Study Results
Results pending
The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.
Basic Information
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Recruitment Status
UNKNOWN
Clinical Phase
PHASE4
Total Enrollment
40 participants
Study Classification
INTERVENTIONAL
Study Start Date
2016-09-30
Study Completion Date
2017-05-31
Brief Summary
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Essential Hypertension is characterized by endothelial dysfunction due to reduced nitric oxide (NO) bioavailability. Impairment in nitric oxide-mediated vasodilatation in human brachial, coronary, and renal arteries has been demonstrated in patients with essential hypertension. Administration of L-arginine, a NO substrate yeld controversial results.
The purpose of the present study, double blind and matched for age, sex and body mass index (BMI), is to assess the efficacy of L-arginine treatment on blood pressure (BP) control and arterial stiffness in patients with stage1 hypertension.
The purpose of the present study, double blind and matched for age, sex and body mass index (BMI), is to assess the efficacy of L-arginine treatment on blood pressure (BP) control and arterial stiffness in patients with stage1 hypertension.
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Detailed Description
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Scientific background
Essential Hypertension is characterized by endothelial dysfunction with impaired vasorelaxation.
Reduced nitric oxide bioavailability, which is considered a hallmark of endothelial dysfunction, plays an important role in mediating blood pressure elevation. Accumulating evidence demonstrates a critical role of nitric oxide in blood pressure regulation. Released from the endothelial cells, nitric oxide increases 30,50-cyclic-guanosine monophosphate (cGMP) production and subsequent cGMP-dependent protein kinase (PKG) activation in the underneath vascular smooth muscle cells (VSMCs), resulting in vasodilatation. The investigators and others have shown that inhibition of NO synthesis increase blood pressure in normal pregnant rats and different animal models. In vivo studies confirmed an essential role of nitric oxide in vasorelaxation of large human arteries. Impairment in nitric oxide-mediated vasodilatation in brachial, coronary, and renal arteries has been demonstrated in patients with essential hypertension.
Several mechanisms have been found responsible for nitric oxide deficiency in hypertension. One of them is deficit of the NO substrate, L-arginine. L-arginine transport is impaired in hypertensive and normotensive patients with a genetic background of essential hypertension, and the offspring of essential hypertensive patients are characterized by a reduced response to acetylcholine linked to a defect in the nitric oxide pathway. These data represent the link between L-arginine and the onset of essential hypertension. The Km of endothelial nitric oxide synthase for L-arginine is about 3mmol/l, but the concentration of plasma L-arginine rarely falls below 60mmol/l in pathological conditions. An elevation in asymmetric dimethylarginine (ADMA, an endogenous NO competitive inhibitor) levels may explain this 'L-arginine paradox'. The administration of excess exogenous L-arginine displaces the competitive inhibitor, improves intracellular transport of this amino acid, and restores NO production to physiological levels. In fact L-arginine supplementation improved endothelial dysfunction in hypertension.
Administration of L arginine in humans have not shown uniform blood pressure responses. A meta-analysis published in 2011 was able to find only 11 articles dealing with l-arginine administration and blood pressure. The population studies were heterogeneous. Compared with placebo, oral L-arginine intervention was associated with an average net change ranging from -23.0 to 2.8 mm Hg for SBP and from -11.0 to 1.0 mm Hg for diastolic BP. Most trials showed an intervention-related trend toward BP reductions, but only a few reached statistical significance.
Endothelial dysfunction leads to an increase in arterial stiffness, a known marker that increases cardiovascular morbidity and mortality. Arterial stiffness can be measured by non invasive methodology, e.g.; measuring carotid-femoral pulse wave velocity, augmentation index, aortic pulse pressure and aortic systolic blood pressure.
Whether administration of l-arginine improved arterial stiffness in patients with mild hypertension it is not known.
Arginoline is a dietary supplement that contains L-arginine at a concentration of 5 g/L. It is possible to dilute with water or take chilled. It is produced by Pharmayeda, an Israeli industry.
Clinical observational studies \[personal communication\] have shown that at a dose of 60 ml\\day \[10 gr of l-arginine\] flow mediated vasodilation improves, suggesting an increase in nitric oxide function.
Methods
Office Blood Pressure (OBP) measurement:
OBP will be measured with a Suntech 247 digital automated device. BP will be determined 3 times at one min. interval each. The mean of the second and third measurements will be noted as the OBP of the visit.
ABPM:
24 hours ABPM will be performed with an Oscar 2 ABPM device of SunTech Medical. The Oscar 2 ABPM device is clinically validated to all 3 internationally recognized protocols (British Heart Society, American Society of Hypertension and the Association for the Advancement of Medical Instrumentation).
Blood pressure is measured in a 20 min. interval at day time and a 30 min. interval at night time. The patients are requested to fill a diary with their activities during the ABPM study, including their subjective evaluation of the sleeping quality.
Measurement of arterial stiffness:
The SphygmoCor X-CEL System (AtCor Medical, Sydney, Australia) will be used.
The system derives (non invasively) the ascending aortic pressure waveform from the brachial waveform using a validated generalised transfer function.
The SphygmoCor X-CEL system measures the carotid-femoral pulse wave velocity (PWV), the speed of the arterial pressure waveform as it travels through the descending aorta to the femoral artery, which is detected from simultaneously measured carotid and femoral arterial pulses.
Design
The study is a matched double blind study with an experimental group and a placebo group. As the number of the groups is small (20 in each group) the patients will be matched according to age, sex and BMI during the recruitment phase, in order to get to comparable groups. The principal investigator is responsible of the matching.
The experimental group will receive arginoline 30 ml twice a day and the placebo group will receive placebo at the same schedule
Visits:
Week -2:
Sign of informed consent
Office BP. Physical examination. BMI.
Blood exams: Hemoglobin (g%), urea (mg%), creatinine (mg%), Natrium (mEq/l), Potassium (mEq/l), alanine transaminase (ALT),Aspartate aminotransferase (AST), gamma-glutamyl transpeptidase (GGT), glucose, cholesterol and triglycerides. and lipid profile.
Urine analysis: microalbuminuria (morning spot)
All patients will receive a booklet with detailed information about healthy life style recommendation to lower blood pressure.
Hypertensive patients on monotherapy will stop treatment.
Week 0
ABPM
Measurement of Central aortic blood pressure and arterial stiffness
Blind group allocation (experimental or placebo group).
Week 2
Office BP measurement.
Week 4
Office BP measurement
Week 6
Office BP measurement
Week 8: ABPM, office BP,
Repeat blood and urine exams as detailed at week -2.
Measurement of Central aortic blood pressure and Arterial stiffness
Statistical evaluation
Will be done using the IBM SPSS statistical software. Pi\<0.05 is considered significative
Essential Hypertension is characterized by endothelial dysfunction with impaired vasorelaxation.
Reduced nitric oxide bioavailability, which is considered a hallmark of endothelial dysfunction, plays an important role in mediating blood pressure elevation. Accumulating evidence demonstrates a critical role of nitric oxide in blood pressure regulation. Released from the endothelial cells, nitric oxide increases 30,50-cyclic-guanosine monophosphate (cGMP) production and subsequent cGMP-dependent protein kinase (PKG) activation in the underneath vascular smooth muscle cells (VSMCs), resulting in vasodilatation. The investigators and others have shown that inhibition of NO synthesis increase blood pressure in normal pregnant rats and different animal models. In vivo studies confirmed an essential role of nitric oxide in vasorelaxation of large human arteries. Impairment in nitric oxide-mediated vasodilatation in brachial, coronary, and renal arteries has been demonstrated in patients with essential hypertension.
Several mechanisms have been found responsible for nitric oxide deficiency in hypertension. One of them is deficit of the NO substrate, L-arginine. L-arginine transport is impaired in hypertensive and normotensive patients with a genetic background of essential hypertension, and the offspring of essential hypertensive patients are characterized by a reduced response to acetylcholine linked to a defect in the nitric oxide pathway. These data represent the link between L-arginine and the onset of essential hypertension. The Km of endothelial nitric oxide synthase for L-arginine is about 3mmol/l, but the concentration of plasma L-arginine rarely falls below 60mmol/l in pathological conditions. An elevation in asymmetric dimethylarginine (ADMA, an endogenous NO competitive inhibitor) levels may explain this 'L-arginine paradox'. The administration of excess exogenous L-arginine displaces the competitive inhibitor, improves intracellular transport of this amino acid, and restores NO production to physiological levels. In fact L-arginine supplementation improved endothelial dysfunction in hypertension.
Administration of L arginine in humans have not shown uniform blood pressure responses. A meta-analysis published in 2011 was able to find only 11 articles dealing with l-arginine administration and blood pressure. The population studies were heterogeneous. Compared with placebo, oral L-arginine intervention was associated with an average net change ranging from -23.0 to 2.8 mm Hg for SBP and from -11.0 to 1.0 mm Hg for diastolic BP. Most trials showed an intervention-related trend toward BP reductions, but only a few reached statistical significance.
Endothelial dysfunction leads to an increase in arterial stiffness, a known marker that increases cardiovascular morbidity and mortality. Arterial stiffness can be measured by non invasive methodology, e.g.; measuring carotid-femoral pulse wave velocity, augmentation index, aortic pulse pressure and aortic systolic blood pressure.
Whether administration of l-arginine improved arterial stiffness in patients with mild hypertension it is not known.
Arginoline is a dietary supplement that contains L-arginine at a concentration of 5 g/L. It is possible to dilute with water or take chilled. It is produced by Pharmayeda, an Israeli industry.
Clinical observational studies \[personal communication\] have shown that at a dose of 60 ml\\day \[10 gr of l-arginine\] flow mediated vasodilation improves, suggesting an increase in nitric oxide function.
Methods
Office Blood Pressure (OBP) measurement:
OBP will be measured with a Suntech 247 digital automated device. BP will be determined 3 times at one min. interval each. The mean of the second and third measurements will be noted as the OBP of the visit.
ABPM:
24 hours ABPM will be performed with an Oscar 2 ABPM device of SunTech Medical. The Oscar 2 ABPM device is clinically validated to all 3 internationally recognized protocols (British Heart Society, American Society of Hypertension and the Association for the Advancement of Medical Instrumentation).
Blood pressure is measured in a 20 min. interval at day time and a 30 min. interval at night time. The patients are requested to fill a diary with their activities during the ABPM study, including their subjective evaluation of the sleeping quality.
Measurement of arterial stiffness:
The SphygmoCor X-CEL System (AtCor Medical, Sydney, Australia) will be used.
The system derives (non invasively) the ascending aortic pressure waveform from the brachial waveform using a validated generalised transfer function.
The SphygmoCor X-CEL system measures the carotid-femoral pulse wave velocity (PWV), the speed of the arterial pressure waveform as it travels through the descending aorta to the femoral artery, which is detected from simultaneously measured carotid and femoral arterial pulses.
Design
The study is a matched double blind study with an experimental group and a placebo group. As the number of the groups is small (20 in each group) the patients will be matched according to age, sex and BMI during the recruitment phase, in order to get to comparable groups. The principal investigator is responsible of the matching.
The experimental group will receive arginoline 30 ml twice a day and the placebo group will receive placebo at the same schedule
Visits:
Week -2:
Sign of informed consent
Office BP. Physical examination. BMI.
Blood exams: Hemoglobin (g%), urea (mg%), creatinine (mg%), Natrium (mEq/l), Potassium (mEq/l), alanine transaminase (ALT),Aspartate aminotransferase (AST), gamma-glutamyl transpeptidase (GGT), glucose, cholesterol and triglycerides. and lipid profile.
Urine analysis: microalbuminuria (morning spot)
All patients will receive a booklet with detailed information about healthy life style recommendation to lower blood pressure.
Hypertensive patients on monotherapy will stop treatment.
Week 0
ABPM
Measurement of Central aortic blood pressure and arterial stiffness
Blind group allocation (experimental or placebo group).
Week 2
Office BP measurement.
Week 4
Office BP measurement
Week 6
Office BP measurement
Week 8: ABPM, office BP,
Repeat blood and urine exams as detailed at week -2.
Measurement of Central aortic blood pressure and Arterial stiffness
Statistical evaluation
Will be done using the IBM SPSS statistical software. Pi\<0.05 is considered significative
Conditions
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Hypertension
Study Design
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Allocation Method
NON_RANDOMIZED
Intervention Model
PARALLEL
Primary Study Purpose
TREATMENT
Blinding Strategy
DOUBLE
Participants
Investigators
Study Groups
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l-arginine
Patients will receive L-arginine 30 ml twice a day for 8 weeks.
Group Type
ACTIVE_COMPARATOR
L-arginine
Intervention Type
DIETARY_SUPPLEMENT
30 ml arginoline contains 5 gr l-arginine
syrup
Patients will receive placebo, 30 ml twice a day for 8 weeks.
Group Type
PLACEBO_COMPARATOR
syrup
Intervention Type
DIETARY_SUPPLEMENT
The same bottle of the experimental group, but without l-arginine
Interventions
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L-arginine
30 ml arginoline contains 5 gr l-arginine
Intervention Type
DIETARY_SUPPLEMENT
syrup
The same bottle of the experimental group, but without l-arginine
Intervention Type
DIETARY_SUPPLEMENT
Other Intervention Names
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Arginoline
placebo
Eligibility Criteria
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Inclusion Criteria
* Stage 1 hypertensive patients, with an office Systolic BP between 140-159 mmHg and/or a diastolic BP between 9-99 mmHg , untreated or treated with monotherapy.
* None to two risk factors \[smoking, hyperlipidemia, obesity , family history of cardiovascular disease\].
* BMI between 25 to 32.
* Twenty for hours ambulatory blood pressure monitor (ABPM) with a mean Systolic BP of 130-149 mmHg and/or a mean Diastolic BP of 80-89 mmHg.
* None to two risk factors \[smoking, hyperlipidemia, obesity , family history of cardiovascular disease\].
* BMI between 25 to 32.
* Twenty for hours ambulatory blood pressure monitor (ABPM) with a mean Systolic BP of 130-149 mmHg and/or a mean Diastolic BP of 80-89 mmHg.
Exclusion Criteria
* Use of any drug that may affect nitric oxide synthesis and/or blood pressure values (nitrates, antihypertensive drugs, non steroidal anti-inflammatory drugs , steroids, pseudoephedrine).
* Diabetes mellitus.
* Renal failure defined as estimated glomerular filtration rate (eGFR) less than 60 ml/min, using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) formula.
* A previous diagnosis of ischemic heart disease, Transient ischemic attack (TIA), Stroke or peripheral arterial disease.
* Patients with recurrent herpes and women who are planning pregnancy during the next year.
* Cancer treated with radiotherapy or chemotherapy during the last year.
* Diabetes mellitus.
* Renal failure defined as estimated glomerular filtration rate (eGFR) less than 60 ml/min, using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) formula.
* A previous diagnosis of ischemic heart disease, Transient ischemic attack (TIA), Stroke or peripheral arterial disease.
* Patients with recurrent herpes and women who are planning pregnancy during the next year.
* Cancer treated with radiotherapy or chemotherapy during the last year.
Minimum Eligible Age
30 Years
Maximum Eligible Age
70 Years
Eligible Sex
ALL
Accepts Healthy Volunteers
No
Sponsors
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Meir Medical Center
OTHER
Sponsor Role
lead
Responsible Party
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Responsibility Role
SPONSOR
Principal Investigators
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Eduardo Podjarny, MD
Role: PRINCIPAL_INVESTIGATOR
Clalit Health Services
Locations
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ADAM Institute of High Blood Pressure, Clalit Health Services
Herzliya, Hasharon Area, Israel
Site Status
Countries
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Israel
Central Contacts
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Facility Contacts
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References
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Tanaka Y, Tang G, Takizawa K, Otsuka K, Eghbali M, Song M, Nishimaru K, Shigenobu K, Koike K, Stefani E, Toro L. Kv channels contribute to nitric oxide- and atrial natriuretic peptide-induced relaxation of a rat conduit artery. J Pharmacol Exp Ther. 2006 Apr;317(1):341-54. doi: 10.1124/jpet.105.096115. Epub 2006 Jan 4.
Reference Type
BACKGROUND
Li Q, Youn JY, Cai H. Mechanisms and consequences of endothelial nitric oxide synthase dysfunction in hypertension. J Hypertens. 2015 Jun;33(6):1128-36. doi: 10.1097/HJH.0000000000000587.
Reference Type
BACKGROUND
Joannides R, Haefeli WE, Linder L, Richard V, Bakkali EH, Thuillez C, Luscher TF. Nitric oxide is responsible for flow-dependent dilatation of human peripheral conduit arteries in vivo. Circulation. 1995 Mar 1;91(5):1314-9. doi: 10.1161/01.cir.91.5.1314.
Reference Type
BACKGROUND
Panza JA, Garcia CE, Kilcoyne CM, Quyyumi AA, Cannon RO 3rd. Impaired endothelium-dependent vasodilation in patients with essential hypertension. Evidence that nitric oxide abnormality is not localized to a single signal transduction pathway. Circulation. 1995 Mar 15;91(6):1732-8. doi: 10.1161/01.cir.91.6.1732.
Reference Type
BACKGROUND
Treasure CB, Klein JL, Vita JA, Manoukian SV, Renwick GH, Selwyn AP, Ganz P, Alexander RW. Hypertension and left ventricular hypertrophy are associated with impaired endothelium-mediated relaxation in human coronary resistance vessels. Circulation. 1993 Jan;87(1):86-93. doi: 10.1161/01.cir.87.1.86.
Reference Type
BACKGROUND
Higashi Y, Oshima T, Ozono R, Watanabe M, Matsuura H, Kajiyama G. Effects of L-arginine infusion on renal hemodynamics in patients with mild essential hypertension. Hypertension. 1995 Apr;25(4 Pt 2):898-902. doi: 10.1161/01.hyp.25.4.898.
Reference Type
BACKGROUND
Taddei S, Virdis A, Mattei P, Ghiadoni L, Sudano I, Salvetti A. Defective L-arginine-nitric oxide pathway in offspring of essential hypertensive patients. Circulation. 1996 Sep 15;94(6):1298-303. doi: 10.1161/01.cir.94.6.1298.
Reference Type
BACKGROUND
Schlaich MP, Parnell MM, Ahlers BA, Finch S, Marshall T, Zhang WZ, Kaye DM. Impaired L-arginine transport and endothelial function in hypertensive and genetically predisposed normotensive subjects. Circulation. 2004 Dec 14;110(24):3680-6. doi: 10.1161/01.CIR.0000149748.79945.52. Epub 2004 Nov 29.
Reference Type
BACKGROUND
Forstermann U, Sessa WC. Nitric oxide synthases: regulation and function. Eur Heart J. 2012 Apr;33(7):829-37, 837a-837d. doi: 10.1093/eurheartj/ehr304. Epub 2011 Sep 1.
Reference Type
BACKGROUND
Boger RH. Asymmetric dimethylarginine, an endogenous inhibitor of nitric oxide synthase, explains the "L-arginine paradox" and acts as a novel cardiovascular risk factor. J Nutr. 2004 Oct;134(10 Suppl):2842S-2847S; discussion 2853S. doi: 10.1093/jn/134.10.2842S.
Reference Type
BACKGROUND
Naseem KM. The role of nitric oxide in cardiovascular diseases. Mol Aspects Med. 2005 Feb-Apr;26(1-2):33-65. doi: 10.1016/j.mam.2004.09.003. Epub 2005 Jan 24.
Reference Type
BACKGROUND
Hishikawa K, Nakaki T, Suzuki H, Kato R, Saruta T. Role of L-arginine-nitric oxide pathway in hypertension. J Hypertens. 1993 Jun;11(6):639-45. doi: 10.1097/00004872-199306000-00008.
Reference Type
BACKGROUND
Ast J, Cieslewicz AR, Korzeniowska K, Bogdanski P, Kazmierczak E, Olszewski J, Skoluda A, Jablecka A. Supplementation with L-arginine does not influence arterial blood pressure in healthy people: a randomized, double blind, trial. Eur Rev Med Pharmacol Sci. 2011 Dec;15(12):1375-84.
Reference Type
BACKGROUND
Ast J, Jablecka A, Bogdanski P, Smolarek I, Krauss H, Chmara E. Evaluation of the antihypertensive effect of L-arginine supplementation in patients with mild hypertension assessed with ambulatory blood pressure monitoring. Med Sci Monit. 2010 May;16(5):CR266-71.
Reference Type
BACKGROUND
Gui S, Jia J, Niu X, Bai Y, Zou H, Deng J, Zhou R. Arginine supplementation for improving maternal and neonatal outcomes in hypertensive disorder of pregnancy: a systematic review. J Renin Angiotensin Aldosterone Syst. 2014 Mar;15(1):88-96. doi: 10.1177/1470320313475910. Epub 2013 Feb 22.
Reference Type
BACKGROUND
Gallagher D, Adji A, O'Rourke MF. Validation of the transfer function technique for generating central from peripheral upper limb pressure waveform. Am J Hypertens. 2004 Nov;17(11 Pt 1):1059-67. doi: 10.1016/j.amjhyper.2004.05.027.
Reference Type
BACKGROUND
Butlin M, Qasem A, Avolio AP. Estimation of central aortic pressure waveform features derived from the brachial cuff volume displacement waveform. Annu Int Conf IEEE Eng Med Biol Soc. 2012;2012:2591-4. doi: 10.1109/EMBC.2012.6346494.
Reference Type
BACKGROUND
Davignon J, Ganz P. Role of endothelial dysfunction in atherosclerosis. Circulation. 2004 Jun 15;109(23 Suppl 1):III27-32. doi: 10.1161/01.CIR.0000131515.03336.f8.
Reference Type
RESULT
Archer SL, Huang JM, Hampl V, Nelson DP, Shultz PJ, Weir EK. Nitric oxide and cGMP cause vasorelaxation by activation of a charybdotoxin-sensitive K channel by cGMP-dependent protein kinase. Proc Natl Acad Sci U S A. 1994 Aug 2;91(16):7583-7. doi: 10.1073/pnas.91.16.7583.
Reference Type
RESULT
Podjarny E, Ben-Chetrit S, Rathaus M, Korzets Z, Green J, Katz B, Bernheim J. Pregnancy-induced hypertension in rats with adriamycin nephropathy is associated with an inadequate production of nitric oxide. Hypertension. 1997 Apr;29(4):986-91. doi: 10.1161/01.hyp.29.4.986.
Reference Type
RESULT
Other Identifiers
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0216-15-COM2
Identifier Type: -
Identifier Source: org_study_id
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