Tissue-localized angiotensin II enhances cardiac and renal disorders in Tsukuba hypertensive mice

Abstract

Tissue Ang II concentration is more important than hypertension in causing cardiac hypertrophy, and both tissue Ang II level and hypertension are important in causing glomerulosclerosis in THM.

Lisinopril Reduces Left Ventricular Hypertrophy and Cardiac Polyamine Concentrations without a Reduction in Left Ventricular Wall Stress in Transgenic Tsukuba Hypertensive Mice.

“…In our previous report (52), THMs showed blood and myocardial Ang II concentrations that were four to five times as high as those in C57BL16 mice. Furthermore, lisinopril and hydralazine were respectively administered to THMs under the same conditions as those of the present experiment.…”

Angiotensin‐Converting Enzyme Genotype Affects the Response of Human Skeletal Muscle to Functional Overload

“…Local RASs have been found in myocardium (Dzau, 1988), smooth muscle (Gibbons & Dzau, 1990) and skeletal muscle (Reneland & Lithell, 1994) and the ACE D allele is associated with higher systemic (Rigat et al 1990) and cardiac tissue ACE activities (Danser et al 1995), although this has not been examined in skeletal muscle. ACE is responsible for the production of angiotensin II, which is a potent growth factor in cardiac and vascular tissue (Geisterfer et al 1988;Kai et al 1998) and ACE also degrades kinins that inhibit growth in cardiac myocytes (Ishigai et al 1997). The D allele has recently been associated with left ventricular hypertrophy in response to physical training (Montgomery et al 1997).…”

“…Angiotensin-converting enzyme (ACE) is a key component of the circulating human renin-angiotensin system (RAS) generating angiotensin II, a vasoconstrictor, and degrading vasodilator kinins. Local ACE expression may also modulate tissue growth processes as both angiotensin II and kinins appear to have growth regulatory effects (Geisterfer et al 1988;Ishigai et al 1997;Kai et al 1998). A functional polymorphism of the ACE gene has been identified, with the absence (deletion, D) rather than the presence (insertion, I) of a 287 base pair fragment associated with higher tissue (Costerousse et al 1993;Danser et al 1995) The response to strength training varies widely between individuals and is considerably influenced by genetic variables, which until now, have remained unidentified.…”

Sympathetic Regulation of the Renal Functions in Rats Reciprocally Congenic for Chromosome 1 Blood Pressure Quantitative Trait Locus

“…For the NE measurement, the samples were homogenized on ice and the protein was removed by centrifugation. The supernatants were then applied to a full-automatic catecholamine analyzer (HLC-725CA II; Tosoh Inc., Tamaguchi, Japan) (19). The results were represented as nmol/g kidney weight (g KW).…”