well, I have not been in research, so I can provide you text book knowledge concerned to your query , " A sequence variation in

the gene encoding the B subunit of a heterotrimeric G protein is commonly found in individuals with hypertension and this variant gene is sus-pected of involvement in obesity and atherosclerosis also. "(Reference: Lehninger Principles of Biochemistry. 5th edn. Nelson and Cox)

Dear Maria,

This is an important question and the area is well researched. It is difficult to explain important genetic contributors towards hypertension. I am involved in active research related to cardiovascular and pulmonary arterial hypertension and just to give you a brief but detailed idea in that area I am sharing some of the important research articles published in this area.

Hope that helps.

Best-

Dear Doctor Maria,

There is greater similarity in blood pressure within families than between families, which indicates a form of inheritance. And it was proved that this finding wasn't due to shared environmental factors. Single gene mutations are proved to cause Mendelian forms of high and low blood pressure. Almost 10 genes have been identified to cause these forms of hypertension. These mutations affect blood pressure by altering renal salt handling. Recently and with the aid of newly developed genetic analysis techniques researchers found statistically significant linkage of blood pressure to several chromosomal regions, including regions linked to familial combined hyperlipidemia.

The colleague Mandal has presented important papers on gentic contributors in hypertension. The interactions between cardiovascular system, kidney and the autonomic nervous system (ANS) have been known for several decades. Genetic aspects contribute to the type and occurrence of hypertension also by affecting the ANS, in the kidney especially by influencing the sympathetic outflow. E.g. several studies have demonstratetd an increased renal noradrenaline (norepinephrine) spillover to plasma in "essential" hypertension. Several treatments have been developed, e.g. denervation of the renal arteries. Most (not all) studies have shown an impressive fall of office BP (follow-up up to 6 years).

Hypertension is no exception: there is astrong link between genetics and the pathology (and also normal function) of the cardiovascular system (and hypertension). Paraphrasing W. Churchill (Nov. 1942) studing genetics and hypertension is "perhaps, the end of the beginning".

Genetic association studies have identified polymorphisms in several candidate genes (e.g. angiotensinogen, angiotensin-converting enzyme, alpha-adducin, beta-adrenergic receptors, nitric oxide synthase III....) but none of these genetic abnormalities have been shown to be responsible for any significant portion of hypertension in the general population. The influence of genetic factors may be accentuated by interaction of several gene polymorphisms or with environmental inputs such as sedentary life style, smoking, dietary factors (high salt, sugar, fat/cholesterol and alcohol intake, low potassium intake) and chronic stress. You can find more for example in the JNC 7 report (see http://hyper.ahajournals.org/content/42/6/1206.long).

There are currently more than 100 candidate genes for essential hypertension, identified through linkage studies and / or association in humans or through experimental studies in animals. This is generally of genes involved directly or indirectly in the salt and water regulation. One of the most studied is probably the ACE gene encoding for angiotensin-converting enzyme I. persons with the genotype D / D has a plasma concentration conversion enzyme of angiotensin twice higher than people with genotype I / I or I / D. the association between ABCB1 and CYP3A5 genes and blood pressure of participants depends on salt consumption and illustrates the importance of gene-gene interactions and gene-environment interactions in the pathogenesis of essential hypertension. A new gene responsible for family hyperkalemic hypertension (Gordon syndrome). A mutation affecting the gene KLHL3 imbalance ionic exchange Na + and Cl- in the kidney and cause an increase in blood pressure. Recently, association studies across the genome have identified new chromosomal regions associated reproducibly, blood pressure in the general population with essential hypertension. These regions contain genes whose role in the regulation of blood pressure was not previously suspected. Although much work remains to be done to identify the specific genes and mutations involved, these findings open the door to the discovery of new pathways involved in control of blood pressure, with the hope of developing new drugs to better address this major public health problem.