Comparison of various genetic hypertensive rat strains.
ABSTRACT Comparative studies on nine genetic hypertensive rat strains [two stroke-prone spontaneously hypertensive rats (SHRSP) and Dahl salt-sensitive (DS) strains, and one strain each of spontaneously hypertensive rats (SHR), Lyon hypertensive rats (LH), Milan hypertensive strain (MHS), genetically hypertensive rats (GH) and Sabra hypertensive rats (SBH)] and their respective controls [two Dahl salt-resistent (DR) strains and one strain each of Wistar-Kyoto rats (WKY), Lyon normotensive rats (LN); Lyon low blood pressure rats (LL), Milan normotensive strain (MNS), genetically normotensive rats (GN) and Sabra normotensive rats (SBN) and their original strain, Sabra rats (SB)], in groups consisting of 6-10 males from each strain, were carried out at 10-12 weeks of age under the same experimental conditions. After checking the developmental course of blood pressure and changes in body weight, they were killed at 12 weeks of age for blood analysis and organ-weight examinations. The SHRSP and SHR showed markedly higher blood pressure levels and earlier blood pressure rises in comparison with other hypertensive strains, although they had higher blood pressure than their respective controls. Among various organ weights examined, all hypertensive strains commonly showed increases in left ventricular weight in proportion to blood pressure rises. Kidney weights were significantly decreased only in MHS compared with MNS, while they were either unchanged or significantly greater in other hypertensive strains. Weights of adrenal glands were greater in the two strains of DS and in LH than in their respective control strains. These comparative data indicate possible differences in the pathogenic mechanism involved in these genetic hypertensive rat strains.
Article: Separate sex-influenced and genetic components in spontaneously hypertensive rat hypertension.[show abstract] [hide abstract]
ABSTRACT: Previous results from our laboratory indicated two major genetic components of spontaneously hypertensive rat (SHR) hypertension, an autosomal component and a Y chromosome component. Two new substrains, SHR/a and SHR/y, were developed using a series of backcrosses to isolate each of these components. The SHR/a substrain has the autosomal loci and X chromosome from the SHR strain and the Y chromosome from the Wistar-Kyoto (WKY) rat strain. The SHR/y substrain has only the Y chromosome from the SHR and autosomal loci and X chromosome from the WKY strain. Throughout these breeding programs parents were chosen at random without selection for blood pressure. Males of both substrains maintained blood pressures over 180 mm Hg. Comparisons of blood pressure in these new substrains with the original parental strains can be used to determine the relative proportions of each genetic component in hypertension. The Y chromosome component contributes 34 mm Hg, which is the difference between SHR/y male and WKY male blood pressure. The total autosomal component contributes 46 mm Hg, which is the difference between SHR/a male and WKY male blood pressure. The autosomal component is a sex-influenced trait; males in the SHR/a strain have significantly higher pressures than SHR/a females. Of the 46 mm Hg estimated for the autosomal component, 41 mm Hg is the result of these loci interacting with male phenotypic sex. This sex-influenced component is separate and distinct from the Y chromosome component.Hypertension 07/1991; 17(6 Pt 2):1097-103. · 6.21 Impact Factor
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ABSTRACT: Angiotensin II-induced phosphorylation of proteins was examined in isolated myocytes from hearts of Dahl rats. A high salt diet induced cardiac hypertrophy in Dahl salt-sensitive rats. Angiotensin II-induced phosphorylation of a 42-kd protein (pp42) was detected by two-dimensional electrophoresis in hypertrophic but not normal ventricular myocytes. Angiotensin II stimulation was time-dependent, with a peak effect at 30 minutes. The half-maximal and maximal concentrations of angiotensin II that stimulated pp42 phosphorylation were 1 and 10 nM, respectively. Phosphorylation of pp42 was a function of cardiac hypertrophy. Phorbol 12-myristate 13-acetate-induced phosphorylation of pp42 indicates the possibility of an association between protein kinase C and the signal transduction pathway of angiotensin II-induced pp42 phosphorylation. Ionomycin and A23187 (both at 1 microM) did not stimulate phosphorylation of pp42. Angiotensin II produced a small increase in the synthesis of myocyte proteins in both normal and hypertrophic cells as shown by [35S]methionine incorporation. However, this increase could not account for the increase in the phosphate content of pp42. This protein was not an isoform of actin nor was it of platelet origin. These results raise the possibility that angiotensin II may play a role in the activation of factors in hypertrophic myocytes; however, further study is required to define a link between phosphorylation of pp42 and the hypertrophic process.Hypertension 12/1992; 20(5):633-42. · 6.21 Impact Factor
Journal of hypertension 07/2009; 27(6):1129-33. · 4.02 Impact Factor