Hypertension (high blood pressure)

http://www.newswire.ca/en/releases/archive/May2009/21/c6035.html

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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 vivoA type of scientific study that analyzes an organism in its natural living environment. mouse model and in vitroA technique of performing a given procedure in a controlled environment outside of a living organism - usually a laboratory. 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-alpha, 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.

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 ARB (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-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 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 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.

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

Hypertension, inflammation and atherosclerosis

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

Inflammation may be a bridge connecting hypertension and atherosclerosis

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.

PMID: 16481882 [PubMed - indexed for MEDLINE]

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.

PMID: 16464884