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Published on: September 22, 2011
Calcium handling by vascular myocytes in hypertension
R C Tostes1, D W Wilde, L M Bendhack
1Department of Physiology, University of Michigan, Ann Arbor 48109-0622, USA. rtostes@usp.br
Insights
Hypertension increases vascular reactivity by altering calcium ion (Ca2+) channel regulation in blood vessels. This leads to elevated intracellular Ca2+ levels and heightened muscle contraction, contributing to high blood pressure.
Area of Science:
- Cardiovascular Physiology
- Molecular Biology
- Hypertension Research
Background:
- Vascular myocyte contraction is regulated by intracellular calcium ions (Ca2+).
- Dysregulation of Ca2+ handling is implicated in the heightened vascular reactivity observed in hypertension.
- Arteries from spontaneously hypertensive rats (SHR) exhibit increased Ca2+ sensitivity and elevated intracellular Ca2+ levels.
Purpose of the Study:
- To investigate the hypothesis that increased membrane Ca2+ channel density and/or function contributes to augmented vascular reactivity in hypertension.
- To elucidate the role of Ca2+ channels in the pathophysiology of hypertension.
Main Methods:
- Comparative analysis of contractile responses in arteries from hypertensive and normotensive rats.
- Assessment of Ca2+ channel activity using Ca2+ channel agonists (e.g., Bay K 8644).
- Measurement of intracellular Ca2+ concentrations in vascular myocytes.
- Electrophysiological studies using voltage-clamp techniques to quantify Ca2+ currents.
Main Results:
- Hypertensive arteries showed increased contractile activity upon depolarization, indicating enhanced voltage-dependent Ca2+ channel activity.
- Ca2+ channel agonists induced greater contractions in hypertensive rat arteries compared to normotensive controls.
- Intracellular Ca2+ levels were significantly elevated in hypertensive vascular myocytes after agonist or depolarization challenges.
- Voltage-clamp recordings revealed nearly double the inward Ca2+ current in myocytes from hypertensive rats versus normotensive rats.
Conclusions:
- Altered Ca2+ channel function and/or increased Ca2+ channel density are key factors in the heightened vascular reactivity associated with hypertension.
- These alterations may result from increased Ca2+ channel synthesis or decreased channel turnover.
- Findings suggest Ca2+ channels as potential therapeutic targets for managing hypertension.
Abstract:
Calcium ions (Ca2+) trigger the contraction of vascular myocytes and the level of free intracellular Ca2+ within the myocyte is precisely regulated by sequestration and extrusion mechanisms. Extensive evidence indicates that a defect in the regulation of intracellular Ca2+ plays a role in the augmented vascular reactivity characteristic of clinical and experimental hypertension. For example, arteries from spontaneously hypertensive rats (SHR) have an increased contractile sensitivity to extracellular Ca2+ and intracellular Ca2+ levels are elevated in aortic smooth muscle cells of SHR. We hypothesize that these changes are due to an increase in membrane Ca2+ channel density and possibly function in vascular myocytes from hypertensive animals. Several observations using various experimental approaches support this hypothesis: 1) the contractile activity in response to depolarizing stimuli is increased in arteries from hypertensive animals demonstrating increased voltage-dependent Ca2+ channel activity in hypertension; 2) Ca2+ channel agonists such as Bay K 8644 produce contractions in isolated arterial segments from hypertensive rats and minimal contraction in those from normotensive rats; 3) intracellular Ca2+ concentration is abnormally increased in vascular myocytes from hypertensive animals following treatment with Ca2+ channel agonists and depolarizing interventions, and 4) using the voltage-clamp technique, the inward Ca2+ current in arterial myocytes from hypertensive rats is nearly twice as large as that from myocytes of normotensive rats. We suggest that an alteration in Ca2+ channel function and/or an increase in Ca2+ channel density, resulting from increased channel synthesis or reduced turnover, underlies the increased vascular reactivity characteristic of hypertension.
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