Hypertension (high blood pressure)


Why is my B/P high? Why does it fluctuate?

There are a variety of medications that doctors use to control hypertension. This article explains the usual treatment of high blood pressure (hypertension).

Hypertension is often a part of the Th1 inflammatory picture. Benicar, even when taken 3 to 4 times per day, is not a very potent anti-hypertensive. At 20mg/day its maximum hypotensive effect is 12 points. See Benicar-Basic Information

Follow your doctor's advice regarding monitoring your blood pressure to determine if your current blood pressure medication/s are effective. Your blood pressure will come down as your Th1 inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. resolves and you will need less blood pressure medication and then may no longer need additional B/P medication. Your doctor will advise you on how and when to adjust your blood pressure medication/s.

If your B/P is too high, we suggest adding a beta blocker, an ACE inhibitor or a calcium channel blocker (in that order of perference) to your ARBA drug which is an angiotensin receptor blocker. One of the ARBs is olmesartan (Benicar). Not all ARBs activate the Vitamin D Receptor. (Benicar).

If your BP rises on the MP

Doctors don't usually change blood pressure medication until there have been several readings in a row that they consider too high. If your doctor advises monitoring your blood pressure, check it once or twice a day at different times, write it down and let your doctor know at the end of the week what your readings have been. You may be able to fax or email your B/P record to your doctor for convenience. You will find information on accurate blood pressure monitors and how to assess your blood pressure in this thread.

Keep in mind that fluctuations in B/P are due to the disease process because the powerful hormone 1,25-D influences many other hormones. Please see: Hormonal Changes Resulting From Changes in 1,25-D.

A safe diuretic

Your doctor is probably familiar with the standard algorithm for treating essential hypertension and may want to use a diuretic.

Do not take a thiazide diuretic to control B/P because it is too hard on kidneys that may already be compromised by inflammation. There is a complete list of thiazide diuretics in Medications to Avoid While on the Marshall Protocol

These diuretics are contraindiated because they are potassium-sparing and might result in hyperkalemia. -spironolactone (Aldactone, Novospironton, Spiractin) -triamterene (Dyrenium) -amiloride (Midamor)

Lasix (furosemide) however, does not cause potassium-retention and is compatible with the MP.

Your doctor will want to monitor serum potassium while you are taking Lasix to make sure it stays within normal limits.

Watch and wait

Because your high blood pressure will stabilize with resolution of your Th1 inflammation, your doctor may want to watch and wait, rather than adjust your secondary blood pressure medication/s frequently.

Members' experiences

“Many with these diseases discover difficulties in blood pressure regulation. In my own experience I have gone from predominantly hypertensive, to wild fluctuations, then to hypotension, and am now hypertensive, again. I think we are seeing an involvement with the ANS (Autonomic Nervous System), hormonal changes, and the body's lack of homeostasis, when blood pressure, heart rate, temperature regulation, respiration, swallowing, and such dysfunctions are noted.” ~Hrts

Inflammation and Hypertension

Hypertension, inflammation and atherosclerosis 1)

Is Vascular Endothelial Growth Factor a Missing Link Between Hypertension and Inflammation?

Inflammation may be a bridge connecting hypertension and atherosclerosis. 2)

Inflammation and hypertension: the search for a link

Elevated high-sensitive C-reactive protein, large arterial stiffness and atherosclerosis: a relationship between inflammation and hypertension?

Inflammation in hypertension.

Savoia C, Schiffrin EL. Curr Opin Nephrol Hypertens. 2006 Mar; 15,(2):152-8

Clinical Research Institute of Montreal, University of Montreal, Montreal, Quebec, Canada.

PURPOSE OF REVIEW: In this review we summarize the recent evidence that highlights the involvement of low-grade inflammation in the development and pathophysiology of hypertension. RECENT FINDINGS: Essential hypertension is characterized by increased peripheral vascular resistance to blood flow, due in large part to vascular remodeling. Vascular changes in hypertension are associated with mechanical and humoral factors that modulate signaling events, resulting in abnormal function, media growth, extracellular matrix deposition and inflammation. Recent evidence suggests that inflammation is present in the vasculature in animal models of hypertension. Inflammatory markers, such as C-reactive protein, are associated with vascular lesions in humans, and are predictive of cardiovascular outcome. In animal and human studies, pro-inflammatory components of the renin-angiotensin-aldosterone system have been demonstrated in large conduit and small arteries in the kidney and heart. Peroxisome proliferator-activated receptor activators are drugs with metabolic properties that have been demonstrated to exert anti-inflammatory effects on the vasculature, and there is now evidence that these actions may be protective for blood vessels. SUMMARY: Inflammatory processes are important participants in the pathophysiology of hypertension and cardiovascular disease. The identification of the mechanisms leading to the activation of inflammation should contribute to the development of specific therapeutic approaches to apply in hypertension and its complications. 3)

Nephrol Dial Transplant. 2006 Apr;21(4):850-3. Epub 2006 Feb 7. Inflammation and hypertension: the search for a link. Pauletto P, Rattazzi M. 4)

Wilke, R. A., R. U. Simpson, et al. (2009). “Genetic variation in CYP27B1 is associated with congestive heart failure in patients with hypertension.” Pharmacogenomics 10(11): 1789-1797. 5)

AIMS: We tested the hypothesis that genetic variation in vitamin D-dependent signaling is associated with congestive heart failure in human subjects with hypertension. MATERIALS & METHODS: Functional polymorphisms were selected from five candidate genes: CYP27B1, CYP24A1, VDRThe Vitamin D Receptor. A nuclear receptor located throughout the body that plays a key role in the innate immune response., REN and ACE. Using the Marshfield Clinic Personalized Medicine Research Project, we genotyped 205 subjects with hypertension and congestive heart failure, 206 subjects with hypertension alone and 206 controls (frequency matched by age and gender). RESULTS: In the context of hypertension, a SNP in CYP27B1 was associated with congestive heart failure (odds ratio: 2.14 for subjects homozygous for the C allele; 95% CI: 1.05-4.39). CONCLUSION: Genetic variation in vitamin D biosynthesis is associated with increased risk of heart failure.

For some, the absence of well-defined causal connections between diseases and surrogate outcomes is a tribute to how truly complicated chronic inflammatory diseases are. D'Agostino’s characterizes hypertension in this way: “There is no reason to believe that hypertension is simply elevated blood pressure. Hypertension is much more complex.”(PMC59603)

Dose-Dependent Arterial Destiffening and Inward Remodeling After OlmesartanMedication taken regularly by patients on the Marshall Protocol for its ability to activate the Vitamin D Receptor. Also known by the trade name Benicar. in Hypertensives With Metabolic Syndrome Stephane Laurent, Pierre Boutouyrie, on behalf of the Vascular Mechanism Collaboration

Patients receiving the highest dose of olmesartan (40 and 80 mg) had an inward carotid remodeling and were shifted toward a lower elastic modulus at a given circumferential wall stress, indicating an improvement in the intrinsic elastic properties of the carotid artery wall material. These data suggest that 40 and 80 mg olmesartan were able to significantly remodel and destiffen the arterial wall material during long-term treatment, partly independently of blood pressure, compared with 20 mg. 6)

Dose-Dependent Arterial Destiffening and Inward Remodeling After Olmesartan in Hypertensives With Metabolic Syndrome


In a CBS interview on video (17 March, 2015) Dr David Agus discussed the finding that vitamin D was useless for lowering blood pressure. Supplementation was also found to be associated with more cancer and heart disease. “Nobody should be taking it…that's the data” said the doctor, who also drew attention to increased risk of bone fracture and kidney stone.

Dear MPKB Reader: You have arrived at one of the articles that has not yet completed the development and review process in the knowledge base. Some of the content here may be helpful, but please know that this page is not complete. There are about 400 articles in the KB, and this is one we are still working on. Thanks for your patience.

Notes and comments

Sallie Q 02.26.2017 added headings, reference , section for member experience

Sallie Q 02.22.2017 moved contents of 1st para out of view as follows


Include here???

Pulmonary hypertension home:diseases:pulmonary_hypertension

Cytomegalovirus Infection Causes an Increase of Arterial Blood Pressure

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Author(s): Cheng JL (Cheng, Jilin)1, Ke QG (Ke, Qingen)2, Jin Z (Jin, Zhuang), Kocher O (Kocher, Olivier)4, Morgan JP (Morgan, James P.)5, Zhang JL (Zhang, Jielin)1, Crumpacker CS (Crumpacker, Clyde S.)1 Source: PLOS PATHOGENS Volume: 5 Issue: 5 Article Number: e1000427 Published: MAY 2009 Times Cited: 5 References: 43 Citation Map Abstract: Cytomegalovirus (CMV) infection is a common infection in adults (seropositive 60-99% globally), and is associated with cardiovascular diseases, in line with risk factors such as hypertension and atherosclerosis. Several viral infections are linked to hypertension, including human herpes virus 8 (HHV-8) and HIV-1. The mechanisms of how viral infection contributes to hypertension or increased blood pressure are not defined. In this report, the role of CMV infection as a cause of increased blood pressure and in forming aortic atherosclerotic plaques is examined. Using in vivo mouse model and in vitro molecular biology analyses, we find that CMV infection alone caused a significant increase in arterial blood pressure (ABp) (p<0.01 similar to 0.05), measured by microtip catheter technique. This increase in blood pressure by mouse CMV (MCMV) was independent of atherosclerotic plaque formation in the aorta, defined by histological analyses. MCMV DNA was detected in blood vessel samples of viral infected mice but not in the control mice by nested PCR assay. MCMV significantly increased expression of pro-inflammatory cytokinesAny of various protein molecules secreted by cells of the immune system that serve to regulate the immune system. IL-6, TNF-alphaA cytokine critical for effective immune surveillance and is required for proper proliferation and function of immune cells., and MCP-1 in mouse serum by enzyme-linked immunosorbent assay (ELISA). Using quantitative real time reverse transcriptase PCR (Q-RT-PCR) and Western blot, we find that CMV stimulated expression of renin in mouse and human cells in an infectious dose-dependent manner. Co-staining and immunofluorescent microscopy analyses showed that MCMV infection stimulated renin expression at a single cell level. Further examination of angiotensin-II (Ang II) in mouse serum and arterial tissues with ELISA showed an increased expression of Ang II by MCMV infection. Consistent with the findings of the mouse trial, human CMV (HCMV) infection of blood vessel endothelial cells (EC) induced renin expression in a non-lytic infection manner. Viral replication kinetics and plaque formation assay showed that an active, CMV persistent infection in EC and expression of viral genes might underpin the molecular mechanism. These results show that CMV infection is a risk factor for increased arterial blood pressure, and is a co-factor in aortic atherosclerosis. Viral persistent infection of EC may underlie the mechanism. Control of CMV infection can be developed to restrict hypertension and atherosclerosis in the cardiovascular system.

  • Legacy content


  • salt avoidance – not recommended given that the body seems to naturally regulate sodium levels independently7)

Effects of olmesartan vs irbesartan on metabolic parameters and visfatin in hypertensive obese women. 8)


CONCLUSION: The administration of olmesartan improved blood pressure, insulin, HOMA, visfatin and lipid profile in hypertensive obese women. Irbesartan improved blood pressure and lipid levels.

Visfatin, glucose metabolism and vascular disease: a review of evidence


Visfatin is is an adipokine involved in inflammatory phenomena, atherosclerosis, and possibly in insulin secretion. Its physiology has begun to be described but its role on diabetes and CAD pathophysiology is still controversial.

New studies may define the possible role of visfatin in the mechanisms of glycemic control, vascular function and atherosclerotic process. These findings may contribute in the identification of higher risk individuals as well as lead to new therapeutic approaches. Genetic studies about the visfatin gene and its variations will also contribute to the elucidation of these phenomena.


Olmesartan reduces arterial stiffness and serum adipocyte fatty acid-binding protein in hypertensive patients. 9)


Olmesartan ameliorated arterial stiffness in patients with hypertension, which may be involved in the reduction of serum A-FABP.

American Journal of Hypertension 2011; 24 3, 362–368. doi:10.1038/ajh.2010.241

Blockade of AT1 Receptors Protects the Blood–Brain Barrier and Improves Cognition in Dahl Salt-Sensitive Hypertensive Rats

Nicolas Pelisch1, Naohisa Hosomi2, Masaki Ueno3, Daisuke Nakano4, Hirofumi Hitomi4, Masaki Mogi5, Kenji Shimada6, Hiroyuki Kobori7, Masatsugu Horiuchi5, Haruhiko Sakamoto3, Masayasu Matsumoto2, Masakazu Kohno1 and Akira Nishiyama4

1Department of Cardiorenal and Cerebrovascular Medicine, Kagawa University Medical School, Kagawa, Japan 2Department of Clinical Neuroscience and Therapeutics, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima, Japan 3Department of Pathology and Host Defense, Kagawa University Medical School, Kagawa, Japan 4Department of Pharmacology, Kagawa University Medical School, Kagawa, Japan 5Department of Molecular Cardiovascular Biology and Pharmacology, Ehime University, School of Medicine, Ehime, Japan 6Department of Neurosurgery, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Japan 7Department of Physiology, Hypertension and Renal Center of Excellence, Tulane University Health Sciences Center, New Orleans, Louisiana, USA. Correspondence: Nicolas Pelisch, (nico@med.kagawa-u.ac.jp)

Received 25 May 2010; First Decision 18 June 2010; Accepted 28 October 2010; Published online 16 December 2010.

Topof page Abstract BackgroundThe present study tested the hypothesis that inappropriate activation of the brain renin–angiotensin system (RAS) contributes to the pathogenesis of blood–brain barrier (BBB) disruption and cognitive impairment during development of salt-dependent hypertension. Effects of an angiotensin II (AngII) type-1 receptor blocker (ARB), at a dose that did not reduce blood pressure, were also examined. MethodsDahl salt-sensitive (DSS) rats at 6 weeks of age were assigned to three groups: low-salt diet (DSS/L; 0.3% NaCl), high-salt diet (DSS/H; 8% NaCl), and high-salt diet treated with ARB, olmesartan at 1 mg/kg. ResultsDSS/H rats exhibited hypertension, leakage from brain microvessels in the hippocampus, and impaired cognitive functions, which were associated with increased brain AngII levels, as well as decreased mRNA levels of tight junctions (TJs) and collagen-IV in the hippocampus. In DSS/H rats, olmesartan treatment, at a dose that did not alter blood pressure, restored the cognitive decline, and ameliorated leakage from brain microvessels. Olmesartan also decreased brain AngII levels and restored mRNA expression of TJs and collagen-IV in DSS/H rats. ConclusionsThese results suggest that during development of salt-dependent hypertension, activation of the brain RAS contributes to BBB disruption and cognitive impairment. Treatment with an ARB could elicit neuroprotective effects in cognitive disorders by preventing BBB permeability, which is independent of blood pressure changes. American Journal of Hypertension (2011). doi:10.1038/ajh.2010.241

Vitamin D and the Prevention of Hypertension and Cardiovascular Diseases: A Review of the Current Evidence

Effect of olmesartan on oxidative stress in hypertensive patients. Mechanistic support to clinical trials derived evidence. Calò LA, Maso LD, Caielli P, Pagnin E, Fusaro M, Davis PA, Pessina AC. Source

Department of Clinical and Experimental Medicine,University of Padova, Italy.


Abstract The role of oxidative stress in the pathophysiology of hypertension and target organ damage is widely recognized. Using a molecular biology approach, we report, in essential hypertensive patients, the effect of the angiotensin II type 1 receptor blocker olmesartan on the mononuclear cell (PBMC) protein expression of major elements in the oxidative stress and vascular remodeling-related pathways, p22(phox) and HO-1, along with the phosphorylation state of ERK1/2 and plasma oxidized low-density lipoproteins (oxLDL). Twenty untreated essential hypertensive patients (range blood pressure: 142-156/94-98 mmHg) were treated with olmesartan medoxomil (20 mg/day for 6 months) and blood samples collected at baseline, 3 and 6 months for PBMC p22(phox) and HO-1 protein expression, phosphorylation state of ERK1/2 (western blot) and oxLDL level (ELISA) evaluations. Olmesartan normalized blood pressure since the third month (149 ± 4.7/94.88 ± 1.9 mmHg vs 137.89 ± 2.08/88.44 ± 2.0 at 3 months and vs 135.44 ± 2.18/85.78 ± 1.2 at 6 months, analysis of variance: p < 0.001). p22(phox) protein level declined at 3 months (7.10 ± 2.61 vs 9.32 ± 2.43 densitometric units (d.u.; p < 0.001), further declining at 6 months (4.55 ± 1.26 d.u., p < 0.001). HO-1 levels increased at 3 months (10.87 ± 1.92 vs 7.70 ± 0.71 d.u., p = 0.001) and remained elevated (11.11 ± 1.89 d.u., p = 0.001), without further increase at 6 months. Phosphorylated ERK1/2 declined at 3 months (3.94 ± 1.44 vs 5.62 ± 1.11 d.u., p = 0.001), further declining at 6 months (1.94 ± 0.87, p < 0.001). oxLDL significantly declined at 3 and 6 months. These results demonstrate that olmesartan inhibits oxidative stress. Given the involvement of oxidative stress and its signaling in atherogenesis, and the available evidence of olmesartan's vasoprotective, anti-inflammatory and antiatherosclerotic effects derived from clinical trials in humans, the results of our study provide a mechanistic rationale for the omelsartan's antioxidant and anti-inflammatory potential translation, in the long term, toward the antiatherosclerotic and antiremodeling effects reported on the clinical ground. 10)

PMID: 21504378


2) , 4)
Inflammation and hypertension: the search for a link.
Pauletto P, Rattazzi M
Nephrol Dial Transplant21p850-3(2006 Apr)
Inflammation in hypertension.
Savoia C, Schiffrin EL
Curr Opin Nephrol Hypertens15p152-8(2006 Mar)
Genetic variation in CYP27B1 is associated with congestive heart failure in patients with hypertension.
Wilke RA, Simpson RU, Mukesh BN, Bhupathi SV, Dart RA, Ghebranious NR, McCarty CA
Pharmacogenomics10p1789-97(2009 Nov)
Can dietary sodium intake be modified by public policy?
McCarron DA, Geerling JC, Kazaks AG, Stern JS
Clin J Am Soc Nephrol4p1878-82(2009 Nov)
Effects of olmesartan vs irbesartan on metabolic parameters and visfatin in hypertensive obese women.
De Luis DA, Conde R, Gonzalez Sagrado M, Aller R, Izaola O, Perez Castrillon JL, Romero E, Castro MJ
Eur Rev Med Pharmacol Sci14p759-63(2010 Sep)
Olmesartan reduces arterial stiffness and serum adipocyte fatty acid-binding protein in hypertensive patients.
Miyoshi T, Doi M, Hirohata S, Kamikawa S, Usui S, Ogawa H, Sakane K, Izumi R, Ninomiya Y, Kusachi S
Heart Vessels26p408-13(2011 Jul)
Effect of olmesartan on oxidative stress in hypertensive patients: mechanistic support to clinical trials derived evidence.
Cal LA, Maso LD, Caielli P, Pagnin E, Fusaro M, Davis PA, Pessina AC
Blood Press20p376-82(2011 Dec)
home/diseases/hypertension.txt · Last modified: 03.15.2017 by sallieq
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