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Mesenteric Artery Contraction and Relaxation Studies Using Automated Wire Myography
Published on: September 22, 2011
[Cellular calcium, vasoconstriction, hypertension]
G Bruschi1, G Regolisti, A Borghetti
1Istituto di Clinica Medica e Nefrologia, Università degli Studi di Parma.
Insights
Hypertension involves altered calcium handling in vascular cells, impacting blood pressure regulation. Understanding these calcium changes is key for developing new antihypertensive therapies.
Area of Science:
- Cardiovascular Physiology
- Molecular Biology
Context:
- Vasomotion control is crucial for blood pressure regulation and a target for antihypertensive treatments.
- Calcium ions (Ca++) act as the final messenger in muscle contraction.
- Both calcium influx and calcium sensitization mechanisms are vital in regulating vascular tone.
Purpose:
- To explore the role of intracellular calcium (Ca++) in the pathophysiology of hypertension.
- To review recent findings on calcium handling in vascular and cardiac myocytes.
- To highlight alterations in cell calcium control associated with different forms of hypertension.
Summary:
- Vasoconstrictors increase Ca++ entry and sensitize the contractile apparatus, while vasodilators have opposing effects.
- Studies show increased vascular myoplasmic Ca++ and enhanced calcium influx via dihydropiridine-sensitive channels in animal models of hypertension.
- Elevated cytoplasmic Ca++ in platelets has been observed in hypertensive patients.
Impact:
- Altered cell calcium control mechanisms may significantly contribute to the development and progression of hypertension.
- Findings emphasize the importance of calcium signaling pathways in cardiovascular homeostasis.
- This research provides a basis for exploring novel therapeutic strategies targeting calcium dysregulation in hypertension.
Abstract:
The control of vasomotion is a central issue in blood pressure regulation and is a primary goal of antihypertensive therapy. Calcium is the final messenger in the contractile mechanism of vascular smooth and cardiac muscle. Vasoconstrictor agents enhance the entry of Ca++ into vascular myocytes; vasodilators usually depress it. The most recent findings, based on direct measures of intracellular Ca++, have also highlighted the importance of calcium-sensitization mechanisms: vasoconstrictors sensitize the contractile apparatus to Ca++; vasodilators have an opposite effect. Cell calcium control alterations have been reported in different forms of hypertension. An increase in vascular myoplasmic Ca++ and a higher rate of calcium influx through specific, dihydropiridine-sensitive calcium channels have been found in genetic or secondary animal models. In hypertensive patients, an elevation of cytoplasmic Ca++ was noted in the platelets. Since Ca++ is a ubiquitous intracellular messenger, these changes may have profound implications for the pathophysiology of hypertension.
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