Acute renal ischemia causes a discrepant pattern of Ang II receptor modulation in aged versus young rats, suggesting potential therapeutic implications for receptor antagonists in aged kidneys.
Answers are grounded in this paper and cite their sources.
Age-specific Ang II receptor changes after renal ischemia are hypothesis-generating in rats; leaves open whether antagonists warrant targeted study.
The properties of Ang II receptors in the aged kidney and their changes after acute renal ischemia are rarely known. The aim of this study was to examine the expression of Ang II receptor mRNA and characteristics of Ang II receptors in the aged kidney and to compare different responsiveness to 45 min of acute renal ischemia in young (3-4 months) and aged (23-24 months) rats. In the normal condition, AT1 mRNA expression was much lower in the aged than that in the young rats. Maximal binding (Bmax) was also lower in the aged (1315 +/- 48 vs. 2035 +/- 257 fmol/mg, p < 0.05). The dissociation constant (KD) of glomerular Ang II receptors, however, was significantly lower in the aged rats compared to the young (6.8 +/- 1.6 vs. 17.4 +/- 2.5 nM). After acute ischemia, the expression of AT1 mRNA decreased in the young rats but increased in the aged rats. Interestingly, Bmax of glomerular Ang II receptors was significantly increased in the aged ischemic rats (1852 +/- 94 vs. 1315 +/- 48 fmol/mg) with unchanged KD. These results show that: (a) the AT1 mRNA expression and the Ang II receptor binding site are decreased with the aging process in the rat kidney; (b) the acute renal ischemia effect on different age groups has a greatly discrepant pattern in respect of Ang II receptor modulation, which may provide a potential therapeutic future for the receptor antagonists in acute renal ischemia in the aged.
No takes yet. Share an insight, caveat, or question.
Lü et al. (1996) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: