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In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model
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Published on: October 27, 2020

Cardiovascular responses to cold exposure.

Zhongjie Sun1

  • 1Department of Physiology, College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA.

Frontiers in Bioscience (Elite Edition)
|December 29, 2009
PubMed
Summary
This summary is machine-generated.

Cold weather worsens hypertension and cardiovascular risks. This review explores the mechanisms of cold-induced hypertension (CIH), focusing on the sympathetic nervous system and renin-angiotensin system.

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07:54

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Published on: March 9, 2021

Area of Science:

  • Cardiovascular Physiology
  • Environmental Health
  • Hypertension Research

Background:

  • Hypertension prevalence increases in winter and cold climates.
  • Cold temperatures exacerbate existing hypertension and trigger cardiovascular events like stroke and heart failure.
  • Animal studies demonstrate cold exposure induces hypertension and cardiac hypertrophy.

Purpose of the Study:

  • To review recent advances in understanding the mechanisms of cold-induced hypertension (CIH).
  • To elucidate how cold temperatures impact cardiovascular systems and contribute to hypertension.
  • To consolidate current knowledge on the molecular and physiological pathways involved in CIH.

Main Methods:

  • Literature review of recent mechanistic investigations into CIH.
  • Analysis of studies on cold exposure effects on the sympathetic nervous system (SNS) and renin-angiotensin system (RAS).
  • Examination of molecular changes including eNOS, nitric oxide (NO), endothelin-1 (ET-1), and related receptors.

Main Results:

  • Cold temperatures activate the sympathetic nervous system (SNS), which initiates CIH via the renin-angiotensin system (RAS).
  • Cold exposure leads to suppressed eNOS expression and reduced nitric oxide (NO) formation.
  • Increased production of endothelin-1 (ET-1) and altered expression of its receptors (ETA up-regulated, ETB down-regulated) are observed.

Conclusions:

  • The sympathetic nervous system and renin-angiotensin system are key mediators of cold-induced hypertension.
  • Imbalances in nitric oxide and endothelin-1 pathways significantly contribute to CIH.
  • Further research into these mechanisms can inform strategies for managing cold-related cardiovascular risks.