Lisinopril is used for treating high blood pressure alone or with other medicines.


How Drinking Alcohol Affects High Blood Pressure


Alcohol from fermented grain, fruit juice and honey has been used for so many years. Fermented beverages and alcoholic drinks existed in the early Egyptian civilization, in China around 7000 BC, in Babylon 2700 BC, in Greece and in South America.
Alcohol was mainly used for medicinal purposes during the sixteenth century. At the start and the middle of the eighteenth century, alcohol in form of spirits was heavily used in Britain. However, in the nineteenth century there were changes in attitudes favoring the moderate use of alcohol. In 1920, a law was passed in the United States that prohibited the manufacture and sale of any intoxicating liquors.
Current research indicates that moderate consumption of alcohol has a beneficial effect on the cardiovascular system and it helps in lowering blood pressure. A pre-clinical study showed decrease in systolic blood pressure on rats that were fed with ethanol over a period of 12 weeks. Two drinks a day for men aged below 65, one drink for men aged 65 and older and one drink a day for women of all ages is regarded to be moderate drinking. Low to moderate drinking prevents the incidence of coronary heart disease and increasing longevity.
Most human societies in the world today, consume alcoholic beverages on a regular basis. But then the abuse of alcohol is a major public health problem in the world right now. For example in the United States, abuse of alcohol affects millions of individuals which leads to loss of thousands of lives every year. Consumption of a high dose of chronic ethanol commonly causes hepatic gastrointestinal, nervous and cardiovascular injuries which leads to physiological dysfunctions.
Clinical studies have found out that consuming chronic ethanol that includes more than three drinks per day leads to high blood pressure and also increases the risk of developing cardiovascular diseases. In heavy drinkers there is a greater increase in systolic blood pressure than diastolic blood pressure. From pre-clinical studies an increase of 7mmHg in the mean arterial pressure was reported when a comparison was made between heavy drinkers and the others.
Few studies have addressed the relationship between alcohol and high blood pressure in older people, and most of them have shown that drinking alcohol affects high blood pressure. The techniques that alcohol uses to cause vascular injury and raise blood pressure remain elusive. But then there are mechanisms that are associated with alcohol-induced high blood pressure.
The following are a number of mechanisms through which alcohol affects your blood pressure:

1. Central nervous system in alcohol-induced-high blood pressure

The relatively greater effect that drinking alcohol has on systolic pressure compared to diastolic pressure indicates that an imbalance exists between the central nervous system, factors affecting cardiac output and peripheral vascular effects of alcohol. There is strong evidence that suggest that alcohol initiates central and peripheral reactions which in a synergetic manner can lead to high blood pressure. In addition, alcohol increases sympathetic outflow due to the secretion of corticotrophin-releasing hormone. Research suggests that the relationship between alcohol and high blood pressure exists because of the temporal sequence of alcohol use and blood pressure measurement. Patients may avoid drinking alcohol before going to visit a doctor. And the measurements taken may indicate an increase in blood pressure which could be due to excessive central-nervous-system excitability and the adrenaline rush caused by the withdrawal.

2. Baroreceptors in alcohol induced-high blood pressure

It was found out that Alcohol diminishes the baroreceptor reflex through interaction with the receptors in the brain stem. Investigators reported that baroreceptor reflex curves when challenged with vasoconstrictors were shifted up and reduced in ethanol fed rats compared to controls. These findings show that there is an impairment of the baroreceptor control and sympathetic system. There was a greater decrease in heart rate noticed in ethanol treated rats compared to control rats which indicates an increase in sympathetic activity. When there is an increase in sympathetic activity, the baroreceptors are impaired which when activated, inhibits the sympathetic nervous system leading to an increase in blood pressure.

3. Sympathetic nervous system in alcohol-induced high blood pressure

Several studies indicated that consumption of alcohol led to an increase in the sympathetic nervous system activity and discharge of sympathetic amines. Alcohol intake can lead to high blood pressure because alcohol affects the autonomic nervous system. However, old people may have a different reaction to factors that trigger their autonomic nervous system than younger people because of the alterations in the sympatho-adrenal which occurs during ageing. The rise in sympathetic outflow is not only expected to induce adrenoreceptor-mediated reactions such as vasoconstriction, heart rate increase, but also stimulating oxidation reactions.
Direct recordings from research indicate that short-term intake of alcohol by humans and both short and long term administration of ethanol, leads to the stimulation of sympathetic-nerve discharge in rats. Moreover, increases in blood pressure and sympathetic activity in ethanol fed rats is centrally mediated. There is a high possibility of alcohol stimulating the adrenal glands to release adrenaline which in turn results to heart rate, cardiac output and high blood pressure. Reports suggest high blood pressure in rats is caused by alcohol through sympathetic activation which looks to be centrally mediated.

4. Renin-angiotensin-aldosterone system in alcohol induced high blood pressure

Intake of alcohol affects the serum levels of vasoactive substances such as renin-aldosterone. Antihypertensive drugs offer protection against the responses caused by alcohol in human endothelial cells indicating the involvement of renin-angiotensin system. Reports indicate that there is a significant rise in plasma rennin activity among people who drink a lot of alcohol compared to those who drink moderately or mildly. However it’s worth noting that alcohol consumption leads to the expansion of extracellular fluid which causes an increase in blood pressure. The expansion of the extracellular fluid is as a result of significant increase of plasma vasopressin levels and plasma rennin activity which indicates increased sympathetic activity.
Recent studies show a significant increase in blood and aortic angiotensin levels in ethanol fed rats. Prolonged elevation of serum angiotensin converting enzyme activity in people who drink alcohol causes an increase in angiotensin levels. When alcohol was administered to dogs, it caused a sustained rennin-angiotensin activity which increased plasma levels and renin activity, left ventricular ACE enzyme activity and left ventricular myocyte receptor expression.

5. Cortisol in alcoholic-induced high blood pressure

There are studies that show the role of cortisol in alcohol-induced high blood pressure. Reports indicate that there is an increase in cortisol levels after alcohol intake while there is a decrease in plasma cortisol levels when alcohol is withdrawn. Increased cortisol levels in alcoholics may be as a result of a direct stimulation of adrenocorticotropic hormone by arginine vasopressin which in turn causes an increase in blood pressure.
The effect on blood pressure could be because of mineralocorticoid activity of cortisol or catecholamine hypersensitivity. Alcohol causes the stimulation of corticotrophin releasing hormone in rats which results in increased cortisol levels, sympathetic stimulation and increase in blood pressure in rats.

6. Increased intracellular calcium and vascular reactivity in alcoholic-induced high blood pressure

Rats fed with ethanol showed constriction of blood vessels which resulted from greater shifts in the binding of the calcium ion in arterial and arteriolar smooth muscle cells which in turn causes an increase in sensitivity to endogenous vasoconstrictors.
Heavy drinking of alcohol has been reported to cause a deficiency of blood and intracellular magnesium, which affects cellular homeostasis through the attenuation of plasmalemmal ATPase activity. It was found out that increases in both cytosolic free calcium and calcium uptake led to an increase in blood pressure in ethanol fed rats. Intra-arterial infusion of alcohol leads to a reduced hand and forearm blood flow in human beings which is as a result of direct vasoconstriction. However, there were no significant responses of alpha-adrenergic receptor mediated constriction of the aorta that was indicated after high intake of ethanol in rats. On the other hand, the endothelium-relaxation which was induced by acetylcholine was reduced in rats that were fed with chronic ethanol.

7. Endothelium and oxidative stress in alcohol-induced high blood pressure

Imbalance of angiotensin II, endothelin-1 and nor-epinephrine and vasodilator nitric oxide plays an important role in alcoholic-induced high blood pressure. Alcohol does not only stimulate the release of endothelin1 and 2 from vascular endothelium, but also it increase the levels of angiotensin II which are known to be potent vasoconstrictors of the blood vessels.
Angiotensin II leads to the production of superoxide by activating NADPH oxidase in the vascular wall. This has been demonstrated in rats with hypertension through angiotensin II infusion. Hypertension resulting from chronic alcohol intake in rats correlates with increased tissue angiotensin II levels and activation of NADPH oxidase activity that causes endothelial injury. Drinking alcohol increases blood pressure by decreasing vasodilators either as a result of the inhibition of endothelial nitric oxide synthase or oxidative injury to the endothelium.
Earlier studies show that drinking a lot of alcohol disrupts the production of nitric oxide from endothelial cells. The reduction in nitric oxide may be as a result of reaction with superoxide anion to form peroxynitrite radicals. The production of NO in the endothelium depends on how endothelial nitric oxide synthase functions and this is regulated by vascular endothelial growth factor. Rats treated with alcohol experience depletion of NO production or NO reaction with superoxide anion to form toxic peroxynitrite radical in the endothelium, thus causing endothelial injury,impairment and increase in blood pressure.

Prevention and treatment of alcoholic-induced high blood pressure

There a few strategies that you can employ to help you control, prevent and treat alcoholic-induced hypertension:

Non-pharmacological prevention and treatment of alcoholic-induced high blood pressure

Studies have shown that reduction in consumption of alcohol in both heavy drinkers and low to moderate drinkers is of beneficial effect in lowering blood pressure and prevention of the development of high blood pressure. Heavy drinkers who decide to reduce the consumption of alcohol can easily lower their systolic pressures by 2 to 4 mmHg and their diastolic pressure by 1 to 2 mmHg. Heavy drinkers who want to reduce their blood pressure should consider cutting back on alcohol consumption. Another pharmacological prevention and treatment is exercise training or physical conditioning. Exercise increases the use and utilization of oxygen in the body. From the rat model experiment, a physiological basis for effect of physical conditioning on alcoholic-induced high blood pressure. When you take part in exercise training, NO is generated in the cardiovascular system by induction of nitric oxide synthase. Physical inactivity can lead to hypertension while taking part in exercise decreases blood pressure and body weight. Studies show that exercise training lowers the blood pressure by suppressing weight gain in rats fed with a lot of alcohol. Therefore, physical conditioning reduces high blood pressure caused by too much drinking of alcohol by increasing the availability of nitric oxide and reducing the oxidative stress response.

Pharmacological treatment of alcoholic-induced high blood pressure

alert No clinical data is available particularly on the efficacy of specific drugs that can be used in the treatment of alcohol-induced high blood pressure. However, reports indicate that taking 2 mg per day of dexamethasone suppresses the acute alcoholic-induced high blood pressure. ACE inhibitors/angiotensin II type 1 blockers have the ability to increase the cardiac output in patients with cardiomyopathy resulting from high consumption of alcohol, and will help in the treatment of alcoholic –induced high blood pressure. Studies have shown that angiotensin II type 1 receptor blockers have the ability to suppress alcoholic cardiomyopathy in dogs. Because of the probability of calcium being involved in the development of alcohol-induced hypertension, the calcium blockers may also be the drug that you can consider using in treating alcohol-induced blood pressure.

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