scholarly journals Maternal Protein Restriction Alters the Renal Ptger1 DNA Methylation State in SHRSP Offspring

Nutrients ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 1436
Author(s):  
Moe Miyoshi ◽  
Masayuki Sato ◽  
Kenji Saito ◽  
Lila Otani ◽  
Katsuhiko Shirahige ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Spontaneously Hypertensive Rat ◽  
Methylation Status ◽  
Salt Sensitivity ◽  
Protein Restriction ◽  
Na Channel ◽  
Prostaglandin E ◽  
Spontaneously Hypertensive ◽  
Methylation State ◽  
Maternal Protein Restriction

We previously reported that maternal protein restriction (LP) during pregnancy increases salt sensitivity in offspring using the Stroke-Prone Spontaneously Hypertensive Rat (SHRSP). In the present study, we focus on DNA methylation profiles of prostaglandin E receptor 1 gene (ptger1), which is known to be associated with hypertension. We evaluated the ptger1 DNA methylation status via bisulfite sequencing, and analyzed the expression of ptger1-related genes. The results of these analyses showed that, compared to controls, the LP-S offspring exhibited both marked ptger1 hypermethylation, and significantly increased ptger1 expression. Moreover, they also exhibited significantly decreased expression of the downstream gene epithelial Na+ channel alpha (enacα). Interestingly, LP offspring that were provided with a standard water drinking supply (W) also exhibited increased ptger1 methylation and expression. Together, these results suggest that maternal protein restriction during pregnancy modulates the renal ptger1 DNA methylation state in SHRSP offspring, and thereby likely mediates ptger1 and enacα gene expression to induce salt sensitivity.

scholarly journals Chloride-Dominant Salt Sensitivity in the Stroke-Prone Spontaneously Hypertensive Rat

Hypertension ◽  
2005 ◽  
Vol 45 (5) ◽  
pp. 867-873 ◽  
Author(s):  
Olga Schmidlin ◽  
Masae Tanaka ◽  
Andrew W. Bollen ◽  
Sai-Li Yi ◽  
R. Curtis Morris
Keyword(s):  
Spontaneously Hypertensive Rat ◽  
Salt Sensitivity ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat

Release of prostaglandins by the mesenteric artery of the renovascular and spontaneously hypertensive rat

1984 ◽  
Vol 62 (1) ◽  
pp. 89-93 ◽  
Author(s):  
Suzanne Desjardins-Giasson ◽  
Jolanta Gutkowska ◽  
Raul Garcia ◽  
Jacques Genest
Keyword(s):  
Wistar Rats ◽  
Spontaneously Hypertensive Rat ◽  
Pressor Response ◽  
Mesenteric Arteries ◽  
Control Group ◽  
Prostaglandin E ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Specific Increase ◽  
Wistar Kyoto

The release of prostaglandin E2 (PGE2) and 6-ketoprostaglandin F1α (6-keto-PGF1α), the stable metabolite of prostacyclin (PGI2), by the perfused mesenteric arteries of renal and spontaneously hypertensive rats (SHR) have been measured. Unstimulated mesenteric arteries from two-kidney one-clip hypertensive rats (2K-1C) released 1.6 times as much PGE2 and 2.7 times as much 6-keto-PGF1α as those of control rats. The release of PGE2 by mesenteric arteries from one-kidney one-clip hypertensive rats (1K-1C) was not significantly different from that of uninephrectomized normotensive rats, but the release of 6-keto-PGF1α was 3.5 times higher in the former than in the latter. Norepinephrine (NE) induced a dose-related increase in perfusion pressure, in PGE2, and 6-keto-PGF1α release in all four groups. However, its effect on the release of PGE2 was more pronounced in 2K-1C than in sham-operated rats. There was no difference between 1K-1C and the uninephrectomized group. The effect of NE on the release of 6-keto-PGF1α was significantly higher for both renal hypertensive groups. These results indicate that the release of PGE2 is more dependent on the loss of renal mass than on hypertension, while the reverse applies to the release of 6-keto-PGF1α. Unstimulated mesenteric arteries from SHR released less PGE2 and less 6-keto-PGF1α than those of Wistar–Kyoto normotensive rats (WKY), but the release was not significantly different from Wistar rats. Under NE stimulation, WKY mesenteric arteries showed almost no increase in release of PGs. Compared with those of Wistar rats, SHR mesenteric arteries showed a greater pressor response to NE, a lower PGE2 release, and the same release of 6-keto-PGF1α. These findings reveal the difficulty of selecting an appropriate control group in studies involving SHR. We concluded that in renal hypertensive rats the specific increase of PGI2 release by arterial tissue may represent an important adaptive mechanism to the elevated blood pressure. However, this mechanism seems not to be involved in SHR.

Voltage-gated Na+ Channel Blockers Reduce Functional Bladder Capacity in the Conscious Spontaneously Hypertensive Rat

Urology ◽  
2012 ◽  
Vol 79 (6) ◽  
pp. 1410.e1-1410.e6 ◽  
Author(s):  
Angela K. Clouse ◽  
Malcolm J. Jugus ◽  
Stephen H. Eisennagel ◽  
Nicholas J. Laping ◽  
Timothy D. Westfall ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rat ◽  
Bladder Capacity ◽  
Na Channel ◽  
Channel Blockers ◽  
Spontaneously Hypertensive ◽  
Voltage Gated ◽  
Hypertensive Rat

A new inbred Wistar-Kyoto rat substrain exhibiting apparent salt sensitivity and borderline hypertension

2002 ◽  
Vol 283 (3) ◽  
pp. H1181-H1190 ◽  
Author(s):  
Adamu Alemayehu ◽  
Laura Breen ◽  
Morton P. Printz
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Spontaneously Hypertensive Rat ◽  
Systolic Pressure ◽  
Salt Sensitivity ◽  
Spontaneously Hypertensive ◽  
Borderline Hypertension ◽  
Genomic Studies ◽  
Wistar Kyoto ◽  
La Jolla

The normotensive Wistar-Kyoto (WKY) rat strain is a traditional control for the spontaneously hypertensive rat (SHR). We found trait differences between two inbred normotensive WKY strains, derived originally from different vendors, and compared these two strains from La Jolla-Taconic Farms (WKY/lj-tf) and La Jolla-Charles River (WKY/lj-cr) with the inbred SHR/lj-cr for cardiovascular, diurnal, and activity traits under normal and high (8%) NaCl diets. Marked genetic diversity was found between the two vendor-derived WKY. By using an extended study design and radiotelemetry, we compared WKY/lj-cr, WKY/lj-tf, and SHR/lj-cr with the following results: systolic pressure (120 ± 1, 133 ± 1, 168 ± 3 mmHg, respectively); diurnal variation in heart rate (ΔHR: 46 ± 3, 71 ± 4, 57 ± 2 beats/min, respectively); and salt sensitivity of arterial pressure (Δsystolic: 10 ± 1, 21 ± 1, 20 ± 1 mmHg, respectively). The WKY/lj-tf genotype apparently results in compromised control of arterial pressure and heart rate, especially during high NaCl intake, and greater susceptibility to high pressure (i.e., high NaCl-induced secondary changes). WKY/lj-tf thus constitutes a new inbred borderline hypertensive WKY substrain offering unique opportunities for genomic studies into the development of genetic hypertension.

Renal and Vascular Wall Prostaglandins in Spontaneously Hypertensive Rats

1982 ◽  
Vol 63 (s8) ◽  
pp. 253s-255s ◽  
Author(s):  
Yukio Ozawa ◽  
Keika Kan ◽  
Konosuke Konishi ◽  
Waichi Kitajima ◽  
Yasuo Matsumura
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Aortic Wall ◽  
Spontaneously Hypertensive Rat ◽  
Prostaglandin E ◽  
Prostaglandin I2 ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Medullary Tissue ◽  
Hypertensive Rat ◽  
Wistar Kyoto

1. Renal cortical and medullary tissue and aortic wall were removed from spontaneously hypertensive rats and from age-matched Wistar-Kyoto control animals at ages 30, 60, 90 and 120 days. The tissues were incubated and the release of prostaglandins into the incubation medium was measured. 2. Compared with Wistar-Kyoto control animals, the release of prostaglandin E from renal medullary tissue in spontaneously hypertensive rats was raised at 30 days (pre-hypertensive stage) and 90 days (early hypertensive stage), but decreased later with further establishment of hypertension. No such trend was seen with renal cortical tissue. Tissue release of prostaglandin F tended to be generally high in the spontaneously hypertensive rats compared with that in the control animals, but the difference was not significant. 3. The release of prostaglandin I2, as indicated by measurements of 6-keto prostaglandin F1α, from aortic wall tissue in the spontaneously hypertensive rat during its pre-hypertensive and early hypertensive stages was similar to values obtained in the age-matched control animal. However, aortic wall prostaglandin I2 release in spontaneously hypertensive rats increased thereafter, and was significantly raised at 90 and 120 days. No similar trend was observed with thromboxan A2 release. Release of prostaglandin I2 and thromboxan A2 from renal tissues in spontaneously hypertensive rats did not differ significantly from that in control animals. 4. It is suggested that indomethacin-induced aggravation of hypertension in the spontaneously hypertensive rat may result from suppression of aortic wall prostaglandin I2 formation rather than from the suppression of renal prostaglandin E2 production.

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