Acute Hypertension Impairs Endothelium-Dependent Vasodilatation

1998 ◽  
Vol 94 (6) ◽  
pp. 601-607 ◽  
Author(s):  
Jonas Millgård ◽  
Lars Lind
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Sodium Nitroprusside ◽  
Forearm Blood Flow ◽  
Acute Hypertension ◽  
Flow Measurements ◽  
Sustained Hypertension ◽  
Before And After ◽  
Normotensive Subjects ◽  
Blood Flow Measurements

1. Previous investigations have demonstrated an impaired endothelium-dependent vasodilatation (EDV) in patients with hypertension. The present study aimed to investigate if an acute rise in blood pressure to hypertensive levels impairs EDV in otherwise normotensive subjects. 2. Twenty-seven young, healthy, normotensive subjects were studied. Eight of these underwent evaluation of EDV and endothelium-independent vasodilatation (EIDV) by means of forearm blood flow measurements during local intra-arterial infusions of methacholine (2 and 4 μg/min) and sodium nitroprusside (5 and 10 μg/min), before and after 1 h of sustained hypertension, induced by noradrenaline given intravenously. Identical measurements were made in 11 subjects before and during concomitant local intra-arterial infusion of noradrenaline without change in blood pressure and eight subjects were studied during saline infusions. 3. One hour of sustained hypertension (diastolic blood pressure > 95 mmHg) significantly attenuated both forearm blood flow (17.4 ± 6.8 versus 27.4 ± 6.8 ml · min−1 · 100 ml−1 tissue at baseline, P < 0.05) and forearm vascular resistance decrease (3.2 ± 0.87 versus 7.4 ± 2.5 units at baseline, P < 0.05) during methacholine infusion. These attenuations were significantly more pronounced for methacholine than for sodium nitroprusside (P < 0.05). In contrast, local intra-arterial noradrenaline infusions impaired vasodilatation induced by methacholine and sodium nitroprusside to a similar extent. Saline infusions did not change either EDV or EIDV. 4. Thus, an acute rise in blood pressure to hypertensive levels induced by noradrenaline impaired EDV more than EIDV in otherwise normotensive subjects, while no such selective effect of local noradrenaline was seen, suggesting that a high blood pressure impairs endothelial vasodilator function.

scholarly journals Improved brain perfusion after electrical cardioversion of atrial fibrillation

EP Europace ◽  
2019 ◽  
Vol 22 (4) ◽  
pp. 530-537 ◽  
Author(s):  
Marianna Gardarsdottir ◽  
Sigurdur Sigurdsson ◽  
Thor Aspelund ◽  
Valdis Anna Gardarsdottir ◽  
Lars Forsberg ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Atrial Fibrillation ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Magnetic Resonance ◽  
Brain Perfusion ◽  
Resonance Imaging ◽  
Flow Measurements ◽  
Before And After ◽  
Blood Flow Measurements

Abstract Aims Atrial fibrillation (AF) has been associated with reduced brain volume, cognitive impairment, and reduced cerebral blood flow. The causes of reduced cerebral blood flow in AF are unknown, but no reduction was seen in individuals without the arrhythmia in a previous study. The aim of this study was to test the hypothesis that brain perfusion, measured with magnetic resonance imaging (MRI), improves after cardioversion of AF to sinus rhythm (SR). Methods and results All patients undergoing elective cardioversion at our institution were invited to participate. A total of 44 individuals were included. Magnetic resonance imaging studies were done before and after cardioversion with both brain perfusion and cerebral blood flow measurements. However, 17 did not complete the second MRI as they had a recurrence of AF during the observation period (recurrent AF group), leaving 17 in the SR group and 10 in the AF group to complete both measurements. Brain perfusion increased after cardioversion to SR by 4.9 mL/100 g/min in the whole brain (P &lt; 0.001) and by 5.6 mL/100 g/min in grey matter (P &lt; 0.001). Cerebral blood flow increased by 58.6 mL/min (P &lt; 0.05). Both brain perfusion and cerebral blood flow remained unchanged when cardioversion was unsuccessful. Conclusion In this study of individuals undergoing elective cardioversion for AF, restoration, and maintenance of SR for at least 10 weeks after was associated with an improvement of brain perfusion and cerebral blood flow measured by both arterial spin labelling and phase contrast MRI. In those individuals where cardioversion was unsuccessful, there was no change in perfusion or blood flow.

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.

Four weeks of cycle training increases basal production of nitric oxide from the forearm

1997 ◽  
Vol 272 (3) ◽  
pp. H1070-H1077 ◽  
Author(s):  
B. A. Kingwell ◽  
B. Sherrard ◽  
G. L. Jennings ◽  
A. M. Dart
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Sodium Nitroprusside ◽  
Forearm Blood Flow ◽  
Protective Effects ◽  
Nitric Oxide Synthase Inhibitor ◽  
Nitrite Production ◽  
Cycle Training ◽  
Nitrate And Nitrite

The purpose of this study was to determine whether nontrained vascular beds might contribute to the beneficial effects of exercise, including reduced blood pressure by enhanced nitric oxide production. Thirteen healthy, sedentary male volunteers performed 4 wk of normal sedentary activity and 4 wk of cycle training in a randomized order. At the end of each intervention, venous occlusion plethysmography was used to study the forearm blood flow responses to intra-arterial infusions of the nitric oxide synthase inhibitor N(G)-monomethyl-L-arginine (L-NMMA), acetylcholine, and sodium nitroprusside. Training increased the maximal work-load and maximal oxygen consumption, whereas intrabrachial blood pressure was reduced. L-NMMA caused a greater vasoconstriction after training (P = 0.004). Net nitrate and nitrite consumption by the forearm was less after training both before and after administration of L-NMMA (P = 0.04), consistent with increased nitrate and nitrite production from nitric oxide metabolism. There was no difference in the response to acetylcholine or sodium nitroprusside between the two states. Preliminary studies showed an increase in forearm blood flow and blood viscosity after cycling, suggesting that elevated shear stress in this vascular bed may contribute to endothelial adaptation and the cardiovascular protective effects of exercise training.

REPRODUCIBILITY OF INTESTINAL BLOOD FLOW MEASUREMENTS BEFORE AND AFTER 1 HOUR CYCLING

1995 ◽  
Vol 27 (Supplement) ◽  
pp. S65
Author(s):  
Peters HPF ◽  
D de Leeuw ◽  
R C Lapham ◽  
E Bol ◽  
M S van Leeuwen ◽  
...  
Keyword(s):  
Blood Flow ◽  
Intestinal Blood Flow ◽  
Flow Measurements ◽  
Before And After ◽  
Blood Flow Measurements

Reproducibility of haemodynamic and plasma catecholamine responses to isometric exercise and mental arithmetic in normo- and hyper-tensive subjects

1988 ◽  
Vol 75 (6) ◽  
pp. 615-619 ◽  
Author(s):  
Jacques Lenders ◽  
Harry Houben ◽  
Rudolf Van Valderen ◽  
Jacques Willemsen ◽  
Theo Thien
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Forearm Blood Flow ◽  
Mental Arithmetic ◽  
Pharmacological Intervention ◽  
Handgrip Exercise ◽  
Single Observation ◽  
Plasma Adrenaline ◽  
Normotensive Subjects

1. To determine the reproducibility of a mental arithmetic stress test and a handgrip exercise test, we studied the responses of blood pressure, heart rate, forearm blood flow and plasma catecholamines on two occasions, with an interval of at least 1 week, in 24 normotensive and 22 hypertensive subjects. 2. The se of a single observation of the percentage changes of blood pressure ranged from 3.9 to 9.3% in normotensive subjects and from 3.9 to 7.4% in hypertensive subjects in both tests. For heart rate, these values were 4.9–12.3% in the normotensive subjects and 4.8–5.7% in the hypertensive subjects. However, there was a wide individual scatter of these haemodynamic responses during both tests. The forearm blood flow, only measured during mental arithmetic, had an se of a single observation of 33.7%. 3. In 10 normotensive subjects the se of a single observation of the change in plasma noradrenaline was 0.16 nmol/l during handgrip exercise and 0.09 nmol/l during mental arithmetic. The corresponding values for plasma adrenaline were 0.04 and 0.05 nmol/l. 4. In conclusion, although both tests showed a rather low se of a single observation for the blood pressure and heart rate responses in normo- and hyper-tensive subjects, there was a considerable individual variability. If related to the mean forearm blood flow responses, the se of a single observation of the forearm blood flow response was of similar magnitude. The limited intra-individual reproducibility of both tests should be borne in mind when interpreting pharmacological intervention studies or studies evaluating sympathoadrenal reactivity in cardiovascular disorders.

Effect of Chronic Smoking on Endothelium-Dependent Vascular Relaxation in Humans

1993 ◽  
Vol 85 (1) ◽  
pp. 51-55 ◽  
Author(s):  
Marie-Cécile Jacobs ◽  
Jacques W. M. Lenders ◽  
Jan A. Kapma ◽  
Paul Smits ◽  
Theo Thien
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cigarette Smoking ◽  
Sodium Nitroprusside ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Forearm Blood Flow ◽  
Vascular Relaxation ◽  
Arterial Blood ◽  
Forearm Vascular Resistance

1. Cigarette smoking is one of the major risk factors for the development of atherosclerosis. It is not clear, however, whether chronic cigarette smoking impairs the normal physiological function of the endothelium before the development of morphological vascular lesions. To test this, we investigated endothelium-dependent vascular relaxation in young habitual smoking subjects. 2. In 11 non-smokers and 10 habitual smokers we measured the changes in bilateral forearm blood flow, arterial blood pressure and forearm vascular resistance (ratio between mean arterial blood pressure and forearm blood flow) during three interventions: postocclusive forearm hyperaemia, intrabrachial infusion of methacholine which causes vasodilatation by stimulating the release of endothelium-dependent relaxing factor, and intrabrachial infusion of sodium nitroprusside which causes vasodilatation independently from the endothelium by a direct effect on the vascular smooth muscle wall. 3. During infusion of the highest dose of methacholine, forearm vascular resistance decreased by 91.7 ± 1.4% in the smokers and by 89.9 ± 1.8% in the non-smokers. During infusion of sodium nitroprusside, forearm vascular resistance decreased by 80.0 ± 3.8% in the smokers as compared with 80.7 ± 6.1% in the non-smokers. There was no difference in basal forearm vascular resistance or in post-ischaemic reactive hyperaemia between smokers and non-smokers. Thus, vasodilatation induced by both methacholine and sodium nitroprusside was not significantly different between smokers and non-smokers. 4. We conclude that in young habitual cigarette smokers the endothelium-dependent vasodilatation in the forearm seems to be preserved, suggesting that habitual smoking does not result in permanent endothelial dysfunction in the human forearm.

Accuracy of portal and forearm blood flow measurements in the assessment of the portal pressure response to propranolol

1997 ◽  
Vol 27 (3) ◽  
pp. 496-504 ◽  
Author(s):  
Agustín Albillos ◽  
María Perez-Paramo ◽  
Guillermo Cacho ◽  
Jerónimo Iborra ◽  
Jose Luis Calleja ◽  
...  
Keyword(s):  
Blood Flow ◽  
Forearm Blood Flow ◽  
Portal Pressure ◽  
Pressure Response ◽  
Flow Measurements ◽  
Blood Flow Measurements

Elevated Plasma Adrenaline Reflects Sympathetic Overactivity and Enhanced α-Adrenoceptor-Mediated Vasoconstriction in Essential Hypertension

1981 ◽  
Vol 61 (s7) ◽  
pp. 161s-164s ◽  
Author(s):  
P. Bolli ◽  
F. W. Amann ◽  
L. Hulthén ◽  
W. Kiowski ◽  
F. R. Bühler
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Essential Hypertension ◽  
Forearm Blood Flow ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Plasma Adrenaline ◽  
Pressor Test ◽  
Normotensive Subjects

1. Stressful sympathetic stimulation (cold pressor test) was applied to 18 patients with essential hypertension and 15 normotensive subjects. Intra-arterial blood pressure, heart rate, plasma adrenaline and noradrenaline concentrations as well as forearm blood flow were measured before and during the cold pressor test; tests were repeated after regional postsynaptic α1-adrenoceptor blockade with prazosin. 2. Under basal conditions mean blood pressure (P &lt; 0.001), heart rate (P &lt; 0.01), forearm blood flow (P &lt; 0.001) as well as adrenaline concentration (P &lt; 0.01), but not noradrenaline, was higher in patients with essential hypertension. 3. During the cold pressor test, mean blood pressure, heart rate, plasma adrenaline and noradrenaline concentrations increased and forearm flow decreased (all P &lt; 0.001). 4. Stress-stimulated plasma adrenaline was higher in essential hypertensive patients than in normotensive subjects (P &lt; 0.01). In the former the stress-induced increase in plasma adrenaline correlated with the increase in mean blood pressure (r = 0.514; P &lt; 0.05). 5. Prazosin increased forearm blood flow more in essential hypertension (P &lt; 0.001). This increase correlated with the resting plasma adrenaline in the hypertensive (r = 0.710; P &lt; 0.001), but not in normotensive, subjects. 6. When the cold pressor test was repeated during postsynaptic α1-adrenoceptor blockade forearm blood flow did not decrease; instead it increased further in both groups (P &lt; 0.05). 7. Thus in essential hypertension elevated plasma adrenaline concentration reflects sympathetic overactivity as also expressed by enhanced α-adrenoceptor-mediated vasoconstriction.

Age-independent forearm vasodilatation by acetylcholine and adenosine 5′-triphosphate in humans

1990 ◽  
Vol 78 (1) ◽  
pp. 89-93 ◽  
Author(s):  
Tsutomu Imaizumi ◽  
Akira Takeshita ◽  
Satoshi Suzuki ◽  
Megumu Yoshida ◽  
Shinichi Ando ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Sodium Nitroprusside ◽  
Vascular Resistance ◽  
Brachial Artery ◽  
Forearm Blood Flow ◽  
Resistance Arteries ◽  
Dose Dependent ◽  
Forearm Vascular Resistance ◽  
Age Independent

1. Forearm vasodilator responses to acetylcholine, ATP and sodium nitroprusside were examined in healthy young (20 ± 1 years, n = 9), middle-aged (46 ± 2 years, n = 6) and old (57 ± 1 years, n = 6) subjects. 2. A brachial artery was cannulated with a 20-gauge cannula through which drugs at graded doses were locally infused for 2 min at each dose. During drug infusions, forearm blood flow was continuously measured at 15 s intervals using a plethysmograph. Forearm vascular resistance was calculated from forearm blood flow and mean blood pressure obtained in the opposite arm. Basal forearm blood flow and forearm vascular resistance did not differ between the three groups. 3. Acetylcholine and ATP were used to examine endothelium-dependent vasodilatation, and sodium nitroprusside was used to examine endothelium-independent vasodilatation. All three drugs caused dose-dependent increases in forearm blood flow (P < 0.01) and decreases in forearm vascular resistance (P < 0.01). The increases in forearm blood flow or decreases in forearm vascular resistance in response to infusions of the three drugs did not differ between the three groups. 4. These results suggest that endothelium-dependent and endothelium-independent vasodilatation in forearm resistance arteries do not alter with ageing in humans.

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