Dissociation between force and [Ca2+]i during extra systoles in guinea-pig ventricular muscle microinjected with fura-2
(1999) In Acta Physiologica Scandinavica 165(1). p.1-8- Abstract
- Thin trabeculae were dissected from the right ventricle of guinea-pig heart and stimulated to contract isometrically at 0.5 Hz (26 degrees C). Rapid and transient changes of force were obtained by inducing three extra systoles (ES1-3) at 450-ms intervals. The two regular contractions (P1-2) following (ES1-3) were potentiated. Fura-2 salt was microinjected into the preparation to monitor intracellular calcium ([Ca2+]i). Three distinct phases of [Ca2+]i were seen: (1) a rapid rising phase to about 200 nmol L(-1), (2) a slower rising phase to a peak at 400 nmol L(-1), and (3) a slow decline to about 50 nmol L(-1). During ES1, there was a discrepancy between force, which decreased, and peak [Ca2+]i, which increased to 600 nmol L(-1). It is... (More)
- Thin trabeculae were dissected from the right ventricle of guinea-pig heart and stimulated to contract isometrically at 0.5 Hz (26 degrees C). Rapid and transient changes of force were obtained by inducing three extra systoles (ES1-3) at 450-ms intervals. The two regular contractions (P1-2) following (ES1-3) were potentiated. Fura-2 salt was microinjected into the preparation to monitor intracellular calcium ([Ca2+]i). Three distinct phases of [Ca2+]i were seen: (1) a rapid rising phase to about 200 nmol L(-1), (2) a slower rising phase to a peak at 400 nmol L(-1), and (3) a slow decline to about 50 nmol L(-1). During ES1, there was a discrepancy between force, which decreased, and peak [Ca2+]i, which increased to 600 nmol L(-1). It is likely that the increased [Ca2+]i during the extra systoles reflects increased sarcolemmal calcium inflow, causing post-extra-systolic potentiation. Ryanodine (1-2 microM) was added to inhibit the intracellular calcium release and thus reduce the intracellular [Ca2+]i gradients following excitation. Ryanodine inhibited phase 1 of [Ca2+]i and abolished post-extra-systolic potentiation. There was a close relationship between dF/dt and [Ca2+]i with ryanodine during control and ES1-3. It is likely that fura-2 reports a spatially averaged [Ca2+]i and that phase 1 of the signal therefore apparently underestimates activator calcium in the close vicinity of the contractile elements. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1115226
- author
- Arheden, Håkan LU ; Hellstrand, Per LU and Wohlfart, Björn LU
- organization
- publishing date
- 1999
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- excitation-contraction coupling, calcium, fura-2, force-interval relationships
- in
- Acta Physiologica Scandinavica
- volume
- 165
- issue
- 1
- pages
- 1 - 8
- publisher
- Wiley-Blackwell
- external identifiers
-
- pmid:10072090
- scopus:0032587523
- ISSN
- 0001-6772
- DOI
- 10.1046/j.1365-201x.1999.00457.x
- language
- English
- LU publication?
- yes
- id
- a1f50262-1ce8-4406-a360-364a4072f04a (old id 1115226)
- alternative location
- http://www.ingentaconnect.com/content/bsc/aps/1999/00000165/00000001/art00001
- date added to LUP
- 2016-04-01 15:38:50
- date last changed
- 2022-03-22 05:28:17
@article{a1f50262-1ce8-4406-a360-364a4072f04a,
abstract = {{Thin trabeculae were dissected from the right ventricle of guinea-pig heart and stimulated to contract isometrically at 0.5 Hz (26 degrees C). Rapid and transient changes of force were obtained by inducing three extra systoles (ES1-3) at 450-ms intervals. The two regular contractions (P1-2) following (ES1-3) were potentiated. Fura-2 salt was microinjected into the preparation to monitor intracellular calcium ([Ca2+]i). Three distinct phases of [Ca2+]i were seen: (1) a rapid rising phase to about 200 nmol L(-1), (2) a slower rising phase to a peak at 400 nmol L(-1), and (3) a slow decline to about 50 nmol L(-1). During ES1, there was a discrepancy between force, which decreased, and peak [Ca2+]i, which increased to 600 nmol L(-1). It is likely that the increased [Ca2+]i during the extra systoles reflects increased sarcolemmal calcium inflow, causing post-extra-systolic potentiation. Ryanodine (1-2 microM) was added to inhibit the intracellular calcium release and thus reduce the intracellular [Ca2+]i gradients following excitation. Ryanodine inhibited phase 1 of [Ca2+]i and abolished post-extra-systolic potentiation. There was a close relationship between dF/dt and [Ca2+]i with ryanodine during control and ES1-3. It is likely that fura-2 reports a spatially averaged [Ca2+]i and that phase 1 of the signal therefore apparently underestimates activator calcium in the close vicinity of the contractile elements.}},
author = {{Arheden, Håkan and Hellstrand, Per and Wohlfart, Björn}},
issn = {{0001-6772}},
keywords = {{excitation-contraction coupling; calcium; fura-2; force-interval relationships}},
language = {{eng}},
number = {{1}},
pages = {{1--8}},
publisher = {{Wiley-Blackwell}},
series = {{Acta Physiologica Scandinavica}},
title = {{Dissociation between force and [Ca2+]i during extra systoles in guinea-pig ventricular muscle microinjected with fura-2}},
url = {{http://dx.doi.org/10.1046/j.1365-201x.1999.00457.x}},
doi = {{10.1046/j.1365-201x.1999.00457.x}},
volume = {{165}},
year = {{1999}},
}