Ionic channels in vascular smooth muscle /
Saved in:
| Author / Creator: | Bkaily, Ghassan. |
|---|---|
| Imprint: | Austin : R.G. Landes Co., ©1994. |
| Description: | 117 pages : illustrations (some color) ; 26 cm. |
| Language: | English |
| Series: | Molecular biology intelligence unit Molecular biology intelligence unit (Unnumbered) |
| Subject: | |
| Format: | Print Book |
| URL for this record: | http://pi.lib.uchicago.edu/1001/cat/bib/2438317 |
Table of Contents:
- General electrophysiology of vascular smooth muscle (VSM)
- General electrophysiology of vascular smooth muscle
- Presence of TTX-sensitive fast Na channels in VSM cells
- Biophysical and pharmacological properties of T-, L- and R-type Ca² channels
- Different types of Ca² channels in excitable cells
- General properties of L- and T-type Ca²⁺ currents
- Receptor-operated Ca²⁺ channel (ROC)
- Resting membrane potential Ca²⁺ channel (R-type)
- Background Ca²⁺ channel (B-type)
- Pharmacology of Ca²⁺ channels in excitable muscle.
- Ionic currents in vascular smooth muscle
- Properties of different types of channels in VSM
- Pharmacology of different types of Ca² channels in VSM
- Regulation of different types of Ca² channels in VSM by second messengers
- Regulation of calcium channels by protein kinase A
- Modulation of L-type Ca² channels in heart cells seems not to be the same as in VSM cells
- Regulation by protein kinase G
- Modulation of the channels
- Regulation of Ca²⁺ channels by C-kinase
- Regulation of calcium channels by IP₃
- Regulation of Ca²⁺ channels by G proteins.
- Regulation of R-type Ca² channels by insulin and ET-1 in VSM
- Insulin induces a sustained increase of [Ca]i
- Endothelin-1
- Differences in sensitivity of VSM to ET-1
- Different pharmacological profiles of Bay K 8644 and ET-1
- G protein involvement on ET-1 and insulin induced sustained increase in [Ca]i in VSM cells
- Regulation of Ca² channels in VSM by monocyte-released factors
- Effect of isradipine on the vasoactive properties of PAF
- PAF activation of a sustained increase of [Ca]i
- Regulation of Ca² channels by bradykinin in VSM cells.
- Bradykinin induced sustained increase of [Ca]i in VSM cells
- Bradykinin does not affect the delayed outward K current but increases both T- and L-type Ca² currents
- Biophysical and pharmacological properties of vascular K channels
- Delayed outward K⁺ current
- Ca²⁺-dependent K⁺ current
- ATP-dependent K⁺ current
- Presence of five types of K⁺ channels in aortic VSM cells
- cGMP-sensitive K⁺ channels in VSM
- Regulation of K⁺ channels in aortic cells by cyclic nucleotides.
- Effect of ANF on the 100 pS (80-120 pS) K channel in rabbit aortic single cells, using the cell-attached mode
- Effect of increasing [cGMP]i on the 100 pS single K channel using the cell-attached configuratioon
- Angiotensin II blocked the macroscopic delayed outward K current in single aortic cells of the rabbit
- Possible role of Ca²⁺ and K⁺ channels in VSM pathophysiology
- Possible role of T- and L-type channels in vascular pathology
- Possible role of the R-type channel in vascular pathology.
- Localization of R-type Ca² channels using laser confocal scanning microscopy.
