How the skin controlled blood pressure

Skin plays a surprising role in regulating blood pressure and heart rate, Skin is the largest organ, covering two square metres in humans - helps regulate blood pressure and heart rate in response to changes in the amount of oxygen available in the environment.

High blood pressure is associated with cardiovascular disease, such as heart attack and stroke. For the vast majority of cases of high blood pressure, there is no known cause. It is often associated with reduced flow of blood through small blood vessels in the skin and other parts of the body, a symptom which can get progressively worse if the hypertension is not treated.

Previous research has shown that when a tissue is starved of oxygen - as can happen in areas of high altitude, or in response to pollution, smoking or obesity, for example - blood flow to that tissue will increase. In such situations, this increase in blood flow is controlled in part by the 'HIF' family of proteins.

To investigate what role the skin plays in the flow of blood through small vessels, a team of researchers exposed mice to low-oxygen conditions. These mice had been genetically modified so that they are unable to produce certain HIF proteins in the skin.

The study was set up to understand the feedback loop between the skin and the cardiovascular system. By working with mice. Researchers were able to manipulate key genes involved in this loop. They discovered that in mice lacking one of two proteins in the skin HIF-1α or HIF-2α, the response to low levels of oxygen changed compared to normal mice and that this affected their heart rate, blood pressure, skin temperature and general levels of activity.

Mice lacking specific proteins controlled by the HIFs also responded in a similar way.
In addition, the response of normal, healthy mice to oxygen starvation was more complex than expected. In the first ten minutes, blood pressure and heart rate rise, and this is followed by a period of 36 hours where blood pressure and heart rate decrease below normal levels. 48 hours after exposure to low levels of oxygen and blood pressure the heart rate levels had returned to normal.

Loss of the HIF proteins or other proteins involved in the response to oxygen starvation in the skin, was discovered to change when this process starts and how long it takes. Skin's response to low levels of oxygen may have substantial effects on how the heart pumps blood around the body.
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Why babies should not face the bed while sleeping

According to the latest research, the abnormality in the brain's control of head and neck movement, breathing, heartbeat and the body's responses to deprivation of oxygen supplied, could be the reason why some babies sleeping on their front are more at risk of sudden infants death syndrome SIDS.

SIDS is so devastating because it occurs with no warning and no obvious signs of illness, the exact cause of death in SIDS has not been identified, multiple studies have pointed to a subset of SIDS babies that are not entirely 'normal' before death. These infants all seem to have some form of underlying vulnerability, exposing them to increased risk.

Abnormality within key regions of the brainstem in SIDS babies, specifically in parts of the brainstem that control breathing and movements of the head and neck. This abnormality is directly linked to SIDS cases.
The abnormality is in the transmission in the brain of a neuro-peptide, known as "substance P", and its binding with an associated neuroreceptor, "neurokinin-1" (NK1R).

Substance P and the NK1R neuroreceptor play a critical role in the brain's control of the respiratory system, the cardiovascular system, and in how the body responds to hypoxia- deprivation of oxygen at the cell level. An infant with this abnormality is likely to have impaired respiratory and motor responses to life-threatening challenges during sleep.
Abnormality is a key reason why it is more dangerous for babies to sleep on their front.

If a child has this underlying vulnerability in its brain chemistry, and its breathing becomes compromised by sleeping on its front, that child is at greater risk of death because its body cannot respond in the normal way. The baby can't lift its head, and its breathing and heartbeat will be compromised.

The study has shown that the abnormality in substance P is significantly influenced by prematurity and male sex, which may explain the increased risk of SIDS in premature and male infants.
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Alcohol affects levels of cholesterol through epigenetics

In an analysis of the epigenomes of people and mice, researchers discovered that drinking alcohol may induce changes to a cholesterol regulating gene. The findings suggest that these changes to the gene, PCSK9, may be responsible for some of the differences in how cholesterol is processed in people who drink alcohol, or may affect those taking a relatively new class of PCSK9 cholesterol-lowering drugs designed to reduce LDL cholesterol.

Chronic alcohol use can have detrimental effects on the liver and the cardiovascular system. Regulation of PCSK9 seems to correlate with this pattern and may be a significant underlying factor behind the variations in the relationship between cholesterol and cardiovascular disease when it comes to alcohol use. Researchers measure how drinking of alcohol can leads to changes in which genes are expressed.

They examined information from DNA chips- microarrays that can show which genes have chemical methyl groups added across the whole genome. These chips looked at about 500,000 methyl groups at a time. methylation affects the level of gene expression. The researchers used different sets of data: DNA from the brains of deceased people with documented alcohol dependence compared to healthy controls and DNA from blood samples of people who had documented alcohol dependence with healthy controls.

When the investigators cross-compared epigenetic data from the sets of data to find out what changes occurred in common in the two data sets and what changes did not, the common factor highlighted the gene PCSK9. The human liver samples from people with alcohol dependence who underwent a liver transplant and noticed a similar pattern: more methylation on PCSK9 and unexpectedly lower PCSK9 protein levels. In samples from people who abused alcohol, the researchers detected that PCSK9 gene expression was only a third of the level in people who didn't abuse alcohol.

Alcohol is metabolized by the liver and can cause liver damage if used in large amounts over long periods of time. In people, PCSK9 is found at its highest levels in liver, but is also found in other tissues, such as brain and blood. PCSK9 binds to the bad cholesterol receptors and blocks uptake and breakdown of bad cholesterol by cells, leading to accumulation in the bloodstream, where it presumably clogs arteries.
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