Showing papers by "Nilesh J. Samani published in 1993"
TL;DR: Findings show that two independent loci influence different haemodynamic components of blood pressure, and that pulse pressure has a specific genetic determination.
Abstract: Several genetic loci involved in blood pressure regulation have recently been localized in experimental models of hypertension, but the manner in which they influence blood pressure remains unknown. Here, we report a study of the Lyon hypertensive rat strain showing that different loci are involved in the regulation of steady-state (diastolic pressure) and pulsatile (systolic – diastolic, or pulse pressure) components of blood pressure. Significant linkage was established between diastolic blood pressure and a microsatellite marker of the renin gene (REN) on rat chromosome 13, and between pulse pressure and the carboxypeptidase B gene (CPB) on chromosome 2. These findings show that two independent loci influence different haemodynamic components of blood pressure, and that pulse pressure has a specific genetic determination.
127 citations
TL;DR: It is demonstrated that a recently identified gene of yet unknown function, termed SA, cosegregates with an increase in blood pressure in F2 rats derived from a cross of the spontaneously hypertensive rat with normotensive Wistar-Kyoto rats, providing strong evidence for a primary genetic involvement of the kidney in hypertension.
Abstract: The role of the kidney in initiating hypertension has been much debated Here we demonstrate that a recently identified gene of yet unknown function, termed SA, which is differentially expressed in the kidney of the spontaneously hypertensive rat, cosegregates with an increase in blood pressure in F2 rats derived from a cross of the spontaneously hypertensive rat with normotensive Wistar-Kyoto rats, accounting for 28 and 21% of the genetic variability in systolic and diastolic blood pressures, respectively Further, the genotype at this locus appears to determine the level of expression of the gene in the kidney The findings provide strong evidence for a primary genetic involvement of the kidney in hypertension
93 citations
TL;DR: The cosegregation of blood pressure with plasma cholesterol and, to a lesser degree, with insulin levels, which was observed in the present study provides the first direct evidence that these phenotypes are associated and are not due simply to genetic drift in the Lyon model.
Abstract: Objective: A large population of F 2 rats, obtained from a cross between male Lyon hypertensive (LH) rats and female Lyon normotensive (LN) rats, was studied in order to assess the relationship between increased body weight, hyperlipidaemia and high blood pressure which characterize LH rats. Methods: Mean arterial pressure (MAP) was recorded in male, conscious, freely moving LH, LN, F 1 and F 2 rats aged 30 weeks. Plasma total cholesterol, high-density lipoprotein-, low-density lipoprotein- and very low-density lipoprotein-cholesterol, phospholipids, triglycerides, insulin and glucose were measured. Results: In the F 2 cohort it was observed that high MAP was a recessive trait that depends on several genes and was unrelated to body weight
46 citations
TL;DR: No evidence of linkage between the hsp70 gene locus, and by implication other genes located within the rat RT1 complex, and blood pressure is found in the cross of SHR and WKY rats.
Abstract: Objective: To investigate the involvement of the heat-shock protein 70 (hsp70) locus, located in the rat major histocompatibility complex (RT1), in hypertension of the spontaneously hypertensive rat (SHR). Previous studies have shown abnormal expression of hsp70 in the SHR and an association of the SHR hsp70 allele with increased blood pressure in recombinant inbred strains derived from a cross of SHR with Brown-Norway rats. Design: SHR were crossed with normotensive Wistar-Kyoto (WKY) rats to produce a large cohort of F 2 rats segregating for blood pressure and hsp70 alleles
19 citations
TL;DR: An rSr' pattern with QRS duration of less than 0.12 s in the right precordial leads can be due to incomplete right bundle branch block or can be a normal electrophysiological variant, to identify other ECG features that may help to distinguish between these two possibilities.
Abstract: An rSr' pattern with QRS duration of less than 0.12 s in the right precordial leads can be due to incomplete right bundle branch block (which may progress to complete right bundle branch block) or can be a normal electrophysiological variant. To identify other ECG features that may help to distinguish between these two possibilities, ECGs of 15 patients who progressed from normal to complete right bundle branch block through an intermediate rSr' pattern of incomplete right bundle branch block were analysed. The following features in the right precordial leads (V1, V2) that preceded or accompanied the appearance of the rSr' were identified: diminution of the S wave depth (100%), inversion of ratio of the S wave depth to SV1 > SV2 (93%), slurring of the downstroke or upstroke of the S wave (27%) and prolongation of the QRS duration to > or = 0.10 s (73%). When a further 79 subjects with rSr' pattern in the right precordial leads and QRS duration of 1.0 and those with SV1/SV2 1.0 were found to be significantly older (59.8 +/- 18.4 years vs 32.8 +/- 18.1 years, P or = 0.10 s (74% vs 7%).(ABSTRACT TRUNCATED AT 250 WORDS)
9 citations
Journal Article•
2 citations
1 citations