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Local and cellular Ca 2+ transients in smooth muscle of pressurized rat resistance arteries during myogenic and agonist stimulation
Author(s) -
Miriel Victor A.,
Mauban Joseph R. H.,
Blaustein Mordecai P.,
Gil Wier W.
Publication year - 1999
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1999.0815p.x
Subject(s) - vasoconstriction , phenylephrine , vasodilation , cyclopiazonic acid , vascular smooth muscle , mesenteric arteries , chemistry , artery , medicine , calcium , anatomy , biophysics , biology , smooth muscle , blood pressure
1 Confocal laser scanning microscopy was used to visualize Ca 2+ transients in the vascular smooth muscle cells (VSMC) of intact, pressurized rat mesenteric resistance arteries loaded with fluorescent calcium indicators. Vasoconstriction was assessed by measuring inner arterial diameter. All arteries were studied at 70 mmHg intralumenal pressure and 37 °C. 2 In the control condition of myogenic tone the arteries were constricted to 62 % ( n = 10 ) of their passive diameter (p.d.). The [Ca 2+ ] i in most VSMC of these arteries was constant over time. In a small percentage (< 10 %) of cells in each artery, [Ca 2+ ] i oscillated regularly. Local calcium transients (Ca 2+ sparks) were observed in five arteries studied with confocal linescan imaging. 3 Activation of α‐adrenoceptors by phenylephrine (PE, 1.0 μM) induced further vasoconstriction of pressurized arteries (to 27 % of p.d.). In this condition, [Ca 2+ ] i oscillations were prominent in a large percentage (83 %) of the VSMC. The Ca 2+ oscillations ranged in frequency from 4 to 22 min −1 , and were usually asynchronous between cells. 4 High [KCl] o (65 mM) induced nearly comparable vasoconstriction to PE (37 % of p.d.) but [Ca 2+ ] i oscillated in only about 13 % of cells in each artery. 5 Block of L‐type Ca 2+ channels (with nifedipine) in arteries activated by PE caused nearly full vasodilatation, but did not abolish the Ca 2+ oscillations. Subsequent block of the sarcoplasmic reticulum Ca 2+ pump (with cyclopiazonic acid) abolished Ca 2+ oscillations in all cells. 6 We conclude that Ca 2+ entering VSMC via L‐type Ca 2+ channels has an obligatory role in force development, both in myogenic tone and during α 1 ‐adrenoceptor activation. The oscillatory pattern of [Ca 2+ ] i that persists in the absence of Ca 2+ entry via L‐type Ca 2+ channels is ineffective in activating contraction.