This review highlights that increased membrane excitability, gap junctions, and endothelial dysfunction drive abnormal arterial tension oscillations in hypertensive animals.
No immediate clinical implications from rat models; leaves open translation of vascular oscillation mechanisms to human hypertension.
The mechanisms of oscillatory contraction of arterial smooth muscle in vitro are discussed. 2. The membrane potential and cytoplasmic free Ca2+ concentration in smooth muscle cells oscillate in the presence of agonists. 3. The oscillatory change in the membrane potential of smooth muscle cells is related to Ca2+ release from intracellular stores. 4. Gap junctions between smooth muscle cells play important roles in the synchronized oscillation of the cytoplasmic free Ca2+ concentration in this population of cells. 5. Endothelial cells may increase or decrease the tension oscillation of smooth muscle cells. 6. In arteries from hypertensive rats, an increase in membrane excitability and the number of gap junctions between smooth muscle cells and impaired endothelial function are the main factors responsible for the modulation of tension oscillation.
No takes yet. Share an insight, caveat, or question.
Shimamura et al. (1999) studied this question.