6 OCTOBER 2011 | The International Consortium for Blood Pressure Genome-Wide Association Studies
A genome-wide association study (GWAS) identified 16 novel genetic loci influencing blood pressure and cardiovascular disease risk. These loci include genes previously known or suspected to regulate blood pressure, as well as new clues to blood pressure physiology. A genetic risk score based on 29 genome-wide significant variants was associated with hypertension, left ventricular wall thickness, stroke, and coronary artery disease, but not kidney disease or kidney function. The study also found associations with blood pressure in East Asian, South Asian, and African ancestry individuals. The findings provide new insights into the genetics and biology of blood pressure and suggest potential novel therapeutic pathways for cardiovascular disease prevention.
The study used a multi-stage design in 200,000 individuals of European descent to identify 29 independent SNPs at 28 loci significantly associated with systolic and diastolic blood pressure. These variants had small effects on blood pressure, but their directions of effect were consistent across SBP, DBP, and hypertension. Some of the associations were in or near genes involved in pathways known to influence blood pressure. The study also evaluated the association of these variants with blood pressure in non-European ancestry groups and found significant associations in East Asian, South Asian, and African populations.
The study also created a genetic risk score to assess the association of the variants with hypertension and clinical measures of hypertensive complications. The risk score was significantly associated with SBP and DBP in non-European ancestry groups. The study also identified several loci with plausible connections to blood pressure via genes implicated in renal physiology or kidney disease. The study found that some of the associations were in or near genes involved in natriuretic peptide and related nitric oxide signaling pathways.
The study also identified two loci with plausible connections to blood pressure via genes implicated in renal physiology or kidney disease. The study found that some of the associations were in or near genes involved in natriuretic peptide and related nitric oxide signaling pathways. The study also identified missense variants in two genes involved in metal ion transport that were associated with blood pressure. The study found that the genetic risk score was significantly associated with blood-pressure-related organ damage and clinical cardiovascular disease, but not kidney disease. The study also found that the genetic risk score was positively associated with left ventricular wall thickness, occurrence of stroke, and CAD, but not with chronic kidney disease or measures of kidney function. The study concluded that blood pressure elevation may in part be a consequence rather than a cause of subclinical kidney disease.A genome-wide association study (GWAS) identified 16 novel genetic loci influencing blood pressure and cardiovascular disease risk. These loci include genes previously known or suspected to regulate blood pressure, as well as new clues to blood pressure physiology. A genetic risk score based on 29 genome-wide significant variants was associated with hypertension, left ventricular wall thickness, stroke, and coronary artery disease, but not kidney disease or kidney function. The study also found associations with blood pressure in East Asian, South Asian, and African ancestry individuals. The findings provide new insights into the genetics and biology of blood pressure and suggest potential novel therapeutic pathways for cardiovascular disease prevention.
The study used a multi-stage design in 200,000 individuals of European descent to identify 29 independent SNPs at 28 loci significantly associated with systolic and diastolic blood pressure. These variants had small effects on blood pressure, but their directions of effect were consistent across SBP, DBP, and hypertension. Some of the associations were in or near genes involved in pathways known to influence blood pressure. The study also evaluated the association of these variants with blood pressure in non-European ancestry groups and found significant associations in East Asian, South Asian, and African populations.
The study also created a genetic risk score to assess the association of the variants with hypertension and clinical measures of hypertensive complications. The risk score was significantly associated with SBP and DBP in non-European ancestry groups. The study also identified several loci with plausible connections to blood pressure via genes implicated in renal physiology or kidney disease. The study found that some of the associations were in or near genes involved in natriuretic peptide and related nitric oxide signaling pathways.
The study also identified two loci with plausible connections to blood pressure via genes implicated in renal physiology or kidney disease. The study found that some of the associations were in or near genes involved in natriuretic peptide and related nitric oxide signaling pathways. The study also identified missense variants in two genes involved in metal ion transport that were associated with blood pressure. The study found that the genetic risk score was significantly associated with blood-pressure-related organ damage and clinical cardiovascular disease, but not kidney disease. The study also found that the genetic risk score was positively associated with left ventricular wall thickness, occurrence of stroke, and CAD, but not with chronic kidney disease or measures of kidney function. The study concluded that blood pressure elevation may in part be a consequence rather than a cause of subclinical kidney disease.