Disease relevance of SHR

• Histological examination of the kidney of renin-immunized SHR showed a chronic autoimmune interstitial nephritis characterized by the presence of immunoglobulins, mononuclear cell infiltration, and fibrosis around the juxtaglomerular apparatus [1].
• METHODS: Rats of four inbred strains (Lewis, Brown Norway, Fischer, and SHR) were immunized with native or recombinant bovine RPE65, or with S-antigen (S-Ag), emulsified with complete Freund adjuvant, and treated simultaneously with killed Bordetella pertussis bacteria, as indicated [2].
• In vivo studies in SHR rats confirmed the ability of moxonidine to normalize hypertension by an action within the RVLM and confirmed the correspondence of I1 binding affinity and antihypertensive efficacy [3].
• SHR rats had both severe glomerulonephritis and severe pulmonary hemorrhage [4].

High impact information on SHR

• The increase in renin antibody in renin-immunized SHR was associated with a significant drop in blood pressure (tail-cuff method) that became similar to that of the WKY control rats after four injections [1].
• The chronic blockade of the renin-angiotensinogen reaction in renin-immunized SHR produced an almost-complete disappearance of Ang II (0.8 %/- 7 fmol/ml; control SHR, 30.6 +/- 15.7 fmol/ml) and a 50% reduction in urinary aldosterone [1].
• In conclusion, these studies indicate that both steroid hormone transport and metabolism are augmented in the lymphoid neoplastic state, and both processes may alter the concentration of cellular exchangeable hormone and, thus, steroid hormone receptor occupancy in lymphoid neoplasms [5].
• The reaction of ethyl chloroformate with amino compounds has been evaluated as a simple route to carbon-11 labeling of steroid hormone-receptor-based imaging agents [6].
• This is the first report of the identification of specific amino acid residues in the binding site of a steroid hormone receptor [7].

Biological context of SHR

• Perfusion of renin-immunized, salt-depleted SHR with converting enzyme inhibitor caused no further decrease in blood pressure but significantly decreased blood pressure in salt-depleted control rats [1].
• Both endogenous and exogenous compounds and their metabolites may act as activators of SHR and disruptors of endocrine, cellular and lipid homeostasis [8].
• We identified a BglII RFLP between BN.lx and SHR rats [9].
• Consistent with the increased ATPase activity, phosphorylation of MLC20 was increased by 2.8 times as much in the SHR compared with the WKY electrically stimulated arterial muscle [10].

Anatomical context of SHR

• First principal component (FPC) values were determined for shear force (SHR) and palatability attributes of tenderness, connective tissue amount, flavor, and juiciness (JUC) [11].
• Increased maximum velocity of shortening (Vmax), increased shortening ability (delta Lmax) and decreased relaxation rate have been reported for arterial smooth muscle from 16- to 18-week-old spontaneously, hypertensive rats (SHR) compared with age-matched normotensive Wistar-Kyoto rats (WKY) [10].
• Experimental autoimmune glomerulonephritis with pulmonary hemorrhage was induced in rats of 4 inbred strains, F344/DuCrj, LEW/Crj, WKY/NCrj and SHR/NCrj, by the injection of a nephritogenic antigen from bovine glomerular basement membrane [4].
• NGFI-B and Ad4BP are steroid hormone receptor-like transcription factor that may control steroidogenesis, growth and differentiation in the adrenal cortex [12].
• In conclusion, these results demonstrate that in studies of steroid hormone receptor expression in the cervix, careful description of sampling site and depth are necessary if the results are to be interpreted meaningfully [13].

References