Linkage but lack of association for blood pressure and the a-adducin locus in normotensive twins
Busjahn A,Aydin A, von Treuenfels N, Faulhaber H-D, Gohlke H-R, Knoblauch H, Schuster H, and Luft FC
J. Hypertens. 1999; 10: 1437-1441

Background a-adducin is a cytoskeletal protein involved with sodium-pump activity in the renal tubule. The a-adducin gene locus has been linked to hypertension and a polymorphism identified which is associated with hypertension; however, the role of the a-adducin gene locus in normal blood pressure regulation is not defined. We performed a combined linkage and association study in normotensive MZ and DZ twins and their parents to address this issue.
Methods We studied 126 MZ and 70 DZ twin pairs and parents of DZ twins. Blood pressure and cold-pressor blood pressure values were obtained. Cardiac dimensions were measured echocardiographically. Three microsatellites adjacent to the a-adducin gene were studied as well as the 460 Trp mutation in the a-adducin gene. Results We obtained strong evidence for linkage (p<0.001) between the a-adducin gene locus and systolic blood pressure. However, we were not able to associate the 460 Trp mutation with higher blood pressures, cold-pressor responses, or cardiac dimensions.
Conclusions The a-adducin gene locus is relevant to blood pressure regulation in normal subjects. Failure to find association between higher blood pressures and the 460 Trp mutation suggests that this mutation may become important only when hypertension is triggered, or that other variations in a-adducin are present which have not yet been discovered.

Quantitative trait loci for blood pressure exist near the IGF-1, the Liddle syndrome, the angiotensin II-receptor gene and the renin loci in man
Nagy-Z; Busjahn-A; Bahring-S; Faulhaber-HD; Gohlke-HR; Knoblauch-H; Rosenthal-M; Mller-Myhsok-B; Schuster-K; Luft-FC

Blood pressure (BP) is heritable and finding quantitative trait loci that influence BP is an important step in identifying genes responsible for BP regulation. Sixty-six pairs of dizygotic (DZ) twin subjects and their parents were used in a sib-pair analysis to look for linkage of selected candidate genes to the quantitative trait BP. Microsatellite markers were tested in the vicinity of the gene loci for insulin-like growth factor-1 (IGF-1), Liddle syndrome, autosomal-dominant hypertension with brachydactyly, angiotensinogen, angiotensin II type I receptor, angiotensin-converting enzyme, renin, and lipoprotein lipase. BP was measured in a standardized manner. Heart size was determined echocardiographically. Significant linkage was found at the IGF-1, Liddle syndrome, and AT(1) receptor gene for systolic BP. Linkage for diastolic BP was found at the autosomal-dominant hypertension with brachydactyly locus. Both systolic and diastolic BP were linked to the renin gene locus. The linkage was most consistent for the IGF-1 gene locus and systolic Bg. Linkage was also found between the IGF-1 gene locus and posterior cardiac wall thickness, septal thickness, and left ventricular mass index. It is suggested that these quantitative trait loci may be important for the subsequent detection of allelic variants for elevated BP. Furthermore, these results linking the IGF-1 gene locus to both BP and cardiac dimensions underscore the importance of the IGF-1 gene as a candidate gene for cardiovascular disease.

Genetic and environmental influences on coping styles: A twin study
Busjahn-A; Faulhaber-HD; Freier-K; Luft-FC
PSYCHOSOMATIC-MEDICINE. JUL-AUG 1999; 61 (4) : 469-475

Objective: Coping styles are generally considered to be environmentally driven, primarily by family influences. However, because personality traits are commonly influenced by genetic effects, we hypothesized that heredity is also important for coping. Methods: We tested this hypothesis by assessing 19 coping styles, as well as four secondary coping factors, by questionnaire in 212 pairs of monozygotic and dizygotic twins. We then examined heredity by structural equation modeling. Results: All coping styles showed evidence of genetic influences. The coping styles shared one common genetic factor. In addition, each coping style was also influenced by other separate genetic factors. Shared environment had no significant influence on coping styles. Three of 19 more specific coping styles showed shared environmental effects as well as genetic influences, 14 were solely under genetic influences, and two showed only shared environment effects. Conclusions: We suggest that hereditary effects on certain coping style preferences cannot be explained solely by genetic influences on major personality traits and temperament. An analysis of the relationships between coping and personality in twin subjects may elucidate the distinction between genetic and environmental effects.