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How does alcohol weaken heart muscles and why does it increase blood pressure both temporarily and long term? Is the long term effect due to increase of plaque or is it due to other effects?

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The actual mechanism through which alcohol increases blood pressure is poorly understood (1,2). However, there is a mountain of evidence that shows that there is a strong correlation between alcohol intake and hypertension (small, infrequent amounts may have positive effects whereas excessive consumption has very negative effects (3)).

Back to the underlying mechanisms however, there is a good paper by Kazim Husain, Rais A Ansari, and Leon Ferder, which presents all the possible mechanisms that may contribute to alcohol-induced hypertension. The core ideas are as follows:

Mechanisms of alcohol-induced hypertension. CNS: Central nervous system; SNS: Sympathetic nervous system; RASAS: Renin-angiotensin system and aldosterone system. Image taken from: Husain et al - 2014 - Alcohol-induced hypertension: Mechanism and prevention

Central nervous system in alcohol-induced hypertension

[..] greater effect [of] alcohol on systolic blood pressure compared with diastolic blood pressure may indicate an imbalance between central nervous system factors influencing cardiac output and the peripheral vascular effects of alcohol

Baroreceptors in alcohol-induced hypertension

Alcohol diminishes the baro (presso) reflex by interacting with receptors in the brain stem, i.e. nucleus tractus solitarii and rostral ventrolateral medulla.

Sympathetic nervous system in alcohol-induced hypertension

Several studies reported increased sympathetic nervous system activation and discharge of sympathetic amines after alcohol consumption.

Renin-angiotensin-aldosterone system in alcohol-induced hypertension

The serum levels of vasoactive substances such as renin-aldosterone have been reported to be affected by alcohol ingestion in vivo or ethanol in vitro.

Cortisol in alcohol-induced hypertension

Certain studies have implicated the role of cortisol in alcohol-induced rise in blood pressure. Potter et al have reported a significant rise in plasma cortisol levels following alcohol consumption and a drop in plasma cortisol levels when alcohol intake was discontinued.

Increased intracellular calcium and vascular reactivity in alcohol-induced hypertension

Rats treated with ethanol showed constriction of blood vessels due to greater shifts in the binding of the calcium ion (Ca2+) in arterial and arteriolar smooth muscle cells causes increased sensitivity to endogenous vasoconstrictors.

Endothelium and oxidative stress in alcohol-induced hypertension

Imbalance of specific endogenous vasoconstrictor such as angiotensin II, endothelin-1 and nor-epinephrine and vasodilator nitric oxide (NO) may also play an important role in alcohol-induced hypertension. Alcohol stimulates the release of endothelin 1 and 2 from vascular endothelium in a dose dependent manner. Alcohol also increases the angiotensin II levels in the blood and vessels. Endothelin 1 and 2 as well as angiotensin II are known to be potent vasoconstrictors of the blood vessels.

References:

  1. Husain et al - 2014 - Alcohol-induced hypertension: Mechanism and prevention
  2. Saunders et al 1981 - Alcohol-induced hypertension
  3. Grønbæk et al - 2009 - The positive and negative health effects of alcohol‐ and the public health implications
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