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Source of calcium for contractile responses of large and small human intramyometrial arteries
A Kostrzewska1, B Modzelewska, S Batra
1Department of Biophysics, Medical Academy, ul. Mickiewicza 2A, 15-230 Bialystok, Poland.
Insights
This study reveals that small human intramyometrial arteries rely heavily on extracellular calcium for vasopressin-induced contractions, unlike large arteries which also depend on intracellular calcium stores.
Area of Science:
- Physiology
- Vascular Biology
- Pharmacology
Background:
- Vasopressin (AVP) plays a role in regulating vascular tone.
- Calcium ions (Ca2+) are critical for smooth muscle contraction.
- Understanding calcium signaling in different arterial sizes is crucial for cardiovascular research.
Purpose of the Study:
- To investigate the distinct roles of intracellular and extracellular calcium in vasopressin-induced responses in human intramyometrial arteries.
- To compare the calcium dependency of large versus small arteries in response to AVP.
Main Methods:
- Vessel-based functional assays were used to measure arterial contractility.
- Experiments involved varying extracellular calcium concentrations and using calcium store depletors like Thapsigargin (TSG).
- Pharmacological agents such as Nimodipine were employed to assess calcium channel involvement.
Main Results:
- Both large and small arteries showed similar sensitivity to AVP.
- Small arteries were highly dependent on extracellular Ca2+, with responses abolished in Ca2+-free solutions.
- Large arteries demonstrated significant dependence on both extracellular and intracellular Ca2+ for maximal responses.
Conclusions:
- Human intramyometrial small arteries primarily utilize extracellular calcium for AVP-mediated contractions.
- Large intramyometrial arteries rely on both extracellular calcium influx and intracellular calcium release.
- These findings highlight differential calcium handling mechanisms in human uterine arteries of varying sizes.
Abstract:
The role of calcium (Ca(2+)) released from intracellular stores and the entry of extracellular Ca(2+) for vasopressin (AVP)-induced responses in large and small, human, intramyometrial arteries was investigated. There was no statistical difference as revealed by pD(2) values (-log EC(50)), in the sensitivity of large and small vessels to AVP. Nimodipine caused an inhibition of contractions induced by low concentrations (10(-10) mol/l) of AVP in both types of vessels but, at higher concentration (>10(-10) mol/l), whereas responses in small arteries were diminished, in large arteries they remained unchanged. In Ca(2+)-free solution, responses of large and small arteries to potassium and to 10(-10) mol/l AVP were abolished. With 10(-6) mol/l AVP, response in small arteries was completely inhibited, whereas in large arteries it was reduced by approximately 50%. Additional experiments were done on large arteries. Thapsigargin (TSG), which causes depletion of internal Ca(2+) stores, caused a significant reduction in responses. Following treatment with TSG, responses to AVP in Ca(2+)-free solution were almost completely inhibited but arteries responded again when incubated in normal physiological salt solution. The results indicate that in contrast to large arteries, small arteries are highly dependent on extracellular Ca(2+). Response of large arteries showed considerable dependence on Ca(2+) stored internally particularly, for maximum activation.