Strain Report - Rat Genome Database

Send us a Message



Submit Data |  Help |  Video Tutorials |  News |  Publications |  Download |  REST API |  Citing RGD |  Contact   

Strain: MHS/N

Symbol: MHS/N
Strain: MHS
Substrain: N
Full Name: Milan Hypertensive Strain
RGD ID: 60987
Citation ID: RRID:RRRC_00169
Ontology ID: RS:0001371
Alleles: Add2;   Add1
Type: inbred
Source: Department of Sciences and Biomedical Technologies, University of Milan, Milan, Italy
Origin: Milan Hypertensive Strain: Outbred Wistar rats with brother x sister mating and selection for high systolic blood pressure (Bianchi et al 1974, Barber et al, 1994).
Coat Color: Albino
Inbred Generations: F36
Last Known Status: Extinct






References

References - curated
# Reference Title Reference Citation
1. Inbred Strains Festing, MFW, Inbred Strains, The Laboratory Rat, 1979, Baker HK, Lindsey JR, Weisbroth SH, 55-72, Academic Press
2. Update to previous Strain Data Festing, MFW, Personal Communication Update, Feb-2000
3. Data registered by the Rat Resource & Research Center Personal Communication with Rat Resource & Research Center
4. RGD Strain RSO annotation pipeline RGD Automated Pipelines
5. Genetic mapping of blood pressure quantitative trait loci in Milan hypertensive rats. Zagato L, etal., Hypertension 2000 Nov;36(5):734-9.

Region


Additional Information

RGD Curation Notes
Note Type Note Reference
strain_characteristics Reviewed by Bianchi et al (1984). Other papers describing this strain include Clark et al, (1994), Muller et al, (1995) 1004
strain_characteristics Reviewed by Bianchi et al (1984). Other papers describing this strain include Clark et al, (1994), Muller et al, (1995) 634612
strain_phys_biochem At weaning, mean systolic blood pressure not different from that of MNS at about 119 mmHg, but by about 50 days the mean systolic blood pressure has risen to about 170 mmHg and heart rate is about 350-360 beats per minute. Kidney weight is reduced at all ages, and left ventricular weight increased from 100 days of age compared with MNS. Erythrocytes are smaller than in MNS. Hypertension can be transplanted from MHS to MNS by kidney transplantation, and this can be done in the very early and mid-hypertensive phase. There are signs of volume expansion and increased water intake. The MHS strain may be a useful animal model of renal hypertension mechanisms responsible for essential hypertension in subgroups of human patients. A factor capable of interacting with the ouabain receptor on the sodium-potassium ATPase of tubular cells is present in the kidneys, it can be removed by prolonged washout (Foulkes et al, 1992), and is present at higher levels in MRS than from the normotensive controls (Ferrandi et al, 1992, 1993). Faster sodium transport may be a primary abnormality responsible for the hypertension (Salardi et al, 1993). There are also defects in the regulation of adenylyl cyclase in vascular smooth muscle cell membranes (Clark et al, 1993). A point mutation in each of two genes coding for the membrane skeletal protein adducin is associated with blood pressure (Bianchi et al, 1994). 1004
strain_phys_biochem At weaning, mean systolic blood pressure not different from that of MNS at about 119 mmHg, but by about 50 days the mean systolic blood pressure has risen to about 170 mmHg and heart rate is about 350-360 beats per minute. Kidney weight is reduced at all ages, and left ventricular weight increased from 100 days of age compared with MNS. Erythrocytes are smaller than in MNS. Hypertension can be transplanted from MHS to MNS by kidney transplantation, and this can be done in the very early and mid-hypertensive phase. There are signs of volume expansion and increased water intake. The MHS strain may be a useful animal model of renal hypertension mechanisms responsible for essential hypertension in subgroups of human patients. A factor capable of interacting with the ouabain receptor on the sodium-potassium ATPase of tubular cells is present in the kidneys, it can be removed by prolonged washout (Foulkes et al, 1992), and is present at higher levels in MRS than from the normotensive controls (Ferrandi et al, 1992, 1993). Faster sodium transport may be a primary abnormality responsible for the hypertension (Salardi et al, 1993). There are also defects in the regulation of adenylyl cyclase in vascular smooth muscle cell membranes (Clark et al, 1993). A point mutation in each of two genes coding for the membrane skeletal protein adducin is associated with blood pressure (Bianchi et al, 1994). 634612

Nomenclature History
Date Current Symbol Current Name Previous Symbol Previous Name Description Reference Status
2012-04-18 MHS/N  Milan Hypertensive Strain  MHS/N  Milan Hypertensive Strain  Name updated 68913 APPROVED

Database Acc Id Source(s)
RRRC RRRC:00169 RGD