Cerebral artery sarcoplasmic reticulum Ca(2+) stores and contractility: changes with development.

Area of Science:

• Cardiovascular Physiology
• Developmental Biology
• Smooth Muscle Pharmacology

Background:

• Sarcoplasmic reticulum (SR) Ca(2+) stores are crucial for regulating vascular smooth muscle contraction.
• Developmental changes in cerebral artery function may alter the contribution of SR Ca(2+) stores to norepinephrine (NE)-induced responses.

Purpose of the Study:

• To investigate the role of SR Ca(2+) stores in NE-induced contraction of fetal and adult sheep middle cerebral arteries (MCA).
• To determine if developmental changes influence the reliance on SR Ca(2+) stores for cerebral artery contraction.

Main Methods:

• Measured NE-induced tension and intracellular Ca(2+) ([Ca(2+)](i)) in fetal and adult sheep MCA.
• Utilized thapsigargin and ryanodine to assess the contribution of SR Ca(2+) stores and ryanodine receptors.
• Performed experiments in the presence and absence of extracellular Ca(2+).

Main Results:

• Thapsigargin significantly reduced NE-induced responses in adult MCA but not in fetal MCA.
• Absence of extracellular Ca(2+) markedly impaired NE-induced responses in adult MCA, with minimal effect on fetal MCA.
• Ryanodine application mimicked NE-induced responses, which were abolished in zero extracellular Ca(2+).

Conclusions:

• SR Ca(2+) stores play a significantly lesser role in NE-induced contraction of fetal MCA compared to adult MCA.
• Fetal cerebral artery contraction is predominantly mediated by Ca(2+) influx through plasma membrane L-type Ca(2+) channels.
• The ryanodine receptor in both fetal and adult MCA appears coupled to plasma membrane channels, influencing contraction.