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[G proteins-phosphoinositide pathways in hypertension].

Hu Sj, Yao‐Wei Huang, Li Y

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Abstract

The second messenger inositol-1,4,5-trisphosphate (InsP3) comes from two major pathways, one is initiated by a family of G protein-linked receptors and the other by receptors linked by tyrosine kinases. These separate receptors activate phospholipase C to hydrolyse phosphatidylinositol-4,5-bisphosphate to give both diacylglycerol and InsP3. The latter then mobilizes stored calcium and promotes an influx of external calcium. The alpha subunit of a newly discovered G protein (Gq) has recently been shown to stimulate the activity of PLC-beta 1. The alpha subunits of the Gq class of G proteins includes G alpha q, G alpha 11, G alpha 14, G alpha 15 and G alpha 16. The important pathologic changes in hypertension are arteriolar spasm and wall thickening. Many vasoactive substances can induce contractile response and proliferation of vascular smooth muscle cells and increase InsP3 level. However, the hypertension does not cause any persistent change in Gq.

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What this paper is about

The second messenger inositol-1,4,5-trisphosphate (InsP3) comes from two major pathways, one is initiated by a family of G protein-linked receptors and the other by receptors linked by tyrosine kinases. These separate receptors activate phospholipase C to hydrolyse phosphatidylinositol-4,5-bisphosphate to give both diacylglycerol and InsP3. The latter then mobilizes stored calcium and promotes an influx of external calcium. The alpha subunit of a newly discovered G protein (Gq) has recently been shown to stimulate the activity of PLC-beta 1. The alpha subunits of the Gq class of G proteins includes G alpha q, G alpha 11, G alpha 14, G alpha 15 and G alpha 16. The important pathologic changes in hypertension are arteriolar spasm and wall thickening. Many vasoactive substances can induce contractile response and proliferation of vascular smooth muscle cells and increase InsP3 level. However, the hypertension does not cause any persistent change in Gq.

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Available abstract

The second messenger inositol-1,4,5-trisphosphate (InsP3) comes from two major pathways, one is initiated by a family of G protein-linked receptors and the other by receptors linked by tyrosine kinases. These separate receptors activate phospholipase C to hydrolyse phosphatidylinositol-4,5-bisphosphate to give both diacylglycerol and InsP3. The latter then mobilizes stored calcium and promotes an influx of external calcium. The alpha subunit of a newly discovered G protein (Gq) has recently been shown to stimulate the activity of PLC-beta 1. The alpha subunits of the Gq class of G proteins includes G alpha q, G alpha 11, G alpha 14, G alpha 15 and G alpha 16. The important pathologic changes in hypertension are arteriolar spasm and wall thickening. Many vasoactive substances can induce contractile response and proliferation of vascular smooth muscle cells and increase InsP3 level. However, the hypertension does not cause any persistent change in Gq.

Key concepts: Gq alpha subunit, Phospholipase C, Second messenger system, G protein, Diacylglycerol kinase, Inositol trisphosphate, Phosphatidylinositol, Receptor

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[G proteins-phosphoinositide pathways in hypertension]. — Research Paper | ScholarLens