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.

Renal interstitial hydrostatic pressure during pressure natriuresis in hypertension

1988 ◽  
Vol 255 (5) ◽  
pp. R756-R759 ◽  
Author(s):  
A. A. Khraibi ◽  
F. G. Knox
Keyword(s):  
Hydrostatic Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Left Kidney ◽  
Hypertensive Rats ◽  
Polyethylene Matrix ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Fractional Excretion Of Sodium ◽  
Wistar Kyoto ◽  
Pressure Natriuresis

The objective of this study was to test the hypothesis that changes in renal perfusion pressure (RPP) are not fully transmitted to the renal interstitium in spontaneous hypertension in comparison with normotensive states. Okamoto spontaneously hypertensive and normotensive Wistar-Kyoto rats were used in this study. Renal interstitial hydrostatic pressure (RIHP) was measured directly and continuously via a polyethylene matrix that was implanted chronically in the left kidney 3 wk before RIHP measurement. When RPP was allowed to increase from 136 +/- 0.5 to 162 +/- 1.3 mmHg in male spontaneously hypertensive rats, RIHP was not significantly changed from 3.7 +/- 0.9 to 4.6 +/- 1.1 mmHg, and fractional excretion of sodium (FENa) increased significantly from 0.26 +/- 0.12 to 0.65 +/- 0.15% (P less than 0.05). When RPP was allowed to change from 104 +/- 0.9 to 127 +/- 1.3 mmHg in male Wistar-Kyoto rats, RIHP increased markedly from 4.0 +/- 0.3 to 7.2 +/- 0.4 mmHg (P less than 0.05), and FENa was significantly elevated from 0.27 +/- 0.08 to 2.02 +/- 0.55% (P less than 0.05). In conclusion, spontaneously hypertensive rats have a blunted increase in RIHP and pressure natriuresis response in comparison with Wistar-Kyoto rats. Thus, in Okamoto spontaneously hypertensive rats, the effect of RPP on RIHP is attenuated, leading to a blunted pressure natriuresis response.

Effect of acute renal denervation and ANF on renal function in adult spontaneously hypertensive rats

1991 ◽  
Vol 261 (4) ◽  
pp. R835-R841
Author(s):  
D. M. Pollock ◽  
W. J. Arendshorst
Keyword(s):  
Renal Function ◽  
Spontaneously Hypertensive Rats ◽  
Renal Denervation ◽  
Renal Nerves ◽  
Hypertensive Rats ◽  
Water Excretion ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Fractional Excretion Of Sodium ◽  
Shr And Wky Rats

Experiments were designed to evaluate the influence of the renal efferent nerves on baseline renal function and on the renal response to atrial natriuretic factor (ANF) in euvolemic anesthetized 10- to 12-wk-old spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) and Munich-Wistar (MW) rats. Acute unilateral renal denervation produced increases in absolute and fractional excretion of sodium and water by the ipsilateral kidney that were similar in SHR and WKY rats; larger responses were observed in MW rats. Excretion by the contralateral innervated kidney was unchanged in each group. Intravenous infusion of ANF (0.25 microgram.kg-1.min-1) caused a diuresis and natriuresis that was similar in the three strains and independent of changes in glomerular filtration rate and renal blood flow. The excretory responses to ANF were larger in denervated than in innervated kidneys. The magnitude of the natriuresis and diuresis produced by ANF was directly related to the pre-ANF rate of urinary excretion, suggesting independent and additive effects of acute renal denervation and ANF on tubular reabsorption. The exaggerated response in the acutely denervated kidney can be explained by removal of a modulatory effect of the renal efferent nerves and associated increases in tubular flow and delivery to more distal ANF-sensitive sites. The denervation responses suggest that the renal efferent nerves have similar effects on sodium and water reabsorption in anesthetized SHR and WKY rats at 10-12 wk of age. The renal nerves and ANF appear to play a larger role in the acute control of sodium and water excretion in MW rats compared to rats of the Okamoto-Aoki strain.

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.

scholarly journals Role of NO on pressure-natriuresis in Wistar-Kyoto and spontaneously hypertensive rats

1993 ◽  
Vol 43 (1) ◽  
pp. 205-211 ◽  
Author(s):  
Hideki Ikenaga ◽  
Hiromichi Suzuki ◽  
Naohito Ishii ◽  
Hajime Itoh ◽  
Takao Saruta
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Pressure Natriuresis

Role of renal nerves in onset and maintenance of spontaneous hypertension

1982 ◽  
Vol 243 (2) ◽  
pp. H284-H288 ◽  
Author(s):  
R. A. Norman ◽  
D. J. Dzielak
Keyword(s):  
Arterial Pressure ◽  
Renal Denervation ◽  
Indirect Measurement ◽  
Renal Nerves ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Norepinephrine Content ◽  
Wistar Kyoto

Renal denervation has been reported to delay development of hypertension in Okamoto spontaneously hypertensive rats (SHR) but to have no effect on the final hypertensive state. However, functional reinnervation begins to occur about 1 mo after renal denervation. The arterial pressure of SHR undergoing repeated bilateral renal denervations at the age of 4, 7, 10, 13, and 16 wk was compared with that in sham-operated SHR. In addition, the effect of successive renal denervations at 4, 7, and 10 wk of age in Wistar-Kyoto (WKY) control rats was determined. Both indirect measurement of pressure by the tail-cuff technique and mean arterial pressure (MAP) measurement indicated that renal denervation prevents full expression of hypertension in SHR. MAP in 19-wk-old renal-denervation SHR averaged 159 +/- 5.1 mmHg (SE) vs. 178 +/-0 4.2 mmHg in sham-operated SHR. Renal denervation had no effect on arterial pressure of WKY rats. Renal norepinephrine content in the renal-denervated WKY rats and SHR was less than 20% of that in the sham-operated groups. Successive bilateral renal denervations every 3 wk blocks 30-40% of the expected progressive elevation of arterial pressure in aging SHR.

scholarly journals Effects of renal denervation on pressure-natriuresis in spontaneously hypertensive rats.

1993 ◽  
Vol 57 (11) ◽  
pp. 1097-1105 ◽  
Author(s):  
JIRO KUBOTA ◽  
HIKARU NISHIMURA ◽  
MASAKUNI UEYAMA ◽  
KEISHIRO KAWAMURA
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Renal Denervation ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Pressure Natriuresis

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.

Effect of renal denervation on the development of hypertension in spontaneously hypertensive rats

1978 ◽  
Vol 56 (5) ◽  
pp. 818-822 ◽  
Author(s):  
R. L. Kline ◽  
P. M. Kelton ◽  
P. F. Mercer
Keyword(s):  
Urine Output ◽  
Spontaneously Hypertensive Rats ◽  
Renal Denervation ◽  
Time Course ◽  
Fluid Intake ◽  
Systolic Pressure ◽  
Systolic Arterial Pressure ◽  
Renal Nerves ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

The involvement of the renal nerves in the development of hypertension in Okamoto spontaneously hypertensive rats (SHR) was investigated by performing bilateral renal denervation in a group (n = 7) of SHR at 8 weeks of age. A sham-operated group (n = 7) of SHR served as surgical controls. Systolic arterial pressure was recorded twice a week until 14 weeks of age using a tail cuff method. Renal denervation significantly (P < 0.01) altered the time course for development of hypertension, although both groups eventually developed hypertension. During the 6-week observation period, there were no significant differences in body weight, average 24-h food and fluid intake, urine output, or Na+ and K+ excretion between the two groups. At 20 weeks of age there were no significant, differences in systolic pressure, average fluid intake, or urine output between the sham and denervated groups. These results suggest that the renal nerves may be involved in the early phase of development of hypertension in the SHR. The possibility that altered renal function may be the mechanism of the above effects is discussed.

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