Calcium-Handling Defects and Smooth Muscle Pathophysiology

Kwan, Chiu‐Yin

doi:10.1007/978-1-4612-5172-9_12

Cited by 5 publications

(2 citation statements)

References 70 publications

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“…Nevertheless there is evidence that changes in blood cells do reflect similar alterations in more relevant tissues. Thus, analogous abnormalities of sodium influx, sodium efflux, phosphoinositol turnover and calcium handling in vascular smooth muscle and other tissues have been reported in the spontaneously hypertensive rat [3,4,26,56,60,62,69,70]. This supports the view that these membrane defects are widespread and that circulating blood cells may be analogous to vascular smooth muscle.…”

Section: Plasma Membrane and Hypertensionsupporting

confidence: 78%

Ion transport in hypertension: are changes in the cell membrane responsible?

et al. 1986

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Disturbances in several, distinct cell membrane ion transport processes have been demonstrated in essential hypertension but their variable relationship to blood pressure in different populations has made it difficult to achieve a unifying hypothesis. We suggest that altered composition of the lipid fraction of the cell membrane is the common underlying factor. This would produce many of the reported perturbations of cell membrane properties and function, not all of which relate directly to the development of hypertension, but which act as markers for the underlying abnormality. However, functions such as phosphoinositol turnover, calcium binding and Ca2+,Mg2+-ATPase dependent calcium efflux, which are influenced by the lipid composition of the membrane, provide a possible link between the membrane disturbance, intracellular calcium, vascular smooth muscle contraction and blood pressure. Alteration in the lipid content of the cell membrane not only provides an explanation for the variability in the ion transport abnormalities between populations but perhaps also for some of the variability in blood pressure within a single population. It also provides a potential means of influencing blood pressure by dietary intervention.

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Section: Plasma Membrane and Hypertensionsupporting

confidence: 78%

Ion transport in hypertension: are changes in the cell membrane responsible?

et al. 1986

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“…It has been well known that excitation–contraction (E‐C) coupling of vascular smooth muscles of spontaneously hypertensive rats (SHR) differs from that of normotensive rats 1–3 . Changes in E‐C coupling have been reported not only in vascular smooth muscle, but also in visceral smooth muscle 1,3–6 . Some experiments on the changes in E‐C coupling in smooth muscle have been performed investigating the effects of caffeine.…”

Section: Introductionmentioning

confidence: 99%

Reduced effect of caffeine on twitch contraction of oesophageal striated muscle from stroke‐prone spontaneously hypertensive rats

Sekiguchi

Kawata

Shimamura

et al. 2003

Clin Exp Pharma Physio

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1. There are known differences in the sensitivity to caffeine between skeletal muscle (soleus) of normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). The present study was performed in order to examine differences in the effects of caffeine on twitch contraction between visceral striated muscle using the outer layer of the oesophagus from WKY rats and stroke-prone SHR (SHRSP). 2. Caffeine, at concentrations ranging from 0.3 to 10 mmol/L, exhibited potentiating effects on twitch contraction in preparations from both WKY rats and SHRSP. The potentiating effect of caffeine was markedly less prominent in preparations from SHRSP compared with preparations from WKY rats. 3. The rate of contraction and relaxation, the time to peak tension and 80% relaxation time were not significantly altered by caffeine at concentrations lower than 3 mmol/L in preparations from either strain. 4. With 10 mmol/L caffeine, the rate of relaxation was markedly reduced and the 80% relaxation time was prolonged, with no significant changes in the rate of contraction, in preparations from WKY rats. These changes were significantly smaller in preparations from SHRSP. 5. The duration of the action potential was greater in preparations from SHRSP than in preparations from WKY rats, although the membrane potential and the amplitude of the action potential were not significantly different between preparations from WKY rats and SHRSP. 6. Caffeine, at 10 mmol/L, prolonged the duration of the action potential in preparations from both strains. The effect of caffeine was not different between preparations from WKY rats and SHRSP. 7. The results of the present study suggest that caffeine augments release of Ca2+ from the sarcoplasmic reticulum (SR) at low concentrations and attenuates Ca2+ re-uptake at 10 mmol/L. Decreased reactivity of SR to caffeine may be a cause of the lesser potentiation of twitch contraction by caffeine in preparations from SHRSP.

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Calcium-Membrane Interactions in Smooth Muscle in Relation to Hypertension

Kwan

1986

Essential Hypertension

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Calcium-Handling Defects and Smooth Muscle Pathophysiology

Cited by 5 publications

References 70 publications

Ion transport in hypertension: are changes in the cell membrane responsible?

Ion transport in hypertension: are changes in the cell membrane responsible?

Reduced effect of caffeine on twitch contraction of oesophageal striated muscle from stroke‐prone spontaneously hypertensive rats

Calcium-Membrane Interactions in Smooth Muscle in Relation to Hypertension

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