Related article: Science behind Olmesartan, section on cardiovascular_disease
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, it is possible to add 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).
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-DPrimary biologically active vitamin D hormone. Activates the vitamin D nuclear receptor. Produced by hydroxylation of 25-D. Also known as 1,25-dihydroxycholecalciferol, 1,25-hydroxyvitamin D and calcitirol. influences many other hormones. Please see: #hormonal_adjustments resulting from changes in 1,25-D.
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 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.. There is a complete list of thiazide diuretics in Medications to Avoid While on the Marshall ProtocolA curative medical treatment for chronic inflammatory disease. Based on the Marshall Pathogenesis.
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.
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.
Hypertension, inflammation and atherosclerosis 1)
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?
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)
see also 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. Ralph B D'Agostino characterizes hypertension in this way: “There is no reason to believe that hypertension is simply elevated blood pressure. Hypertension is much more complex.” 6)
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. 7)
“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
Comparative effectiveness of an angiotensin receptor blocker, olmesartan medoxomil, in older hypertensive patients. 8)
The administration of olmesartan improved blood pressure, insulin, HOMA, visfatin and lipid profile in hypertensive obese women. Irbesartan improved blood pressure and lipid levels. 9)
Olmesartan ameliorated arterial stiffness in patients with hypertension, which may be involved in the reduction of serum A-FABP. 10)
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 olmesartan's antioxidant and anti-inflammatory potential translation, in the long term, toward the antiatherosclerotic and antiremodeling effects reported on the clinical ground. 11)