Renin Response to Volume Contraction and Indomethacin in Spontaneously Hypertensive Rats

1981 ◽  
Vol 60 (5) ◽  
pp. 479-482 ◽  
Author(s):  
J. L. Cangiano ◽  
Carmen Rodriguez-Sargent ◽  
L. Nascimento ◽  
M. Martinez-Maldonado
Keyword(s):  
Sharp Increase ◽  
Spontaneously Hypertensive Rats ◽  
Plasma Renin ◽  
Prostaglandin Synthesis ◽  
Restricted Diet ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Volume Contraction ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Wistar Kyoto

1. The effects of volume contraction and indomethacin on renin response were examined in spontaneously hypertensive rats and Wistar-Kyoto normotensive rats. Volume contraction was induced by frusemide or by salt-restricted diet combined with frusemide administration. 2. Plasma renin levels were not altered by either procedure in spontaneously hypertensive rats (5.2 ± 0.8 versus 5.6 ± 0.9 ng h−1 ml−1). Normotensive rats responded to volume contraction with a sharp increase in plasma renin activity (13.1 ± 1.2 to 23.3 ± 1.1 ng h−1 ml−1). 3. Intraperitoneal injection of indomethacin for 1 week did not alter basal renin levels in either group. In contrast, indomethacin pretreatment caused renin to rise in response to frusemide in spontaneously hypertensive rats (4.7 ± 0.8 to 27.1 ± 1.8 ng h−1 ml−1). 4. These findings suggest that a prostaglandin normally inhibits the renin response of spontaneously hypertensive rats to frusemide-induced volume contraction. Inhibition of prostaglandin synthesis allows volume contraction to stimulate renin release.

Hypertension transmitted by kidneys from stroke-prone spontaneously hypertensive rats

1989 ◽  
Vol 257 (2) ◽  
pp. F197-F203 ◽  
Author(s):  
R. Rettig ◽  
H. Stauss ◽  
C. Folberth ◽  
D. Ganten ◽  
B. Waldherr ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Transplantation ◽  
Spontaneously Hypertensive Rats ◽  
Plasma Renin ◽  
F1 Hybrids ◽  
Hypertensive Rats ◽  
Plasma Urea ◽  
Spontaneously Hypertensive ◽  
Major Function ◽  
Wistar Kyoto

We determined whether transplantations of kidneys from stroke-prone spontaneously hypertensive rats (SPSHR) and from normotensive Wistar-Kyoto rats (WKY) alter blood pressure in renal graft recipients. Kidneys taken from seven male SPSHR and seven male WKY rats (blood pressure 186 +/- 4.8 and 111 +/- 3.7 mmHg, respectively) at the age of 20 wk were transplanted, using microsurgical techniques, to bilaterally nephrectomized age-matched male F1 hybrids (blood pressure 136 +/- 2.6 and 138 +/- 6.3 mmHg, respectively) bred from SPSHR and WKY parents. After renal transplantation, blood pressure in recipients of SPSHR kidneys rose to 146 +/- 11.8 (week 2), 163 +/- 16.4 (week 3), 192 +/- 17.1 (week 4), 222 +/- 17.7 (week 5), 221 +/- 12.6 (week 6), 218 +/- 20.3 (week 7), and 239 +/- 9.2 mmHg (week 8). There was no significant change in blood pressure in recipients of WKY kidneys. All rats recovered rapidly from surgery. After renal transplantation, there was a significant increase in daily water intake, a decrease in plasma renin activity, and a slight rise in plasma urea concentration. Our data show that transplantation of kidneys from adult SPSHR causes hypertension in normotensive recipients, indicating a major function for the kidney in SPSHR hypertension.

Effect of apocynin treatment on renal expression of COX-2, NOS1, and renin in Wistar-Kyoto and spontaneously hypertensive rats

2006 ◽  
Vol 290 (3) ◽  
pp. R694-R700 ◽  
Author(s):  
A. Paliege ◽  
A. Parsumathy ◽  
D. Mizel ◽  
T. Yang ◽  
J. Schnermann ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nadph Oxidase ◽  
Spontaneously Hypertensive Rats ◽  
Plasma Renin ◽  
Juxtaglomerular Apparatus ◽  
Oxidase Inhibitor ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Cox 2 ◽  
Wistar Kyoto

Macula densa (MD) cells of the juxtaglomerular apparatus (JGA) synthesize type 1 nitric oxide synthase (NOS1) and type 2 cyclooxygenase (COX-2). Both nitric oxide (NO) and prostaglandins have been considered to mediate or modulate the control of renin secretion. Reactive oxygen species (ROS) produced locally by NADPH oxidase may influence NO bioavailability. We have tested the hypothesis that in hypertension elevated ROS levels may modify the expression of NOS1 and COX-2 in the JGA, thereby interacting with juxtaglomerular signaling. To this end, spontaneously hypertensive rats (SHR) and Wistar-Kyoto control rats (WKY) received the specific NADPH oxidase inhibitor, apocynin, during 3 wk. Renal functional and histochemical parameters, plasma renin activity (PRA), and as a measure of ROS activity, urinary isoprostane excretion (IP) were evaluated. Compared with WKY, IP levels in untreated SHR were 2.2-fold increased, and NOS1 immunoreactiviy (IR) of JGA 1.5-fold increased, whereas COX-2 IR was reduced to 35%, renin IR to 51%, and PRA to 7%. Apocynin treatment reduced IP levels in SHR to 52%, NOS1 IR to 69%, and renin IR to 62% of untreated SHR, whereas renin mRNA, COX-2 IR, glomerular filtration rate, PRA, and systolic blood pressure remained unchanged. WKY revealed no changes under apocynin treatment. These data show that NADPH oxidase is an important contributor to elevated levels of ROS in hypertension. Upregulation of MD NOS1 in SHR may have the potential of blunting the functional impact of ROS at the level of bioavailable NO. Downregulated COX-2 and renin levels in SHR are apparently unrelated to oxidative stress, since apocynin treatment had no effect on these parameters.

Vascular prostaglandin synthesis in the spontaneously hypertensive rat

1977 ◽  
Vol 233 (4) ◽  
pp. H493-H499 ◽  
Author(s):  
C. J. Limas ◽  
C. Limas
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Inferior Vena ◽  
Spontaneously Hypertensive Rat ◽  
Vena Cava ◽  
Prostaglandin Synthesis ◽  
Hypertensive Rats ◽  
Blood Pressure Elevation ◽  
Spontaneously Hypertensive ◽  
Prostaglandin Dehydrogenase ◽  
Wistar Kyoto

Vascular prostaglandin synthesis was studied in tissues (aorta and inferior vena cava) obtained from spontaneously hypertensive rats (SHRs) of the Aoki-Okamoto strain and age-matched Wistar-Kyoto (WKYs) controls. PGE2 synthesis in aortas from SHRs was significantly enhanced at 10 wk of age (5.3 +/- 0.7 nmol PGE2/mg protein per 10 min vs. 1.9 +/- 0.03 nmol PGE2/mg protein per min in the WKYs, P less than 0.001) and increased progressively until 22 wk of age; PGE2alpha synthesis in SHRs was not significantly different from WKYs. In the venous walls from SHRs, PGF2alpha was the prostaglandin predominantly synthesized (7.1 +/- 0.6 vs. 1.9 +/- 0.05 nmol PGE2alpha/mg protein per 10 min in the WKY controls, P less than 0.01). The activities of 15-hydroxy prostaglandin dehydrogenase and PGE 9-ketoreductase were also compared in the two groups of animals. The only difference detected was a significant increase in venous PGE 9-ketoreductase of SHR's (7.3 +/- 0.06 vs. 4.8 +/- 0.04 nmol PGF2alpha/mg per min, P less than 0.01). The results suggest that increased vascular synthesis of prostaglandins accompanies the development of spontaneous hypertension and may serve to attenuate the effects of blood pressure elevation.

Role of renal nerves on pressure natriuresis in spontaneously hypertensive rats

1991 ◽  
Vol 260 (1) ◽  
pp. F81-F85 ◽  
Author(s):  
M. Yoshida ◽  
S. Satoh
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Renal Denervation ◽  
Plasma Renin ◽  
Renal Nerves ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Rightward Shift ◽  
Fractional Excretion Of Sodium ◽  
Wistar Kyoto ◽  
Pressure Natriuresis

An abnormal rightward shift of the pressure-natriuresis curve is a well known feature of the renal function in hypertension. The participation of intrinsic neural factors in the kidney in this phenomenon was investigated in anesthetized young and adult spontaneously hypertensive rats (SHR). At 7-8 wk of age, the renal pressure-diuresis curve and pressure-natriuresis curve were shifted to the left in denervated SHR compared with innervated animals. Fractional excretion of sodium was higher, and plasma renin activity was lower in denervated SHR. Glomerular filtration rate was not affected by renal denervation. In 13- to 15-wk-old SHR, renal denervation did not affect the pressure-diuresis and -natriuresis curves, although other parameters were changed compared with the results at 7-8 wk. In Wistar-Kyoto rats, the pressure-diuresis curve was shifted to the left by renal denervation at both ages. These results suggest that the renal nerves have an important effect on the renal pressure-diuresis and -natriuresis curves. However, renal innervation cannot be thought to cause an abnormal rightward shift of the pressure-diuresis and -natriuresis curves in SHR, especially in the established stage of hypertension.

Excess oxygen delivery during muscle contractions in spontaneously hypertensive rats

1995 ◽  
Vol 78 (1) ◽  
pp. 101-111 ◽  
Author(s):  
J. M. Lash ◽  
H. G. Bohlen
Keyword(s):  
Blood Flow ◽  
Oxygen Saturation ◽  
Oxygen Delivery ◽  
Spontaneously Hypertensive Rats ◽  
Muscle Contractions ◽  
Hypertensive Rats ◽  
Hemoglobin Oxygen Saturation ◽  
Spontaneously Hypertensive ◽  
Tissue Po2 ◽  
Wistar Kyoto

These experiments determined whether a deficit in oxygen supply relative to demand could account for the sustained decrease in tissue PO2 observed during contractions of the spinotrapezius muscle in spontaneously hypertensive rats (SHR). Relative changes in blood flow were determined from measurements of vessel diameter and red blood cell velocity. Venular hemoglobin oxygen saturation measurements were performed by using in vivo spectrophotometric techniques. The relative dilation [times control (xCT)] of arteriolar vessels during contractions was as large or greater in SHR than in normotensive rats (Wistar-Kyoto), as were the increases in blood flow (2 Hz, 3.50 +/- 0.69 vs. 3.00 +/- 1.05 xCT; 4 Hz, 10.20 +/- 3.06 vs. 9.00 +/- 1.48 xCT; 8 Hz, 16.40 +/- 3.95 vs. 10.70 +/- 2.48 xCT). Venular hemoglobin oxygen saturation was lower in the resting muscle of SHR than of Wistar-Kyoto rats (31.0 +/= 3.0 vs. 43.0 +/- 1.9%) but was higher in SHR after 4- and 8-Hz contractions (4 Hz, 52.0 +/- 4.8 vs. 43.0 +/- 3.6%; 8 Hz, 51.0 +/- 4.6 vs. 41.0 +/- 3.6%). Therefore, an excess in oxygen delivery occurs relative to oxygen use during muscle contractions in SHR. The previous and current results can be reconciled by considering the possibility that oxygen exchange is limited in SHR by a decrease in anatomic or perfused capillary density, arteriovenular shunting of blood, or decreased transit time of red blood cells through exchange vessels.

scholarly journals Aging Additively Influences Insulin- and Insulin-Like Growth Factor-1-Mediated Endothelial Dysfunction and Antioxidant Deficiency in Spontaneously Hypertensive Rats

Biomedicines ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 676
Author(s):  
Kunanya Masodsai ◽  
Yi-Yuan Lin ◽  
Sih-Yin Lin ◽  
Chia-Ting Su ◽  
Shin-Da Lee ◽  
...  
Keyword(s):  
Growth Factor ◽  
Endothelial Dysfunction ◽  
Spontaneously Hypertensive Rats ◽  
No Production ◽  
Organ Bath ◽  
Insulin Like Growth Factor ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Nos Inhibitors ◽  
Wistar Kyoto

This study aimed to investigate the aging-related endothelial dysfunction mediated by insulin and insulin-like growth factor-1 (IGF-1) and antioxidant deficiency in hypertension. Male spontaneously hypertensive rats (SHRs) and age-matched normotensive Wistar–Kyoto rats (WKYs) were randomly divided into 24-week-old (younger) and 48-week-old (older) groups, respectively. The endothelial function was evaluated by the insulin- and IGF-1-mediated vasorelaxation of aortic rings via the organ bath system. Serum levels of nitric oxide (NO), malondialdehyde (MDA), catalase, and total antioxidant capacity (TAC) were examined. The insulin- and IGF-1-mediated vasorelaxation was significantly impaired in both 24- and 48-week-old SHRs compared with age-matched WKYs and was significantly worse in the 48-week-old SHR than the 24-week-old SHR. After pretreatments of phosphoinositide 3-kinase (PI3K) or NO synthase (NOS) inhibitors, the insulin- and IGF-1-mediated vasorelaxation became similar among four groups. The serum level of MDA was significantly increased, while the NO, catalase, and TAC were significantly reduced in the 48-week-old SHR compared with the 24-week-old SHR. This study demonstrated that the process of aging additively affected insulin- and IGF-1-mediated endothelial dysfunction in SHRs, which could be partly attributed to the reduced NO production and antioxidant deficiency.

Effects of dietary Ca2+ on erythrocyte Na+-transport systems in spontaneously hypertensive rats

1991 ◽  
Vol 81 (1) ◽  
pp. 107-112 ◽  
Author(s):  
K. Fujito ◽  
M. Yokomatsu ◽  
N. Ishiguro ◽  
H. Numahata ◽  
Y. Tomino ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Transport Systems ◽  
Hypertensive Rats ◽  
Na Transport ◽  
Spontaneously Hypertensive ◽  
Na Pump ◽  
Wistar Kyoto ◽  
Increased Activity ◽  
Regulation Of Blood Pressure

1. The purpose of this study was to determine the effect of dietary Ca2+ intake on blood pressure and erythrocyte Na+ transport in spontaneously hypertensive rats. 2. Spontaneously hypertensive rats and Wistar-Kyoto rats were fed diets with three different Ca2+ contents, 0.1% (low-Ca2+ diet), 0.6% (normal-Ca2+ diet) and 4.0% (high-Ca2+ diet), between 6 and 20 weeks of age. At 20 weeks of age, the levels of erythrocyte Na+ efflux, as well as Na+ and K+ contents in erythrocytes, were measured. 3. On the low-Ca2+ diet, spontaneously hypertensive rats showed an enhancement of hypertension. Conversely, on the high-Ca2+ diet, they showed an attenuation of the increase in blood pressure. Spontaneously hypertensive rats had a lower erythrocyte Na+ content and increased activity of the Na+ pump at higher levels of dietary Ca2+. Passive Na+ permeability and Na+-K+ co-transport were similar in spontaneously hypertensive rats on the low-, normal- and high-Ca2+ diets. There were no significant differences in blood pressure and in Na+ pump activity in WKY on the three different diets. 4. It is concluded that dietary Ca2+ might affect the regulation of blood pressure in spontaneously hypertensive rats by changing the activity of Na+ pump in the cell membrane.

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