Related Experiment Videos
Dysfunction of calcium handling by smooth muscle in hypertension
Insights
Altered calcium ion handling in vascular smooth muscle contributes to hypertension. Studies in animal models reveal defects in calcium transport across cell membranes, particularly in genetic hypertension, suggesting broader membrane issues.
Area of Science:
- Cardiovascular Physiology
- Cellular Biology
- Hypertension Pathophysiology
Background:
- Ion handling by vascular smooth muscle cell membranes is crucial for blood pressure regulation.
- Dysfunction in ion binding and transport (potassium, sodium, calcium, magnesium) is linked to hypertension.
- Calcium ion (Ca2+) regulation is vital for vascular smooth muscle function; its derangement can elevate blood pressure.
Purpose of the Study:
- To review and evaluate evidence on calcium ion handling alterations in vascular smooth muscle across different hypertension models in animals.
- To assess the role of cytoplasmic Ca2+ concentration regulation in hypertension.
- To explore the contribution of impaired Ca2+ regulation to increased peripheral resistance and elevated blood pressure.
Main Methods:
- Review of studies utilizing subcellular membrane fractionation techniques.
- Analysis of Ca2+ binding and transport in vascular and nonvascular smooth muscle membranes.
- Comparison of data from genetic and experimental hypertensive rat models.
Main Results:
- Decreased active transport of Ca2+ across plasma membrane vesicles observed in some forms of hypertension.
- This membrane abnormality is present in nonvascular smooth muscles and other tissues in genetic hypertension.
- The abnormality is not consistently observed in experimental hypertension models.
Conclusions:
- Altered Ca2+ transport is a feature in certain forms of hypertension.
- Evidence suggests potential general membrane defects in spontaneous (genetic) hypertension.
- Further research is needed to fully understand the implications of these membrane abnormalities.
Abstract:
Dysfunction of ion handling, including binding and fluxes (passive and active transport) of physiologically important ions such as potassium, sodium, calcium, and magnesium, by vascular smooth muscle cell membranes has repeatedly been reported to be associated with the pathophysiology of hypertension. The specific purpose of this review is to summarize and evaluate the evidence for alterations of calcium ion (Ca2+) handling by vascular smooth muscle in various forms of hypertension in the animal model on the basis that regulation of cytoplasmic Ca2+ concentration is a complex and yet vitally important process for a normal function of vascular smooth muscle and that derangement of such a regulation may result in excessive retention of cytoplasmic Ca2+, contribute toward increase of total peripheral resistance, and ultimately lead to elevation of blood pressure. Emphasis is placed upon the consideration of the usefulness of the subcellular membrane fractionation technique in studies of binding and transport of Ca2+ by vascular and nonvascular smooth muscle membranes from genetic as well as experimental hypertensive rats. The limitations of the interpretation of data using such an approach are also considered. Decreased active transport of Ca2+ across isolated plasma membrane vesicles from large and small arteries occurs in several but not all forms of hypertension. This membrane abnormality also occurs in nonvascular smooth muscles and other tissues or cells not confined to the cardiovascular system in genetic hypertension, but not in experimental hypertension. A hypothesis of general membrane defects in spontaneous hypertension is proposed.(ABSTRACT TRUNCATED AT 250 WORDS)