Background-Evaluation of metabolic syndrome (MetS) characteristics across an age spectrum from childhood to adulthood has been limited by a lack of consistent MetS criteria for children and adults and by a lack of adjustment for environmental factors. We used the pediatric and adult International Diabetes Federation (IDF) criteria to determine whether gender-and race-specific differences in MetS and its components are present in adolescents as in adults after adjustment for socioeconomic status (SES) and lifestyle factors.

To define whether intrarenal renin and angiotensinogen synthesis and distribution are affected by angiotensin-converting enzyme (ACE) inhibition, a control group of adult, male Wistar-Kyoto rats (n = 7) was compared with a group of rats treated with enalapril (n = 8) for 5 days. Kidney renin and angiotensinogen mRNA levels were detected by Northern and dot blot analysis, using full-length rat renin and angiotensinogen cDNAs. Renin mRNA levels in the enalapril-treated group were 4.6-fold higher than in the control group (P less than 0.05). Angiotensinogen mRNA levels were not significantly different. The intrarenal distribution of renin assessed by immunocytochemistry was markedly different between the two groups of rats. Whereas in the control kidney renin was localized in a juxtaglomerular position, in the kidneys from enalapril-treated rats, renin immunoreactivity of the afferent arteriole extended well beyond the juxtaglomerular loci in the direction of the interlobular artery. The percent of afferent arteriolar length immunostained for renin was higher in the enalapril-treated (53 +/- 17%) than in the control (33 +/- 15) group. Similarly, the ratio of immunostained juxtaglomerular apparatuses (JGA) over total number of JGA and the ratio of immunostained arteries over total number of arteries were higher in the enalapril-treated (0.84 +/- 0.017; 0.68 +/- 0.03) than in the control (0.67 +/- 0.034; 0.43 +/- 0.045) group (P less than 0.05). We conclude that chronic ACE inhibition enhances intrarenal renin synthesis and increases renin expression upstream from the glomerulus and in new sites in blood vessels.(ABSTRACT TRUNCATED AT 250 WORDS)

To determine whether angiotensin II (ANG II) modulates renal growth and renin and angiotensin type 1 (AT1) gene expression via AT1 during development, weanling rats were given ANG II antagonist losartan (DuP 753) for 3 wk. Body weight (g), kidney weight (g), and kidney weight-to-body weight ratio were lower in losartan-treated rats (162 +/- 7, 1.6 +/- 0.06, and 9.5 +/- 0.1 x 10(-3)) than in control rats (184 +/- 5, 1.8 +/- 0.07, and 10.1 +/- 0.1 x 10(-3); P < 0.05). Renal DNA content (mg/kidney) was lower in losartan-treated (2.4 +/- 0.17) than in control rats (3.3 +/- 0.31; P < 0.05), whereas protein-to-DNA and RNA-to-DNA ratios were similar in losartan-treated and control rats. Renin mRNA levels were sevenfold higher in losartan-treated than in control rats, as determined by quantitative standardized dot blot analysis. In addition, blockade of AT1 with losartan induced recruitment of renin-synthesizing and renin-containing cells in the renal vasculature, as determined by immunocytochemistry and in situ hybridization. To establish whether AT1 blockade has a direct effect on renin gene expression, freshly isolated renin-producing cells were exposed in vitro to losartan (10(-6) M) or culture media (control). Losartan induced a twofold increase in steady-state renin mRNA levels above control (P < 0.05). Intrarenal AT1 mRNA levels were not altered by losartan given either in vivo or in vitro to freshly dispersed cells. To define whether immature renin-secreting cells are responsive to ANG II, renin release was determined by reverse hemolytic plaque assay.(ABSTRACT TRUNCATED AT 250 WORDS)

We investigated the effect of angiotensin II (ANG II) and enalapril on accumulation of renin messenger RNA (mRNA) and on renal renin distribution (immunohistochemical analysis). Adult Wistar-Kyoto rats received enalapril (0.2 mg/ml) in distilled drinking water for 8 or 12 days. On day 5 of enalapril treatment, an osmotic minipump was implanted in the peritoneum that caused sustained release of ANG II (200 ng.kg-1.min-1) or vehicle (bovine serum albumin) for 3 or 7 days. Control rats received water for 8 or 12 days and osmotic minipump implantation (containing vehicle solution) on the 5th day. Renin mRNA was identified by hybridization with a 32P-labeled full-length complementary DNA and was detected by autoradiography. Enalapril treatment increased renal renin mRNA specific activity (renin mRNA/total RNA). Subsequent infusion of angiotensin II for 3 or 7 days decreased renal renin mRNA specific activity. In addition, renin immunostaining increased along the afferent arteriole after enalapril treatment; however, enalapril-induced spread of renin immunostaining was not inhibited by ANG II. Thus ANG II attenuates the accumulation of renin mRNA stimulated by enalapril treatment without alteration of renal renin distribution. The lack of effect of ANG II on renal renin distribution may be due to the length of turnover time for stored protein. These findings suggest the shortloop negative feedback of ANG II on renin reflects inhibition of renin synthesis by ANG II. Therefore, we propose that ANG II exerts a direct inhibitory effect on renin by regulation of renin gene expression in renal vasculature.

Enzymatic dispersion and density gradient (Percoll) sedimentation were used to isolate a population of renin-containing, granule-laden cells (density 1.067 g/ml) from rat kidney cortex. Using immunohistochemistry (light microscopy) and electron microscopy, we defined the presence and ability of these cells to store renin protein(s). A 1000 base pair rat renin complementary DNA was used to show that these cells express the renin gene. The reverse hemolytic plaque assay defined the functional properties of the renin-containing cell. The data are consistent with the postulated inverse relationship between calcium concentration and release of renin. Thus, we have isolated a population of functional rat kidney cells that synthesize, store, and release renin.