The Effect of Felodipine on Blood Pressure, Heart Rate, Forearm Blood Flow and the Response to Venous Occlusion in Normal Man

1984 ◽  
Vol 67 (s9) ◽  
pp. 3P-3P
Author(s):  
Peter MacE ◽  
Terence Stallard ◽  
Paul Davies ◽  
William Littler
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Forearm Blood Flow ◽  
Venous Occlusion ◽  
Normal Man

scholarly journals Cardiovascular and Autonomic Responses after a Single Bout of Resistance Exercise in Men with Untreated Stage 2 Hypertension

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Marcus Vinicius Machado ◽  
Thais de Paola Chequer Barbosa ◽  
Thais Camasmine Chrispino ◽  
Fabricia Junqueira das Neves ◽  
Gabriel Dias Rodrigues ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Resistance Exercise ◽  
Vascular Reactivity ◽  
Forearm Blood Flow ◽  
Area Under The Curve ◽  
Venous Occlusion ◽  
Antihypertensive Medications ◽  
Single Bout

The aim of this paper is to assess the integrated responses of ambulatory blood pressure (BP), cardiac autonomic modulation, spontaneous baroreflex sensitivity (BRS), and vascular reactivity after a single bout of resistance exercise (RE) in men with stage 2 hypertension who have never been treated before. Ten hypertensive men were subjected to a RE session of three sets of 20 repetitions and an intensity of 40% of the 1-repetition maximum (RM) test in seven different exercises. For the control (CTR) session, the volunteers were positioned on the exercise machines but did not perform any exercise. Forearm blood flow was measured by venous occlusion plethysmography. We also analyzed the heart rate variability (HRV), ambulatory BP, blood pressure variability (BPV), and BRS. All measurements were performed at different timepoints: baseline, 20 min, 80 min, and 24 h after both RE and CTR sessions. There were no differences in ambulatory BP over the 24 h between the RE and CTR sessions. However, the area under the curve of diastolic BP decreased after the RE session. Heart rate (HR) and cardiac output increased for up to 80 and 20 min after RE, respectively. Similarly, forearm blood flow, conductance, and vascular reactivity increased 20 min after RE ( p < 0.05 ). In contrast, HRV and BRS decreased immediately after exercise and remained lower for 20 min after RE. We conclude that a single bout of RE induced an increase in vascular reactivity and reduced the pressure load by attenuating AUC of DBP in hypertensive individuals who had never been treated with antihypertensive medications.

Effects of caffeine on blood pressure, heart rate, and forearm blood flow during dynamic leg exercise

1998 ◽  
Vol 85 (1) ◽  
pp. 154-159 ◽  
Author(s):  
Jason W. Daniels ◽  
Paul A. Molé ◽  
James D. Shaffrath ◽  
Charles L. Stebbins
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Systolic Blood Pressure ◽  
Skin Temperature ◽  
Rectal Temperature ◽  
Forearm Blood Flow ◽  
Dynamic Exercise ◽  
Ang Ii ◽  
Leg Exercise

This study examined the acute effects of caffeine on the cardiovascular system during dynamic leg exercise. Ten trained, caffeine-naive cyclists (7 women and 3 men) were studied at rest and during bicycle ergometry before and after the ingestion of 6 mg/kg caffeine or 6 mg/kg fructose (placebo) with 250 ml of water. After consumption of caffeine or placebo, subjects either rested for 100 min (rest protocol) or rested for 45 min followed by 55 min of cycle ergometry at 65% of maximal oxygen consumption (exercise protocol). Measurement of mean arterial pressure (MAP), forearm blood flow (FBF), heart rate, skin temperature, and rectal temperature and calculation of forearm vascular conductance (FVC) were made at baseline and at 20-min intervals. Plasma ANG II was measured at baseline and at 60 min postingestion in the two exercise protocols. Before exercise, caffeine increased both systolic blood pressure (17%) and MAP (11%) without affecting FBF or FVC. During dynamic exercise, caffeine attenuated the increase in FBF (53%) and FVC (50%) and accentuated exercise-induced increases in ANG II (44%). Systolic blood pressure and MAP were also higher during exercise plus caffeine; however, these increases were secondary to the effects of caffeine on resting blood pressure. No significant differences were observed in heart rate, skin temperature, or rectal temperature. These findings indicate that caffeine can alter the cardiovascular response to dynamic exercise in a manner that may modify regional blood flow and conductance.

Effect of intravenous infusion of adrenaline on the cardiovascular responses to distal body subatmospheric pressure in man

1988 ◽  
Vol 75 (4) ◽  
pp. 389-394 ◽  
Author(s):  
I. W. Fellows ◽  
I. A. MacDonald ◽  
T. Bennett ◽  
D. P. O'Donoghue
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Forearm Blood Flow ◽  
Cardiovascular Responses ◽  
Saline Infusion ◽  
Subatmospheric Pressure ◽  
Arterial Blood ◽  
Adrenaline Infusion

1. On two separate occasions, at least 1 week apart, seven young healthy male subjects received intravenous infusions of either adrenaline [0.27 nmol (50 ng) min−1 kg−1] or saline (154 mmol/l NaCl), plus ascorbic acid (5.68 mmol/l), over 30 min. 2. On each occasion, the subjects were exposed to distal body subatmospheric pressure (DBSP), 0 to 50 mmHg (0 to 6.65 kPa) in 10 mmHg (1.33 kPa) steps, before infusion, during the final 15 min of the infusion, and at 15 min and 30 min after the cessation of the infusion. 3. Venous adrenaline concentrations of 2.85 ±0.22 nmol/l were achieved during the adrenaline infusion, compared with 0.49 ± 0.07 nmol/l during the saline infusion (P < 0.001). At 15 min and at 30 min after cessation of the adrenaline infusion, venous adrenaline concentrations had fallen to levels similar to those achieved after the cessation of the saline infusion. 4. Heart rate rose significantly from 58 ±4 beats/min to 67 ±4 beats/min during the adrenaline infusion (P < 0.05), but there was no further significant change in response to 50 mmHg (6.65 kPa) DBSP. At 30 min after the cessation of the adrenaline infusion, heart rate rose from 60 ± 4 beats/min to 78 ± 7 beats/min in response to 50 mmHg DBSP. This increase was significantly greater than that observed before the adrenaline infusion [58 ± 4 beats/min to 69 ±7 beats/min during 50 mmHg (6.65 kPa) DBSP; P < 0.01]. 5. During the infusion of adrenaline, systolic arterial blood pressure rose and diastolic arterial blood pressure fell, but the blood pressure responses to DBSP were unaffected. 6. Forearm blood flow increased significantly during adrenaline infusion but there was no significant difference in the fall in forearm blood flow during DBSP compared with the values before infusion. At 15 min after the cessation of the adrenaline infusion, forearm vascular resistance rose proportionately more in response to DBSP than it had before the adrenaline infusion (P < 0.05). 7. These results are consistent with adrenaline-mediated facilitation of sympathetic neuronal release of noradrenaline in the heart and in the forearm vascular bed.

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.

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.

Haemodynamic effects of physiological concentrations of circulating noradrenaline in man

1988 ◽  
Vol 75 (5) ◽  
pp. 469-475 ◽  
Author(s):  
Peter C. Chang ◽  
Eugene Kriek ◽  
Jacques A. Van Der Krogt ◽  
Gerard-Jan Blauw ◽  
Peter Van Brummelen
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Vascular Resistance ◽  
Forearm Blood Flow ◽  
Haemodynamic Effects ◽  
Plasma Noradrenaline ◽  
Arterial Blood ◽  
Forearm Vascular Resistance ◽  
Venous Plasma

1. To define the role of circulating noradrenaline in cardiovascular regulation, threshold concentrations for haemodynamic effects were determined in arterial and venous plasma of eight healthy volunteers. 2. Five doses of noradrenaline, 0–54 ng min−1 kg−1, were infused intravenously in random order and single-blind for 15 min per dose. Changes in intra-arterial blood pressure, heart rate, forearm blood flow and forearm vascular resistance were determined, and plasma noradrenaline was measured in arterial and venous blood samples. 3. Significant increases in systolic and diastolic blood pressure were found at arterial and venous plasma noradrenaline concentrations (means ±sem) of 3.00 ± 0.23 and 1.35 ±0.12 nmol/l, respectively. A significant decrease in heart rate was found at arterial and venous plasma noradrenaline concentrations of 8.99 ± 0.69 and 3.09 ± 0.60 nmol/l, respectively. The lower doses of noradrenaline tended to increase forearm blood flow and to decrease forearm vascular resistance, whereas the higher doses had no consistent effect on forearm haemodynamics. 4. During the noradrenaline infusions 73 ± 5% of the increase in arterial plasma noradrenaline concentration was extracted in the forearm. 5. The venous plasma noradrenaline threshold concentration was found to be much lower than previously reported. It is concluded that arterial and venous plasma noradrenaline concentrations which are readily encountered in physiological circumstances elicit haemodynamic effects.

Forearm vasoconstriction in response to noradrenaline and NG-monomethyl-L-arginine in essential hypertension

1999 ◽  
Vol 97 (3) ◽  
pp. 277-282 ◽  
Author(s):  
Barry J. KNEALE ◽  
Philip J. CHOWIENCZYK ◽  
Sally E. BRETT ◽  
JohnR. COCKCROFT ◽  
James M. RITTER
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Essential Hypertension ◽  
Forearm Blood Flow ◽  
Venous Occlusion ◽  
Control Group ◽  
No Production ◽  
Primary Role ◽  
Consistent Finding ◽  
And Control

A role for abnormal NO production in essential hypertension remains controversial. Blunted vasoconstriction of forearm resistance vasculature in response to NG-monomethyl-⌊-arginine (⌊-NMMA; an inhibitor of NO biosynthesis), relative to the response to noradrenaline, has been reported in hypertensive patients and interpreted as evidence of reduced basal NO biosynthesis. We sought to determine whether reduced sensitivity of forearm vasculature to the vasoconstrictor action of l-NMMA relative to that of noradrenaline is a consistent finding in essential hypertension. We studied a group of patients (n = 32; blood pressure 176±4/102±2 mmHg; means±S.E.M.) and a group of healthy normotensive controls (n = 32; blood pressure 130±2/75±1 mmHg). Noradrenaline (60–240 pmol·min-1) and ⌊-NMMA (1–4 μmol·min-1) were infused into the brachial artery, and forearm blood flow was measured by venous occlusion plethysmography. The effects of each vasoconstrictor were similar in hypertensive and control subjects. The highest dose of l-NMMA reduced forearm blood flow by 0.75±0.12 ml·min-1·dl-1 in the control group and by 0.89±0.10 ml·min-1·dl-1 in the hypertensive group. The study had 90% power (with P = 0.05) to detect a 10% difference in forearm blood flow response between the hypertensive and control groups. We conclude that reduced sensitivity of forearm resistance vasculature to the vasoconstrictor action of l-NMMA is not a universal feature of essential hypertension. This argues against a primary role for reduced basal NO biosynthesis in skeletal muscle resistance vessels in the pathogenesis of essential hypertension.

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