By A. G. Motulsky, W. Burke (auth.), Kare Berg M. D., Ph. D., Dr. Victor Bulyzhenkov, Dr. Yves Christen, Pierre Corvol M. D. (eds.)
Cardiovascular ailments are the important reason behind mortality in lots of built nations and are expanding in significance in constructing nations the place communicable ailments are being introduced below keep an eye on. it really is anticipated that heart ailment (CRD) and cerebrovascular ailments are accountable for among 40-50% of all deaths. Righ blood strain is usual in all industrialized societies and contributes importantly to CRD. it truly is popular that genetic components play a massive function within the etiology and pathogenes es of cardiovascular ailments and give a contribution to an individual's susceptibility or resistance to the illness. the applying of contemporary genetic concepts has ended in the id of polymorphie markers which are interested in the conventional legislation and serve as of the cardiovascular procedure. lots of those may perhaps give a contribution to the person modifications within the hazard for CRD and high blood pressure. it really is referred to now that numerous hazard elements or protecting components with appreciate to cardiovascular ailments are strongly motivated via genes, and it really is now attainable to spot person genes contributing to cardiovascular threat. a wide financial institution of genetic wisdom appropriate to CRD and high blood pressure has turn into to be had in the past years. for this reason, it truly is now believed that CRD, for instance, can be a solid version for a feasibility research to figure out a fashion through which preventive measures might be applied.
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Extra resources for Genetic Approaches to Coronary Heart Disease and Hypertension
However, considering hypertension as a homogeneous disease is artificial and we can also imagine that, in a small sub set of patients, the renin locus might exert a greater contribution. Both our results and those N aftilan et al. may appear a bit disappointing when compared to the results obtained by Rapp et al. (1989) on the Dahl rat and by Kurtz et al. (1990) on spontaneously hypertensive rats (SHR). Both groups have analyzed the F2 generation obtained by crossing rats from inbred hypertensive strains (Dahl-sensitive or SHR) with normotensive rats (Dahl resistant or inbred Lewis rat) to obtain F1 rats and then by intercrossing F1 rats to obtain F2 rats.
In the erythrocytes of WW hybrids, calcium content was equal to that of WKY rats and lower than that in the WS and SS groups, which in turn had significantly lower levels than SHR (Fig. 1). This trait is probably under polygenie control, but the c-src locus has definite influence upon it. All the results of these studies lead to the conc1usion that the locus of DNA marked by the RFLP in c-src contains gene(s) whieh determine the increased Na+ - K+ cotransport and Ca2 + accumulation in the erythrocytes of rats with spontaneous hypertension.
1989). Plasma angiotensinogen concentration and plasma angiotensin-I converting enzyme (ACE) concentration are stable in a given individual. Plasma angiotensinogen was found to be higher in plasma of hypertensives than in normotensives in the classical work of Walker et al. (1979), but this parameter has not been investigated in family studies. The genetic control of ACE, on the other hand, has been extensively investigated. A first study was conducted in normal nuclear families. The results demonstrated a familial resemblance for plasma ACE level (Cambien et al.