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Related Experiment Videos

Receptor-mediated Ca++ entry in blood vessels.

R K Hester1

  • 1Department of Medical Pharmacology and Toxicology, College of Medicine, Texas A&M University, College Station 77843.

Microcirculation, Endothelium, and Lymphatics
|February 1, 1989
PubMed
Summary

This study quantifies receptor-mediated calcium entry (RMCa++E) versus potential-dependent calcium entry (PDCa++E) in rabbit arteries. RMCa++E plays a significant role in agonist-induced responses, with distinct pathways varying by agonist and blood vessel type.

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Area of Science:

  • Pharmacology
  • Cardiovascular Physiology
  • Cellular Signaling

Background:

  • Agonist-induced vascular smooth muscle contraction involves calcium (Ca++) influx and release.
  • Distinguishing between receptor-mediated Ca++ entry (RMCa++E) and potential-dependent Ca++ entry (PDCa++E) is crucial for understanding vascular responses.
  • Rabbit aorta and renal artery exhibit differential responses to various agonists, suggesting distinct calcium handling mechanisms.

Purpose of the Study:

  • To quantitatively delineate the relative contributions of RMCa++E and PDCa++E in agonist-induced responses in rabbit aorta and renal artery.
  • To investigate the role of specific agonists (norepinephrine, histamine, serotonin) in activating these distinct calcium entry pathways.
  • To explore the influence of magnesium (Mg++) and lanthanum (La+++) on RMCa++E and PDCa++E.

Main Methods:

  • Utilized a Ca++-free solution with EGTA and D600 to selectively inhibit PDCa++E.
  • Administered varying concentrations of norepinephrine (NE), histamine (Hist), and serotonin (5HT) to rabbit aorta and renal artery preparations.
  • Quantified developed force to assess Ca++ release and RMCa++E components, and evaluated the effects of Mg++ and La+++.

Main Results:

  • Agonist-induced Ca++ release was concentration-dependent, with NE > Hist > 5HT.
  • RMCa++E significantly contributed to total developed force in aorta (NE: 91%, Hist: 71%, 5HT: 37%) and renal artery (NE: 78%).
  • The capacity to stimulate RMCa++E was inversely related to sensitivity to the PDCa++E blocker D600, and Mg++ modulated Ca++ sensitivity.

Conclusions:

  • Receptor-mediated Ca++ entry is a major determinant of agonist-induced contraction in rabbit aorta and renal artery.
  • Pharmacologically distinct Ca++ channels exist and are differentially activated by specific agonist-receptor interactions in a potential-independent manner.
  • These findings highlight the complex and selective regulation of calcium signaling in vascular smooth muscle.

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