Calcium-channel blockers, ABA and stomatal closure

 

 

Partial inhibition of ABA-induced stomatal closure by calcium-channel blockers.

by McAinsh M. R., Brownlee C., Hetherington A. M. (1991)

 

martin_mcainsh
Martin R Mcainsh, Lancaster University
OLYMPUS DIGITAL CAMERA
Colin Brownlee, Marine Biological Association of the UK, Plymouth
AS-272722915754002@1442033618447_l
Alistair M. Hetherington, School of Biological Sciences, University of Bristol, UK

in Proceedings of the Royal Society B: Biological Sciences, 243 (1308). pp. 195-201.- doi: 10.1098/rspb.1991.0031 –

CrossRef Full Text | Google Scholar – 

http://rspb.royalsocietypublishing.org/content/243/1308/195

Abstract

ABA-induced increases in [Ca$^{2+}$]$_{\text{cyt}}$ (cytosolic free Ca$^{2+}$) may result from Ca$^{2+}$ influx from the apoplast and/or release from intracellular stores. In this paper, Ca$^{2+}$-channel blockers have been used to investigate this question in the detached epidermis of Commelina communis.

Examples from the benzothiazepine, dihydropyridine and phenylalkylamine series all inhibited ABA-induced stomatal closure: ($\pm $) verapamil > nifedipine > diltiazem. Inhibition was partial, the magnitude of the effect being dependent on both the concentration of ABA and that of the channel blocker. The maximum inhibition observed in the presence of 100 nM ABA was approximately 66% at high (100 nM) concentrations of ($\pm $) verapamil or nifedipine.

In the near absence of extracellular Ca$^{2+}$ (2 mM EGTA) ABA-induced stomatal closure was reduced by approximately 22% and the inhibition by Ca$^{2+}$-channel blockers abolished. Inhibition by ($\pm $) verapamil was totally reversible and exhibited signs of stereospecificity, the s(-) enantiomer being a more potent inhibitor of ABA-induced stomatal closure than the R(+) enantiomer.

Bay K 8644 (a fluorinated analogue of nifedipine) exhibited biphasic action on 500 $\mu $M Ca$^{2+}$-induced stomatal closure, i.e. agonistic at low concentrations (10 nM), antagonistic at high concentrations (> 10 nM to 100 $\mu $M), but did not affect ABA-induced stomatal closure.

These results suggest that Ca$^{2+}$ release from intracellular stores may be important in the ABA-induced increase in [Ca$^{2+}$]$_{\text{cyt}}$ associated with stomatal closure. They do not, however, exclude a contribution of Ca$^{2+}$ influx from the apoplast.

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Published by

Willem Van Cotthem

Honorary Professor of Botany, University of Ghent (Belgium). Scientific Consultant for Desertification and Sustainable Development.

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