G proteins and hypertension: An alternative candidate gene approach Winfried Siffert  Kidney International  Volume 53, Issue 6, Pages 1466-1470 (June 1998) DOI: 10.1046/j.1523-1755.1998.00934.x Copyright © 1998 International Society of Nephrology Terms and Conditions

Figure 1 Platelet activating factor-evoked Ca2+ signals in B lymphoblasts. Lymphocytes from normotensive (NT) and hypertensive (HT) subjects were immortalized with Epstein Barr virus. Pertussis toxin-sensitive Ca2+ signals were determined in fura-2-loaded cells upon stimulation with 100 nmol/liter platelet activating factor. Data are mean ± SD; *P < 0.05. (modified from[32]) Kidney International 1998 53, 1466-1470DOI: (10.1046/j.1523-1755.1998.00934.x) Copyright © 1998 International Society of Nephrology Terms and Conditions

Figure 2 Signal transduction pathways activated upon stimulation of Gi proteins. A variety of hormones including norepinephrine (via α2-adrenergic receptors), angiotensin II, and thrombin activate receptors coupled to Gi proteins. Activated α and βγ subunits influence a variety of intracellular second messenger systems including ion channels, adenylyl cyclase, and the ras-raf-MAP-kinase (MAPK) pathway. Furthermore, βγ subunits can directly activate isoforms of phospholipase Cβ (PLC), thereby inducing activation of protein kinase C (PKC) and an elevation of the intracellular Ca2+ concentration. Enhanced activation of G proteins is predicted to cause a pronounced activation of these pathways, which may ultimately result in increased cell proliferation. Kidney International 1998 53, 1466-1470DOI: (10.1046/j.1523-1755.1998.00934.x) Copyright © 1998 International Society of Nephrology Terms and Conditions