Hypertension and Inflammation

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This is a fantastic site all round... but I figured some might be interested in this page in particular.

 

Clare in Tassie

 

 

 

 

 

 

NephroPal

 

 

 

 

 

 

Hypertension and Inflammation

Posted: 06 Nov 2009 04:28 PM PST

 

The metabolic syndrome is essentially a state of inflammation. Hypertension being a component of the metabolic syndrome is also a reflection of inflammation. How is hypertension caused in this state? There is decreased activity of nitric oxide (NO) and increased activity of Angiotensin II. Nitric oxide causes vasodilitation (dilation of the vessels). Angiotensin II has the following effects:

 

Vasculature: vasoconstriction (constricting the vessels resulting in higher blood pressures)

Neuro: it increases the sensation for salt and thirst. It also increases the secretion of ADH (from the posterior pituitary gland) which tells the kidneys to retain water. Also ACTH is released from the anterior pituitary gland which signals the adrenal glands to produce cortisol.

Adrenal glands: increased production of aldosterone (which tells the kidneys to retain sodium)

Kidneys: causes sodium retention causing blood pressure to go up.

Angiotensin II also stimulates the release of Endothelin-1 (ET-1) which is one of the most potent vasoconstrictors of the body. A recent study from the Medical College of Georgia (click) has discovered that in the kidneys, ET-1 increases the amount of T-cells. This leads to the recruitment of other WBCs. Thus, by means of ET-1, an inflammatory state is created enabling microscopic scarring of the kidney filter. As a result, kidney failure occurs over time. How ET-1 stimulates an increase in T-cells is unclear. Thus, medications like Angiotensin II Receptor Blockers and ACE-inhibitors should not only be seen as blood pressure medications but also anti-inflammatory medications as well. Hormone D (Vitamin D) also decreases the activity of this process through adiponectin. Amazing!

The studies on Vitamin D improving blood pressure are mixed. I personally have not seen a great improvement. I assume that if one continues on a pro-imnflammatory diet, Vitamin D can have so much of an effect. Moreover, as seen in the cartoon and previously discussed, Agniotensin II can activate NF-kB leading the free radical production and cardiac fibrosis. Once again, Vitamin D plays a role in inhibiting this process.

For more information, refer to the entry on the RAAS system (click) and Cardiac Disease and Adiponectin (click)