects of Substance P and ATP in Human Forearm Vessels

1997 ◽  
Vol 92 (2) ◽  
pp. 123-131 ◽  
Author(s):  
Masanari Shiramoto ◽  
Tsutomu Imaizumi ◽  
Yoshitaka Hirooka ◽  
Toyonari Endo ◽  
Takashi Namba ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Substance P ◽  
Sodium Nitroprusside ◽  
Forearm Blood Flow ◽  
Dependent Manner ◽  
Human Forearm ◽  
Before And After ◽  
Dose Dependent

1. It has been shown in animals that substance P as well as acetylcholine releases endothelium-derived nitric oxide and evokes vasodilatation and that ATP-induced vasodilatation is partially mediated by nitric oxide. The aim of this study was to examine whether vasodilator effects of substance P and ATP are mediated by nitric oxide in humans. 2. In healthy volunteers (n = 35), we measured forearm blood flow by a strain-gauge plethysmograph while infusing graded doses of acetylcholine, substance P, ATP or sodium nitroprusside into the brachial artery before and after infusion of NG-monomethyl-l-arginine (4 or 8 μmol/min for 5 min). In addition, we measured forearm blood flow while infusing substance P before and during infusion of l-arginine (10 mg/min, simultaneously), or before and 1 h after oral administration of indomethacin (75 mg). 3. Acetylcholine, substance P, ATP or sodium nitroprusside increased forearm blood flow in a dose-dependent manner. NG-Monomethyl-l-arginine decreased basal forearm blood flow and inhibited acetylcholine-induced vasodilatation but did not affect substance P-, ATP-, or sodium nitroprusside-induced vasodilatation. Neither supplementation of l-arginine nor pretreatment with indomethacin affected substance P-induced vasodilatation. 4. Our results suggest that, in the human forearm vessels, substance P-induced vasodilatation may not be mediated by either nitric oxide or prostaglandins and that ATP-induced vasodilatation may also not be mediated by nitric oxide.

Intracoronary adenosine enhances myocardial reactive hyperemia after brief coronary occlusion

1985 ◽  
Vol 248 (6) ◽  
pp. H812-H817
Author(s):  
D. Saito ◽  
T. Hyodo ◽  
K. Takeda ◽  
Y. Abe ◽  
H. Tani ◽  
...  
Keyword(s):  
Blood Flow ◽  
Left Atrium ◽  
Coronary Occlusion ◽  
Reactive Hyperemia ◽  
Control Level ◽  
Direct Effects ◽  
Intracoronary Infusion ◽  
Hyperemic Flow ◽  
Hyperemic Response

Adenosine is a prime candidate for the role of mediator between myocardial metabolic state and coronary blood flow. However, there are few reports concerning the direct effects of exogenously added adenosine on coronary autoregulation. The present investigation in the open-chest dog studied the effects of a threshold dose of intracoronary adenosine infusion on reactive hyperemia following brief coronary occlusions. The infused dose did not increase nonocclusive flow by greater than 10%. Adenosine enhanced total hyperemic flow at all occlusions tested (5, 10, 15, 20, and 30 s). Aminophylline pretreatment reduced reactive hyperemia below the control level even in the presence of an intracoronary infusion of adenosine. Adenosine injected into the left atrium and intracoronarily infused papaverine did not affect hyperemic response to 5- and 15-s coronary occlusions. The results suggest that a minimum dose of exogenously added adenosine enhances myocardial reactive hyperemia, possibly by potentiating the effects of endogenous adenosine released during ischemia.

scholarly journals Agonist-dependent variablity of contributions of nitric oxide and prostaglandins in human skeletal muscle

2005 ◽  
Vol 98 (4) ◽  
pp. 1251-1257 ◽  
Author(s):  
William G. Schrage ◽  
Niki M. Dietz ◽  
John H. Eisenach ◽  
Michael J. Joyner
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Animal Studies ◽  
Forearm Blood Flow ◽  
Feedback Inhibition ◽  
Venous Occlusion ◽  
No Synthase ◽  
Human Forearm ◽  
Independent Mechanism ◽  
Treatment Order

The relative contributions of endothelium-dependent dilators [nitric oxide (NO), prostaglandins (PGs), and endothelium-derived hyperpolarizing factor (EDHF)] in human limbs are poorly understood. We tested the hypothesis that relative contributions of NO and PGs differ between endothelial agonists acetylcholine (ACh; 1, 2, and 4 μg·dl−1·min−1) and bradykinin (BK; 6.25, 25, and 50 ng·dl−1·min−1). We measured forearm blood flow (FBF) using venous occlusion plethysmography in 50 healthy volunteers (27 ± 1 yr) in response to brachial artery infusion of ACh or BK in the absence and presence of inhibitors of NO synthase [NOS; with NG-monomethyl-l-arginine (l-NMMA)] and cyclooxygenase (COX; with ketorolac). Furthermore, we tested the idea that the NOS + COX-independent dilation (in the presence of l-NMMA + ketorolac, presumably EDHF) could be inhibited by exogenous NO administration, as reported in animal studies. FBF increased ∼10-fold in the ACh control; l-NMMA reduced baseline FBF and ACh dilation, whereas addition of ketorolac had no further effect. Ketorolac alone did not alter ACh dilation, but addition of l-NMMA reduced ACh dilation significantly. For BK infusion, FBF increased ∼10-fold in the control condition; l-NMMA tended to reduce BK dilation ( P < 0.1), and addition of ketorolac significantly reduced BK dilation. Similar to ACh, ketorolac alone did not alter BK dilation, but addition of l-NMMA reduced BK dilation. To test the idea that NO can inhibit the NOS + COX-independent portion of dilation, we infused a dose of sodium nitroprusside (NO-clamp technique) during ACh or BK that restored the reduction in baseline blood flow due to l-NMMA. Regardless of treatment order, the NO clamp restored baseline FBF but did not reduce the NOS + COX-independent dilation to ACh or BK. We conclude that the contribution of NO and PGs differs between ACh and BK, with ACh being more dependent on NO and BK being mostly dependent on a NOS + COX-independent mechanism (EDHF) in healthy young adults. The NOS + COX-independent dilation does not appear sensitive to feedback inhibition from NO in the human forearm.

scholarly journals Activation of ATP-sensitive potassium channels contributes to reactive hyperemia in humans

1996 ◽  
Vol 271 (4) ◽  
pp. H1594-H1598 ◽  
Author(s):  
P. F. Banitt ◽  
P. Smits ◽  
S. B. Williams ◽  
P. Ganz ◽  
M. A. Creager
Keyword(s):  
Blood Flow ◽  
Katp Channel ◽  
Forearm Blood Flow ◽  
Reactive Hyperemia ◽  
Katp Channels ◽  
Venous Occlusion ◽  
Membrane Hyperpolarization ◽  
Flow Response ◽  
Hyperemic Flow ◽  
Basal Flow

Activation of ATP-sensitive potassium (KATP) channels present on vascular smooth muscle cells causes membrane hyperpolarization and vasodilation. The purpose of this study was to determine whether KATP channels contribute to reactive hyperemia in humans. Accordingly, we studied the effect of tolbutamide, a KATP channel inhibitor, on reactive hyperemic forearm blood flow. Forearm blood flow was measured by venous occlusion plethysmography. Forearm ischemia was produced by inflating a sphygmomanometric cuff on the arm to suprasystolic pressures for 5 min. After cuff release, forearm blood flow was measured during the reactive hyperemic phase for 5 min. Tolbutamide (1 mM blood concentration, n = 6) did not affect basal (2.4 +/- 0.2 to 2.2 +/- 0.1 ml.100 ml-1.min-1) or peak reactive hyperemic forearm blood flow (21.9 +/- 3.8 to 22.6 +/- 2.9 ml.100 ml-1.min-1, each P = NS), but it significantly attenuated total hyperemic volume (12.6 +/- 1.7 vs. 9.2 +/- 1.8 ml/100 ml, P < 0.02). Vehicle (n = 6) did not affect basal flow, peak reactive hyperemic flow, or total hyperemia. To determine whether adenosine or endothelium-derived nitric oxide contribute to reactive hyperemia via KATP channels, adenosine (1.5-500 micro grams/min, n = 6) and acetylcholine (30 micrograms/min, n = 6) were infused before and during tolbutamide coinfusion. Tolbutamide did not significantly alter the forearm blood flow response to either adenosine or acetylcholine. In conclusion, KATP channels contribute to vasodilation during reactive hyperemia in humans.

scholarly journals Blood flow in the forearm in patients with Rheumatoid arthritis and healthy subjects under local thermotherapy

2002 ◽  
Vol 58 (2) ◽  
Author(s):  
C. Mucha
Keyword(s):  
Rheumatoid Arthritis ◽  
Blood Flow ◽  
Healthy Subjects ◽  
Forearm Blood Flow ◽  
Human Subjects ◽  
Muscle Blood Flow ◽  
Reactive Hyperemia ◽  
Peripheral Blood Flow ◽  
Healthy Human ◽  
Heat Therapy

Objectives: Muscle blood flow in the forearm of patients with rheuma-toid arthritis and healthy volunteers following treatment with temperature increasingarm baths, mudpacks and short- or decimeter-wave diathermy was studied in thisinvestigation. The aim of the study was to find out the difference of reactive hyperemia between the different temperature methods as well as the influence on theconsensual reaction. Subjects: Eighty patients with rheumatoid arthritis, stage 3 according toSteinbrocker, as well as 80 healthy human subjects had been assigned numerically in the four therapy- and controlgroups. Patients with diseases influencing the peripheral blood flow were excluded. Design: Blood flow was measured by venous occlusion plethysmography in both forearms with the subjects lyingsupine. The application of the local heat therapies had been excluded on the left forearm. The forearm blood flow wasmonitored before heat therapy, directly after as well as in two further 10 minutes intervals. An analysis of variancewas used to determine the influence on blood flow of the response to the heat therapies in patients with rheumatoidarthritis and healthy subjects.Results: Under homogeneous starting conditions and a statistically uniformed high blood flow in rest the reactive values of blood flow on the left-hand side of application and the right consensual side showed high significant differencesbetween all methods of therapy. Differences between the patients and the healthy subjects only showed tendencies withpartially lower reactions, concerning the patients with rheumatoid arthritis. All methods of heat therapy caused a statistically provable consensual reaction that turned out smaller after diathermic methods. Here the post therapeuticreaction of the blood flow on the side of application was also lower or rather shorter. Conclusion: Greater differences of the blood flow in rest between the patients with rheumatoid arthritis and healthysubjects could not be observed. Temperature increasing arm baths and mud packs induced a provable higher increaseof local and consensual forearm blood flow than did diathermic methods. These results lead to the conclusion thatthere are differences in temperature distribution between the methods of therapy. Increasing arm baths and mud packsseem to have a stronger influence on the thermo reflexive skin perfusion.

A restrospective perspective

2005 ◽  
Vol 98 (2) ◽  
pp. 762-763 ◽  
Author(s):  
John Gamble
Keyword(s):  
Blood Flow ◽  
Adrenergic Receptors ◽  
Reactive Hyperemia ◽  
Venous Occlusion ◽  
Venous Occlusion Plethysmography ◽  
Limb Blood Flow ◽  
Major Area ◽  
Vasoactive Factors ◽  
Health And Disease

Venous occlusion plethysmography is a simple but elegant technique that has contributed to almost every major area of vascular biology in humans. The general principles of plethysmography were appreciated by the late 1800s, and the application of these principles to measure limb blood flow occurred in the early 1900s. Plethysmography has been instrumental in studying the role of the autonomic nervous system in regulating limb blood flow in humans and important in studying the vasodilator responses to exercise, reactive hyperemia, body heating, and mental stress. It has also been the technique of choice to study how human blood vessels respond to a variety of exogenously administered vasodilators and vasoconstrictors, especially those that act on various autonomic and adrenergic receptors. In recent years, plethysmography has been exploited to study the role of the vascular endothelium in health and disease. Venous occlusion plethysmography is likely to continue to play an important role as investigators seek to understand the physiological significance of newly identified vasoactive factors and how genetic polymorphisms affect the cardiovascular system in humans.

Venous Constriction in Response to Head-Up Tilt in Man

1972 ◽  
Vol 50 (4) ◽  
pp. 317-320 ◽  
Author(s):  
Lars O. Boréus ◽  
Norman K. Hollenberg
Keyword(s):  
Blood Flow ◽  
Forearm Blood Flow ◽  
Marked Decrease ◽  
Technical Difficulty ◽  
Venous Occlusion ◽  
Venous System ◽  
Postural Stress ◽  
Venous Distensibility ◽  
Head Up Tilt

There has been disagreement about the role of the peripheral venous system in cardiovascular adjustments to postural stress in man. In part this seems to be due to the technical difficulty in determining venous distensibility by plethysmographic techniques in situations where concomitant changes in blood flow occur. We have demonstrated in this study that rapid and consistent increases in forearm venous tone assessed by venous occlusion plethysmography do occur on head-up tilt in man, and that they can be readily masked by the parallel marked decrease in forearm blood flow. It is concluded that the peripheral venous system in man is not designed to function only in states of severe stress but rather plays an important role in moment-to-moment adjustments of cardiovascular activity.

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