PI3Kγ in hypertension: a novel therapeutic target controlling vascular myogenic tone and target organ damage

Cardiovasc Res. 2012 Sep 1;95(4):403-8. doi: 10.1093/cvr/cvs166. Epub 2012 May 19.

Abstract

In the past decade, several studies have characterized a number of cellular and molecular mechanisms that contribute to the regulation of the vascular myogenic response, thus affecting blood pressure regulation. Recently, phosphoinositide 3-kinase γ (PI3Kγ) has been identified as a main regulator of vascular myogenic tone and blood pressure, a result further strengthened by a highly significant genome-wide association of a single nucleotide polymorphism flanking this gene with blood pressure regulation, in a large human population. The goal of this review is to summarize the available information regarding the mechanism whereby PI3Kγ exerts blood pressure control, regulating myogenic tone at the level of L-type calcium channel in smooth muscle cells. Moreover, an overview of the pharmacological approaches available for targeting this signalling pathway shows that PI3Kγ is a suitable candidate for antihypertensive therapy, capable of lowering blood pressure. Finally, a survey of the studies dissecting the role of PI3Kγ in pathological conditions that are typically induced by hypertension in its target organs provides a more complete picture of the high potential of this novel therapeutic approach for fighting hypertension and, at the same time, its target organ damage, independently of blood pressure-lowering effects.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Antihypertensive Agents / pharmacology*
  • Arterial Pressure / drug effects*
  • Arterial Pressure / genetics
  • Calcium Channels, L-Type / metabolism
  • Genetic Predisposition to Disease
  • Humans
  • Hypertension / complications
  • Hypertension / drug therapy*
  • Hypertension / enzymology
  • Hypertension / genetics
  • Hypertension / physiopathology
  • Muscle, Smooth, Vascular / drug effects*
  • Muscle, Smooth, Vascular / enzymology
  • Muscle, Smooth, Vascular / physiopathology
  • Phenotype
  • Phosphatidylinositol 3-Kinase / metabolism
  • Phosphoinositide-3 Kinase Inhibitors*
  • Polymorphism, Single Nucleotide
  • Protein Kinase Inhibitors / pharmacology*
  • Signal Transduction / drug effects

Substances

  • Antihypertensive Agents
  • Calcium Channels, L-Type
  • Phosphoinositide-3 Kinase Inhibitors
  • Protein Kinase Inhibitors
  • Phosphatidylinositol 3-Kinase