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

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.

2002 ◽  
Vol 103 (s2002) ◽  
pp. 53S-58S ◽  
Author(s):  
Charles J. FERRO ◽  
William G. HAYNES ◽  
Malcolm F. HAND ◽  
David J. WEBB

The importance of endothelin-1 (ET-1) in the pathophysiology of essential hypertension is unclear. We therefore compared the effects of endothelin ETA receptor blockade and the stimulation of ETA and ETB receptors, and their interaction with the sympathetic nervous system, in the forearm resistance vessels of patients with essential hypertension and healthy control subjects. A total of 27 untreated patients with essential hypertension (blood pressure >160/100mmHg) and 25 normotensive (blood pressure <140/90mmHg) age- and sex-matched control subjects participated in these studies. A total of 10 patients and 10 controls took part in each phase. Locally active doses of study drugs were infused into the non-dominant brachial artery, while forearm blood flow was measured by venous occlusion plethysmography. A 60min infusion of BQ-123 (an ETA receptor antagonist; 100nmol/min) significantly increased forearm blood flow by 40±8% in hypertensive patients and by 35±5% in controls, with no difference between groups (P = 0.49). Forearm vasoconstriction to ET-1 (an ETA and ETB receptor agonist; 5 pmol/min) for 90min was significantly blunted in hypertensive patients (21±4%) compared with control subjects (37±3%; P = 0.0001). Forearm vasoconstriction to sarafotoxin S6c (an ETB receptor agonist; 10 pmol/min) for 90min was similar in hypertensive patients (44±5%) and control subjects (48±4%; P = 0.95). Sympathetically mediated vasoconstriction produced by lower-body negative pressure was not different in hypertensive patients compared with controls, and was not affected by infusion of ET-1 or sarafotoxin S6c. There were no differences in the observed increase in forearm blood flow with a control vasodilator (sodium nitroprusside) or the observed decrease in forearm blood flow with a control vasoconstrictor (noradrenaline) between hypertensive patients and control subjects. BQ-123 produced a significant increase in forearm blood flow in hypertensive patients, consistent with the anti-hypertensive actions of this agent. In conclusion, forearm vasoconstriction to ET-1, but not to sarafotoxin S6c, was reduced in patients with essential hypertension, consistent with possible down-regulation of the ETA receptor in this condition.


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 ◽  
...  

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.


1981 ◽  
Vol 61 (s7) ◽  
pp. 161s-164s ◽  
Author(s):  
P. Bolli ◽  
F. W. Amann ◽  
L. Hulthén ◽  
W. Kiowski ◽  
F. R. Bühler

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.


2021 ◽  
pp. 72-74
Author(s):  
Deepak Jain ◽  
Ajith Thomas ◽  
Rajinder Singh Gupta

Background: The association of raised serum uric acid levels with various cardiovascular risk factors has often led to the debate of whether raised serum uric acid levels could be an independent risk factor in essential hypertension. Hence, the present study was conducted for assessing the serum uric acid levels in cases of essential hypertension and comparing them with normal healthy, non-hypertensive controls. Materials & Methods: Sixty patients visiting in the department of general medicine, MMIMSR with newly diagnosed cases of essential hypertension [according to the Indian guidelines on Hypertension(IGH) III-2013] , fullling the inclusion criteria and after verifying the exclusion criteria were nally taken up for the study. Sixty controls of age and sex matched were taken from the same catchment area. Results: The mean age of the subjects of the essential hypertension group and control group was found to be 45.75 years and 47.8 years respectively. Mean systolic blood pressure and diastolic blood pressure among the subjects of the essential hypertension group was 161.3 and 102.3 mm of Hg. Mean systolic blood pressure and diastolic blood pressure among the subjects of the control group was 116.8 and 77.4 mm of Hg. Mean serum uric acid levels among the subjects of the essential hypertension group and control group was found to be 6.45 mg/dL and 5.57 mg/dLrespectively. Signicant results were obtained while comparing the mean serum uric acid levels among the subjects of the essential hypertension group and the control group. Hyperuricemia was present in 38.33 percent of the patients (23 patients) of the essential hypertension group and 13.33 percent of the patients (8 patients) of the control group. Signicant results were obtained while comparing the prevalence of hyperuricemia in between the two study groups.Conclusion: An independent relationship of elevated serum uric acid levels with hypertension and indicates the signicance of maintaining normal serum uric acid concentration to prevent hypertension.


1984 ◽  
Vol 67 (s9) ◽  
pp. 3P-3P
Author(s):  
Peter MacE ◽  
Terence Stallard ◽  
Paul Davies ◽  
William Littler

1986 ◽  
Vol 61 (2) ◽  
pp. 673-678 ◽  
Author(s):  
L. I. Sinoway ◽  
T. I. Musch ◽  
J. R. Minotti ◽  
R. Zelis

In an effort to evaluate potential peripheral adaptations to training, maximal metabolic vasodilation was studied in the dominant and nondominant forearms of six tennis players and six control subjects. Maximal metabolic vasodilation was defined as the peak forearm blood flow measured after release of arterial occlusion, the reactive hyperemic blood flow (RHBF). Two ischemic stimuli were employed in each subject: 5 min of arterial occlusion (RHBF5) and 5 min of arterial occlusion coupled with 1 min of ischemic exercise (RHBF5ex). RHBF and resting forearm blood flows were measured using venous occlusion strain-gauge plethysmography (ml X min-1 X 100 ml-1). Resting forearm blood flows were similar in both arms of both groups. RHBF5ex was similar in both arms of our control group (dominant, 40.8 +/- 1.2 vs. nondominant, 40.9 +/- 2.1). However, RHBF5ex was 42% higher in the dominant than in the nondominant forearms of our tennis player population (dominant, 48.7 +/- 4.0 vs. nondominant, 34.4 +/- 3.4; P less than 0.05). This intraindividual difference in peak forearm blood flows was not secondary to improved systemic conditioning since the maximal O2 consumptions in the two study groups were similar (controls, 45.4 +/- 3.9 vs. tennis players, 46.1 +/- 1.7). These findings suggest a primary peripheral cardiovascular adaptation to exercise training in the dominant forearms of the tennis players resulting in a greater maximal vasodilatation.


1979 ◽  
Vol 57 (s5) ◽  
pp. 177s-180s ◽  
Author(s):  
W. Kiowski ◽  
P. Van Brummelen ◽  
F. R. Bühler

1. The relationships between plasma noradrenaline concentration at rest and blood pressure, as well as increase in forearm blood flow in response to a brachial artery infusion of the α-adrenoreceptor-blocking agent phentolamine, were investigated in hypertensive and normotensive subjects of similar age. 2. In 44 hypertensive patients plasma noradrenaline correlated with systolic, diastolic and mean blood pressures, but no difference in the mean plasma noradrenaline concentration was found. 3. In 11 patients and 14 normotensive subjects α-adrenoreceptor blockade resulted in a similar increase in forearm blood flow. Only in the patients, however, was this increase related to plasma noradrenaline and blood pressure. 4. In patients with established essential hypertension plasma noradrenaline can be considered to be a marker of α-adrenoreceptor-mediated vasoconstriction, which, in part, determines the height of the blood pressure.


1963 ◽  
Vol 18 (4) ◽  
pp. 789-793 ◽  
Author(s):  
Frank D. Rohter ◽  
Rene H. Rochelle ◽  
Chester Hyman

Forearm blood flow measurements were made with a venous occlusion plethysmograph on six competitive swimmers and six control subjects at rest and during a prescribed rhythmic exercise throughout a 13-week training and detraining program. The swimmers‗ mean exercise forearm blood flow increased progressively during the training program, reaching a maximum at the peak of training toward the end of the 5th week, after which it decreased to near posttraining levels during the period of detraining. The increase in the swimmer's exercise flow between the 1st week of training (4.02 ± 0.59 ml/100 ml min) and the 5th week of training (6.40 ± 0.56 ml/100 ml min) was statistically significant; their decrease in mean exercise blood flow during the 3rd week of detraining (4.70 ± 0.24 ml/100 ml min) was also statistically significant. There was no significant change in the swimmers' resting blood flow; nor were there significant changes in either the exercise or the resting blood flows of the control group. The technique for measuring blood flow in the forearm during rhythmic exercise is explained. Submitted on December 11, 1962


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