It makes a lot of sense to start this talk by defining the sympathetic nervous system. The sympathetic nervous system (known in laymen’s terms as the “fight-or-flight” response) is the body’s activation of processes that prepare itself for demonstrative physical response. This is largely a reflexive response to new and foreign stimuli, and is in constant contact with the bloodstream to monitor the balance of needs. The actions of the sympathetic nervous system are counteracted by the body’s parasympathetic nervous system, or its resting response. A good way to think of this is as a gas (sympathetic) and brake (parasympathetic) in a motor vehicle.
The sympathetic system responds when strenuous physical activity is needed, and the parasympathetic system acts when the body is safe from outside harm, and can proceed with attending more inner functions, such as food digestion. An imbalance in homeostasis, or the body’s natural resting state (ie. a drop in blood pressure) can send a trigger to the brain that causes the sympathetic nervous system to activate. This is known as the afferent system, or information moving away from the senses toward the brain.
The efferent system, or control moving from the brain, can transmit desires from the brain’s systems to peripheral systems that can carry out functions that increase survival in times of acute stressful need. This division of the sympathetic nervous system consists of 2 neurons: one from the brain that heads to the spinal cord, and one from the spinal cord to the body. It acts directly on the tissue that it is designed to act on. Most of these neurons release norepinephrine and epinephrine, which is also known as adrenaline.
The neurotransmitters of this system (norepinephrine and epinephrine) act directly on blood vessels as one of their functions. Upon acting, the end goal is that more blood is directed to skeletal muscles, and blood is directed away from systems like the gut and kidneys that are not needed during a physically stressful event. The sympathetic nervous system also releases glucose from the body’s stores for the muscles to use as energy to enhance function. It is the optimal muscular response. Blood pressure is typically elevated during these times, and in strenuous exercise can increase to as high as 220mmHg systolic (systolic BP is the higher number of the 2 when measuring blood pressure).
Alcoholism itself is a predisposition for hypertension, and there are several manners in which this occurs. Firstly, a 1997 study showed that acute alcohol ingestion acts directly on the sympathetic nervous system through cortisol, the body’s stress hormone, increasing muscle activation and increasing heart rate, up to 80 minutes after intake. However, as this study showed, alcohol’s properties as a natural vasodilator, which is how blood pressure is lowered, cancel out the effects of increased heart rate and sympathetic activity during an acute drinking episode, resulting in a fairly normal blood pressure.
When alcohol use is chronic, usually in the amount of more than 3 drinks per day, there is an associated increase in blood pressure by about 10-40mmHg systolic. This occurs both at the level of the brain and the periphery of the body. As noted above, when alcohol is consumed, the sympathetic nervous system is activated, which is responsible for increasing blood pressure in the body during times of stress. Simultaneously, alcohol acts on the renin-angiotensin system of the body, which are the hormones used by the kidney to signal the brain to increase blood pressure.
A direct link between alcohol consumption and increased renin (the protein precursor to increasing blood pressure through the kidneys) has been established in previous studies. This is thought to be because of the increased amount of circulating volume that the body is handling while alcohol is in the system. This is also supported by the fact that the most effective blood pressure lowering medication in alcohol-induced hypertension inhibits this renin from acting on the body. Additionally deficiencies of magnesium, which is a natural blood pressure lowering agent, is very common in people who have consistent and high levels of alcohol intake. Finally, the chronic inflammatory state induced by alcohol also naturally elevates the body’s defenses, which increases injury to blood vessels and impairs their ability to relax.
As alluded to above, most patients entering into alcohol withdrawal are already likely in a state of at least mild hypertension. This makes it less straightforward to consider hypertension as a withdrawal symptom, as the presence of hypertension may have occurred prior to cessation of alcohol use. A study by Ceccanti et al. published in the journal Alcohol and Alcoholism made substantial investigation into hypertension during withdrawal on 147 patients, and found a mild increase in blood pressure during the first 24 hours in about half of their subjects. However, they found very strong correlations between days in withdrawal and a decrease in overall blood pressure, usually ending up around 10 points lower than when they were admitted for up to 80% of those involved in the study 18 days later. The severity of withdrawal, they said, was not an indication for hypertension within the first 24 hours. The results of this study were replicated in a study by Soardo et al. in 2006, albeit on a much smaller scale (14 hypertensive alcoholics).
The results of these two studies show the subtleties involved in investigating this topic. Although hypertension is often thought of as a symptom of alcohol withdrawal, the evidence actually correlates to the opposite. In fact, in patients with a heavy drinking past and hypertension, one of the most effective ways they can lower blood pressure is to stop drinking. It is rather the fact that many alcoholics are already hypertensive, that it becomes an observation during withdrawal, for which many people believed was the cause. This is a significant benefit towards alcohol abstinence, as lowering blood pressure very quickly reduces the rate of complications down the road.