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Neurovascular MedicinePursuing Cellular Longevity for Healthy Aging$
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Kenneth Maiese

Print publication date: 2009

Print ISBN-13: 9780195326697

Published to Oxford Scholarship Online: January 2010

DOI: 10.1093/acprof:oso/9780195326697.001.0001

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Role of Protein Kinase C and Related Pathways in Vascular Smooth Muscle Contraction and Hypertension

Role of Protein Kinase C and Related Pathways in Vascular Smooth Muscle Contraction and Hypertension

Chapter:
(p.21) Chapter 2 Role of Protein Kinase C and Related Pathways in Vascular Smooth Muscle Contraction and Hypertension
Source:
Neurovascular Medicine
Author(s):

Xiaoying Qiao

Raouf A. Khalil

Publisher:
Oxford University Press
DOI:10.1093/acprof:oso/9780195326697.003.0002

Intracellular signaling activities in vascular smooth muscles (VSMs) are central in the control of blood vessel diameter and the regulation of peripheral vascular resistance and blood pressure. Several studies have examined the molecular mechanisms underlying VSM contraction under physiological conditions and the pathological alterations that occur in vascular diseases such as hypertension. Vasoconstrictor stimuli activate specific cell surface receptors and cause an increase in intracellular free Ca2+ concentration ([Ca2+]i), which forms a complex with calmodulin, activates myosin light chain (MLC) kinase, and leads to MLC phosphorylation, actin-myosin interaction, and VSM contraction. In unison, activation of protein kinase C (PKC) increases the myofilament force sensitivity to [Ca2+]i and MLC phosphorylation, and maintains VSM contraction. Identifying the subcellular location of PKC may be useful in the diagnosis and prognosis of VSM hyperactivity states associated with hypertension. Targeting of vascular PKC using isoform-specific PKC inhibitors may work in concert with cytokine antagonists, antioxidants, and matrix metalloproteinase inhibitors, and thereby provide new approaches in the treatment of VSM hyperactivity states and certain forms of hypertension that do not respond to Ca2+-channel blockers.

Keywords:   vascular diseases, blood pressure, vascular smooth muscles, protein kinase C, hypertension, muscle contraction, hyperactivity states

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