Gap Junction Protein Locus on Chromosome 18 Cosegregates with Body Weight in the Spontaneously Hypertensive Rat.

In this study. the effect of the herbal prescription Tian Ma Gou Teng Yen (TGY), which is traditionally used to treat certain diseases associated with elevated arterial pressure (AP), on the general development of hypertension was investigated in the spontaneously hypertensive rat (SHR). An aqueous extract of TGY was given orally (0.5 ml/100g body weight) to 5 week old SHR twice a day for six consecutive days followed by one day without herbal therapy. The herbal prescription was administered until the SHR were 16 weeks of age. Admininstration of TGY significantly altered the development and prevented hypertension in SHR. On the other hand, heart rat, body weight, food and water intake, and urine volume and electrolytes were not altered. These data suggest that the effect of TGY on AP was through an action of TGY on sympathetic vasomotor activity.

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Evaluation of Pathological Association between Stroke-Related QTL and Salt-Induced Renal Injury in Stroke-Prone Spontaneously Hypertensive Rat

BioMed Research International ◽

10.1155/2019/5049746 ◽

2019 ◽

Vol 2019 ◽

pp. 1-7

Author(s):

Mohammad Farhadur Reza ◽

Davis Ngarashi ◽

Masamichi Koike ◽

Masaki Misumi ◽

Hiroki Ohara ◽

...

Keyword(s):

Blood Pressure ◽

Genetic Marker ◽

Renal Injury ◽

Spontaneously Hypertensive Rat ◽

Kidney Injury ◽

Cerebral Stroke ◽

Chromosome 18 ◽

Spontaneously Hypertensive ◽

Congenic Strains ◽

Hypertensive Rat

The stroke-prone spontaneously hypertensive rat (SHRSP) suffers from severe hypertension and hypertensive organ damage such as cerebral stroke and kidney injury under salt-loading. By a quantitative trait locus (QTL) analysis between SHRSP and SHR (the stroke-resistant parental strain of SHRSP), two major QTLs for stroke susceptibility were identified on chromosomes 1 and 18 of SHRSP, which were confirmed in congenic strains constructed between SHRSP and SHR. As the progression of renal dysfunction was suggested to be one of the key factors inducing stroke in SHRSP, we examined effects of the stroke-related QTLs on kidney injury using two congenic strains harboring either of SHRSP-derived fragments of chromosomes 1 and 18 in the SHR genome. The congenic strains were challenged with 1% NaCl solution for 4 weeks; measurement of systolic blood pressure and urinary isoprostane level (a marker for oxidative stress) and evaluation of renal injury by quantification of genetic marker expression and histological examination were performed. We found that the congenic rats with SHRSP-derived fragment of chromosome 18 showed more severe renal damage with higher expression of Col1α-1 (a genetic marker for renal fibrosis) and higher urinary isoprostane level. In contrast, the fragment of chromosome 1 from SHRSP did not give such effects on SHR. Blood pressure was not greater in either of the congenic strains when compared with SHR. We concluded that the QTL region on chromosome 18 might deteriorate salt-induced renal injury in SHR through a blood pressure-independent mechanism.

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