Initial orthostatic hypotension and cerebral blood flow regulation: effect of α1-adrenoreceptor activity

2013 ◽  
Vol 304 (2) ◽  
pp. R147-R154 ◽  
Author(s):  
Nia C. S. Lewis ◽  
Philip N. Ainslie ◽  
Greg Atkinson ◽  
Helen Jones ◽  
Emily J. M. Grant ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Orthostatic Hypotension ◽  
Relative Difference ◽  
Cerebral Hypoperfusion ◽  
Adrenergic Blockade ◽  
Absolute Level ◽  
Arterial Blood ◽  
Placebo Trial ◽  
Initial Orthostatic Hypotension ◽  
End Tidal

We examined the hypothesis that α1-adrenergic blockade would lead to an inability to correct initial orthostatic hypotension (IOH) and cerebral hypoperfusion, leading to symptoms of presyncope. Twelve normotensive humans (aged 25 ± 1 yr; means ± SE) attempted to complete a 3-min upright stand, 90 min after the administration of either α1-blockade (prazosin, 1 mg/20 kg body wt) or placebo. Continuous beat-to-beat measurements of middle cerebral artery velocity (MCAv; Doppler), blood pressure (finometer), heart rate, and end-tidal Pco2were obtained. Compared with placebo, the α1-blockade reduced resting mean arterial blood pressure (MAP) (−15%; P < 0.01); MCAv remained unaltered ( P ≥ 0.28). Upon standing, although the absolute level of MAP was lower following α1-blockade (39 ± 10 mmHg vs. 51 ± 14 mmHg), the relative difference in IOH was negligible in both trials (mean difference in MAP: 2 ± 2 mmHg; P = 0.50). Compared with the placebo trial, the declines in MCAv and PetCO2during IOH were greater in the α1-blockade trial by 12 ± 4 cm/s and 4.4 ± 1.3 mmHg, respectively ( P ≤ 0.01). Standing tolerance was markedly reduced in the α1-blockade trial (75 ± 17 s vs. 180 ± 0 s; P < 0.001). In summary, while IOH was little affected by α1-blockade, the associated decline in MCAv was greater in the blockade condition. Unlike in the placebo trial, the extent of IOH and cerebral hypoperfusion failed to recover toward baseline in the α1-blockade trial leading to presyncope. Although the development of IOH is not influenced by the α1-adrenergic receptor pathway, this pathway is critical in the recovery from IOH to prevent cerebral hypoperfusion and ultimately syncope.

scholarly journals Management of initial orthostatic hypotension: lower body muscle tensing attenuates the transient arterial blood pressure decrease upon standing from squatting

2007 ◽  
Vol 113 (10) ◽  
pp. 401-407 ◽  
Author(s):  
C. T. Paul Krediet ◽  
Ingeborg K. Go-Schön ◽  
Yu-Sok Kim ◽  
Mark Linzer ◽  
Johannes J. Van Lieshout ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Orthostatic Hypotension ◽  
Healthy Subjects ◽  
Lower Body ◽  
Blood Pressure Decrease ◽  
Body Muscle ◽  
Arterial Blood ◽  
Pressure Decrease ◽  
Standing Up ◽  
Initial Orthostatic Hypotension

IOH (initial orthostatic hypotension) comprises symptoms of cerebral hypoperfusion caused by an abnormally large transient MAP (mean arterial pressure) decrease 5–15 s after arising from a supine, sitting or squatting position. Few treatment options are available. In the present study, we set out to test the hypothesis that LBMT (lower body muscle tensing) attenuates IOH after rising from squatting and its symptoms in daily life. A total of 13 IOH patients (nine men; median age, 27 years) rose from squatting twice, once with LBMT and once without. In addition, seven healthy volunteers (five men; median age, 27 years) were studied in a cross-over study design. They stood up from the squatting position three times, once combined with LBMT. Blood pressure (Finometer) was measured continuously, and CO (cardiac output) by Modelflow and TPR (total peripheral resistance) were computed. MAP, CO and TPR were compared without and with LBMT. Using a questionnaire, the perceived effectiveness of LBMT in the patients' daily lives was evaluated. With LBMT, the minimal MAP after standing up was higher in both groups (19 mmHg in patients and 13 mmHg in healthy subjects). In healthy subjects, the underlying mechanism was a blunted TPR decrease (to 47% compared with 60%; P<0.05), whereas in the patients no clear CO or TPR pattern was discernible. During follow-up, eight out of ten patients using LBMT reported fewer IOH symptoms. In conclusion, LBMT is a new intervention to attenuate the transient blood pressure decrease after standing up from squatting, and IOH patients should be advised about the use of this manoeuvre.

Lower limb-localized vascular phenomena explain initial orthostatic hypotension upon standing from squat

2011 ◽  
Vol 301 (5) ◽  
pp. H2102-H2112 ◽  
Author(s):  
Michael E. Tschakovsky ◽  
Kristine Matusiak ◽  
Catherine Vipond ◽  
Lisa McVicar
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Orthostatic Hypotension ◽  
Arterial Blood Pressure ◽  
Lower Limb ◽  
Potential Contribution ◽  
Vascular Conductance ◽  
Leg Muscles ◽  
Arterial Blood ◽  
Initial Orthostatic Hypotension

The cause(s) of initial orthostatic hypotension (transient fall in blood pressure within 15 s upon active rising) have not been established. We tested the hypothesis that this hypotension is due to local vascular phenomena in contracting leg muscles from the brief effort of standing up. Seventeen young healthy subjects (2 male and 15 female, 22.5 ± 1.0 years) performed an active rise from resting squat after a 10-s squat, a 1-min squat, or a 5-min squat. Beat-by-beat arterial blood pressure, cardiac output, heart rate, and stroke volume (Finometer finger photoplethysmography) and right common femoral artery blood flow (Doppler and Echo ultrasound) were recorded. Data are means ± SE. Quiet standing before squat represented baseline. Peak increases in lower limb and total vascular conductance (ml·min−1·mmHg−1) upon standing were not different within squat conditions (10-s squat, 50.0 ± 12.4 vs. 44.3 ± 5.0; 1-min squat, 54.7 ± 9.2 vs. 50.5 ± 4.5; 5-min squat, 67.4 ± 13.7 vs. 58.8 ± 3.9; all P > 0.574). Mean arterial blood pressure (in mmHg) fell to a nadir well below standing baseline in all conditions despite increases in cardiac output. The hypotension predicted by the increase in leg vascular conductance accounted for this hypotension [observed vs. predicted (in mmHg): 10-s squat, −17.1 ± 2.1 vs. −18.3 ± 5.5; 1-min squat, −22.0 ± 3.8 vs. −25.3 ± 4.9; 5-min squat, −28.3 ± 4.0 vs. −29.2 ± 6.7]. We conclude that rapid contraction induced dilation in leg muscles with the effort of standing, along with a minor potential contribution of elevated lower limb arterio-venous pressure gradient, outstrips compensatory cardiac output responses and is the cause of initial orthostatic hypotension upon standing from squat.

Enhancement of the Antihypertensive Effect of Hydrochlorothiazide in Dogs after Suppression of Renin Release by Beta-Adrenergic Blockade

1975 ◽  
Vol 48 (2) ◽  
pp. 147-151
Author(s):  
C. S. Sweet ◽  
M. Mandradjieff
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Arterial Blood Pressure ◽  
Antihypertensive Effect ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Release ◽  
Antihypertensive Activity ◽  
Adrenergic Blockade ◽  
Arterial Blood

1. Renal hypertensive dogs were treated with hydrochlorothiazide (8−2 μmol/kg or 33 μmol/kg daily for 7 days), or timolol (4.6 μmol/kg daily for 4 days), a potent β-adrenergic blocking agent, or combinations of these drugs). Changes in mean arterial blood pressure and plasma renin activity were measured over the treatment period. 2. Neither drug significantly lowered arterial blood pressure when administered alone. Plasma renin activity, which did not change during treatment with timolol, was substantially elevated during treatment with hydrochlorothiazide. 3. When timolol was administered concomitantly with hydrochlorothiazide, plasma renin activity was suppressed and blood pressure was significantly lowered. 4. These observations suggest that compensatory activation of the renin-angiotensin system limits the antihypertensive activity of hydrochlorothiazide in renal hypertensive dogs and suppression of diuretic-induced renin release by timolol unmasks the antihypertensive effect of the diuretic.

Abstract 2470: Augmented Tonic Activation Of Chemoreceptors May Contribute To Sympathetic Overactivity In Patients With Essential Hypertension

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Maciej Sinski ◽  
Jacek Lewandowski ◽  
Joanna Bidiuk ◽  
Piotr Abramczyk ◽  
Anna Dobosiewicz ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Sympathetic Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Arterial Blood ◽  
Hemoglobin Saturation ◽  
Ambient Oxygen ◽  
Young Subjects ◽  
End Tidal ◽  
Carotid Body Chemoreceptors

Rationale : Peripheral chemoreflex contributes to regulation of arterial blood pressure and chemoreceptors respond not only to hypoxia but they are also continuously activated by normal ambient oxygen concentration. Stimulation of chemoreceptors activates sympathetic traffic and this response may be altered in subjects with essential hypertension.. Objective: The aim of our study was to investigate the effect of deactivation of carotid body chemoreceptors on sympathetic activity directly measured as MSNA (muscle sympathetic nerve activity) in young subjects with mild to moderate untreated hypertension. Methods: Twelve patients with essential hypertension (36±9 years, all men, BMI 29±4 kg/m 2 ,) and 8 controls (37±7, men BMI 27±5kg/m 2 ) participated in the study. None of the patients or controls received any medications. MSNA (burst/minute and mean burst amplitude - au), systolic blood pressure (SBP) and diastolic blood pressure (DBP), heart rate (HR), ECG, hemoglobin saturation with oxygen (Sat%), end tidal CO 2 and respiratory movements were monitored and measured after 10 minute of respiration by non-rebreathing mask with 100% 0 2 or 21% O 2 applied in blinded fashion. Results: Hypertensives had higher resting MSNA (38.6 ±8.6 burst/min vs. 30.3±.7 burst/min, p<0.05), SBP (149.1± 9.9 vs. 124.1 ±11.6, p < 0.05) and DBP (92.1 ±8.6 vs. 78.1 ± 8.9, p< 0.05) than controls. Breathing with 100% oxygen caused significant decrease in MSNA in hypertensives (from 38.6 ± 8.6 burst/min to 26.3 burst/min ± 6.8 and from 100 ± 0 au to 86 ± 18 au, p< 0.05) and no change in MSNA in controls (30.3 ± 5.7 burst/min initially and 27.3 burst/min ± 6.2 after 100% 0 2 , 100 ± 0 au vs. 98 ± 11 au). Blood pressure, end tidal CO 2 , respiration frequency did not change significantly after hyperoxia while HR decreased (from 69.6 ± 9 to 64.1 ± 7 in hypertensives p<0.05 and from 67± 8 to 62.5 ± 7 in controls, p< 0.05). Sat% increased significantly in both groups to 99%. Conclusions: Increased sympathetic activity in young, untreated hypertensives may be caused by the elevated tonic chemoreflex activation.

scholarly journals The preponderance of initial orthostatic hypotension in postural tachycardia syndrome

2020 ◽  
Vol 129 (3) ◽  
pp. 459-466
Author(s):  
Julian M. Stewart ◽  
Archana Kota ◽  
Mary Breige O’Donnell-Smith ◽  
Paul Visintainer ◽  
Courtney Terilli ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Heart Rate Variability ◽  
Cerebral Blood Flow ◽  
Orthostatic Hypotension ◽  
Pressure Recovery ◽  
Postural Tachycardia Syndrome ◽  
Postural Tachycardia ◽  
Initial Orthostatic Hypotension

Significant initial orthostatic hypotension (IOH) occurs in ~50% of postural tachycardia syndrome (POTS) patients and 13% of controls. Heart rate and blood pressure recovery are prolonged in IOH sustaining lightheadedness; IOH is more prevalent and severe in POTS. Altered cerebral blood flow and cardiorespiratory regulation are more prevalent in POTS. Altered heart rate variability and baroreflex gain may cause nearly instantaneous lightheadedness in POTS. IOH alone fails to confer a strong probability of POTS.

Hypoxemia raises muscle sympathetic activity but not norepinephrine in resting humans

1989 ◽  
Vol 66 (4) ◽  
pp. 1736-1743 ◽  
Author(s):  
L. B. Rowell ◽  
D. G. Johnson ◽  
P. B. Chase ◽  
K. A. Comess ◽  
D. R. Seals
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Nervous Activity ◽  
Plasma Concentrations ◽  
Random Order ◽  
Sympathetic Nervous Activity ◽  
Severe Hypoxemia ◽  
Arterial Blood ◽  
End Tidal ◽  
Venous Plasma

The experimental objective was to determine whether moderate to severe hypoxemia increases skeletal muscle sympathetic nervous activity (MSNA) in resting humans without increasing venous plasma concentrations of norepinephrine (NE) and epinephrine (E). In nine healthy subjects (20–34 yr), we measured MSNA (peroneal nerve), venous plasma levels of NE and E, arterial blood pressure, heart rate, and end-tidal O2 and CO2 before (control) and during breathing of 1) 12% O2 for 20 min, 2) 10% O2 for 20 min, and 3) 8% O2 for 10 min--in random order. MSNA increased above control in five, six, and all nine subjects during 12, 10, and 8% O2, respectively (P less than 0.01), but only after delays of 12 (12% O2) and 4 min (8 and 10% O2). MSNA (total activity) rose 83 +/- 20, 260 +/- 146, and 298 +/- 109% (SE) above control by the final minute of breathing 12, 10, and 8% O2, respectively. NE did not rise above control at any level of hypoxemia; E rose slightly (P less than 0.05) at one time only with both 10 and 8% O2. Individual changes in MSNA during hypoxemia were unrelated to elevations in heart rate or decrements in blood pressure and end-tidal CO2--neither of which always fell. We conclude that in contrast to some other sympathoexcitatory stimuli such as exercise or cold stress, moderate to severe hypoxemia increases leg MSNA without raising plasma NE in resting humans.

scholarly journals Neurogenic Orthostatic Hypotension. Lessons From Synucleinopathies

2020 ◽  
Author(s):  
Juan Francisco Idiaquez ◽  
Juan Idiaquez ◽  
Juan Carlos Casar ◽  
Italo Biaggioni
Keyword(s):  
Blood Pressure ◽  
Orthostatic Hypotension ◽  
Treatment Options ◽  
Lewy Body Dementia ◽  
Cerebral Hypoperfusion ◽  
Neurogenic Orthostatic Hypotension ◽  
Compression Garments ◽  
Novel Treatments ◽  
Mild Disease ◽  
Noradrenergic Fibers

Abstract Maintenance of upright blood pressure critically depends on the autonomic nervous system and its failure leads to neurogenic orthostatic hypotension (NOH). The most severe cases are seen in neurodegenerative disorders caused by abnormal α-synuclein deposits: multiple system atrophy (MSA), Parkinson’s disease, Lewy body dementia, and pure autonomic failure (PAF). The development of novel treatments for NOH derives from research in these disorders. We provide a brief review of their underlying pathophysiology relevant to understand the rationale behind treatment options for NOH. The goal of treatment is not to normalize blood pressure but rather to improve quality of life and prevent syncope and falls by reducing symptoms of cerebral hypoperfusion. Patients not able to recognize NOH symptoms are at a higher risk for falls. The first step in the management of NOH is to educate patients on how to avoid high-risk situations and providers to identify medications that trigger or worsen NOH. Conservative countermeasures, including diet and compression garments, should always precede pharmacologic therapies. Volume expanders (fludrocortisone and desmopressin) should be used with caution. Drugs that enhance residual sympathetic tone (pyridostigmine and atomoxetine) are more effective in patients with mild disease and in MSA patients with spared postganglionic fibers. Norepinephrine replacement therapy (midodrine and droxidopa) is more effective in patients with neurodegeneration of peripheral noradrenergic fibers like PAF. NOH is often associated with other cardiovascular diseases, most notably supine hypertension, and treatment should be adapted to their presence.

Cardiac arrhythmias resulting from experimental head injury

1976 ◽  
Vol 45 (6) ◽  
pp. 609-616 ◽  
Author(s):  
Delbert E. Evans ◽  
William A. Alter ◽  
Stanley A. Shatsky ◽  
E. Neal Gunby
Keyword(s):  
Blood Pressure ◽  
Head Injury ◽  
Cardiac Arrhythmias ◽  
Cardiovascular Events ◽  
Ventricular Arrhythmias ◽  
Adrenergic Blockade ◽  
Content Type ◽  
Arterial Blood ◽  
Before And After ◽  
Fine Print

✓ The cardiovascular events resulting from experimental head injury were studied to determine the incidence of cardiac arrhythmias and to define the autonomic mechanisms responsible for these changes. Electrocardiograms and arterial blood pressure were recorded in anesthetized monkeys before and after the animals were subjected to temporoparietal head impact. Cardiac arrhythmias and hypotension occurred immediately following impact in every animal studied. Various atrioventricular nodal and ventricular arrhythmias were seen. Cholinergic blockade was found to prevent arrhythmias induced by head injury whereas adrenergic blockade was found to be ineffective.

scholarly journals Orthostatic arterial hypotension

2017 ◽  
Vol 12 (2) ◽  
pp. 12-15
Author(s):  
Camelia C. DIACONU ◽  
◽  
Denisa BUCUR ◽  
Daniel BERCEANU ◽  
Ovidiu Gabriel BRATU ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Elderly Patients ◽  
Orthostatic Hypotension ◽  
Pharmacological Treatment ◽  
Elderly Population ◽  
Autonomic Failure ◽  
Clinical Manifestations ◽  
The Elderly ◽  
Cerebral Hypoperfusion ◽  
Blurred Vision

Orthostatic hypotension is a persistent decrease of systolic blood pressure by at least 20 mm Hg and/or diastolic blood pressure by at least 10 mm Hg in the first 3 minutes upon standing. Orthostatic hypotension is more common in the elderly patients, being one of relatively frequent causes of hospitalization in the elderly population. Orthostatic hypotension may be primary or secondary, acute or chronic. Its etiology is represented in most cases by the primary or secondary autonomic failure. Clinical manifestations of orthostatic hypotension occur after the transition from supine to standing, and are due to cerebral hypoperfusion. These consist of nausea, dizziness, generalized weakness, postural instability, fatigue, blurred vision. Cardiological and neurological consult are necessary for diagnosis. Pharmacological treatment of orthostatic hypotension is often unsatisfactory, imposing combination with non-pharmacological measures.

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