Differential effects of salt on renal hemodynamics and potential pressure transmission in stroke-prone and stroke-resistant spontaneously hypertensive rats

2005 ◽  
Vol 289 (2) ◽  
pp. F305-F313 ◽  
Author(s):  
Isam Abu-Amarah ◽  
Anil K. Bidani ◽  
Rifat Hacioglu ◽  
Geoffrey A. Williamson ◽  
Karen A. Griffin
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Renal Damage ◽  
Function Analysis ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Vascular Bed ◽  
Transfer Function Analysis ◽  
Pressure Transmission ◽  
Renal Vascular ◽  
Potential Pressure

Salt-supplemented stroke-prone spontaneously hypertensive rats (SHRsp) develop more severe hypertension-induced renal damage (HIRD) compared with their progenitor SHR. The present studies were performed to examine whether in addition to increasing the severity of hypertension salt also enhanced the transmission of such hypertension to the renal vascular bed in the SHRsp. “Step” and “dynamic” renal blood flow (RBF) autoregulation (AR) were examined in ∼12-wk-old SHR and SHRsp after 3–5 days of an 8% NaCl diet. During step AR under anesthesia ( n = 8–11), RBF was significantly higher in the SHRsp at all perfusion pressures ( P < 0.01), but AR capacity was not different. Similarly, in separate conscious chronically instrumented rats ( n = 8 each), both blood pressure (BP) and RBF were modestly but significantly higher at baseline before salt in the SHRsp ( P < 0.05). However, transfer function analysis did not show significant differences in the admittance gain parameters. However, after 3–5 days of salt, although average BP was not significantly altered in either strain, RBF increased further in the SHRsp and there was a significantly greater transfer of BP into RBF power in the SHRsp. This was reflected in the significantly higher admittance gain parameters at most frequencies including the heartbeat frequency ( P < 0.05 maximum). These differential hemodynamic effects of salt have the potential to enhance BP transmission to the renal vascular bed and also contribute to the more severe HIRD observed in the salt-supplemented SHRsp.

Changes in angiotensin receptors expression play a pivotal role in the renal damage observed in spontaneously hypertensive rats

2011 ◽  
Vol 300 (2) ◽  
pp. F499-F510 ◽  
Author(s):  
Sharon S. Landgraf ◽  
Mira Wengert ◽  
Jaqueline S. Silva ◽  
Gisele Zapata-Sudo ◽  
Roberto T. Sudo ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Spontaneously Hypertensive Rats ◽  
Renal Damage ◽  
Renin Angiotensin System ◽  
Angiotensin Receptors ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Protein Kinase C Activity ◽  
Kidney Glomerulus ◽  
Wistar Kyoto

The renal renin-angiotensin system plays a central role in the development of hypertension. The aim of this work was to verify the expression of angiotensin II receptors AT1R and AT2R in the microsomal fraction of renal cortex and correlate this with the development of hypertension and renal damage in spontaneously hypertensive rats (SHR) using Wistar-Kyoto rats (WKY) as controls. AT1R expression increased (126%) and AT2R expression decreased (66%) in 4-wk-old SHR; AT2 expression decreased in 14-wk-old SHR (61%) compared with respective age-matched WKY. These modifications were correlated to the increase in protein kinase C activity and decrease in protein kinase A activity. Four-week-old SHR showed large accumulations of macrophages in kidney glomerulus and the tubulointerstitial area, dense cortical collagen deposition, and arterial proliferative changes in the walls of arterioles and medium-sized vessels. Similar modifications were also observed in 14-wk-old SHR. Four-week-old SHR treated with losartan (30 mg·kg−1·day−1) or hydralazine (15 and 30 mg·kg−1·day−1) by gavage for 10 wk did not develop hypertension. The decrease in AT2R expression and renal damage observed in SHR remained even after treatment with hydralazine. On the other hand, losartan treatment prevented the modifications observed in 14-wk-old SHR, indicating that renal injuries are caused specifically by AT1 rather than an increase in blood pressure. Our results indicate that the imbalance in AT1R and AT2R expression is associated with an inflammatory process that contributes to renal injury in adult SHR and to the development of hypertension.

Alterations in renal vascular resistance and reactivity in spontaneous hypertension of rats

1980 ◽  
Vol 238 (3) ◽  
pp. H287-H293 ◽  
Author(s):  
K. H. Berecek ◽  
U. Schwertschlag ◽  
F. Gross
Keyword(s):  
Vascular Resistance ◽  
Dose Response ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Response Curves ◽  
Renal Vasculature ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Dose Response Curves ◽  
Renal Vascular

Vascular resistance and reactivity were investigated in isolated, constant flow perfused kidneys of stroke-prone spontaneously hypertensive rats (SHRSP) and age- and sex-matched normotensive Wistar-Kyoto control rats (WKY rats). Stroke-prone spontaneously hypertensive rats were studied at 4 wk, 2 mo, and 4 mo of age representing different stages of development of hypertension. Resistance in maximally vasodilated vascular beds was greater and the pressure-flow relationship was significantly shifted to the left in kidneys of SHRSP as compared to WKY rats. Responses to norepinephrine, vasopressin, serotonin, and angiotensin II were enhanced in the renal vascular bed of SHRSP. Dose-response curves were shifted to the left, had steeper slopes, decreased thresholds, and increased maximal responses. With longer duration of hypertension, resistance increased, the slopes of the dose-response curves were steeper, and maximum responses greater. The higher resistance and enhanced reactivity in the renal vasculature of SHRSP, already demonstrable in the prehypertensive stage appear to be due to primary structural and functional alterations of the resistance vessels.

High-potassium diet attenuates salt-induced acceleration of hypertension in SHR

1991 ◽  
Vol 260 (1) ◽  
pp. R21-R26 ◽  
Author(s):  
Y. Sato ◽  
K. Ando ◽  
E. Ogata ◽  
T. Fujita
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
High Potassium ◽  
Spontaneously Hypertensive ◽  
Antihypertensive Action ◽  
High K ◽  
Wistar Kyoto ◽  
Renal Vascular

We studied the effects of K supplementation (8% KCl) for 4 wk on blood pressure (BP), Na space, and renal hemodynamics in 5-wk-old, spontaneously hypertensive rats (SHR) or age-matched Wistar-Kyoto rats (WKY) eating normal-NaCl (0.66%) or high-NaCl (8%) diet. In WKY, high-Na and/or high-K diets had no effects on BP. In SHR, Na load accelerated the development of hypertension, whereas K supplementation did not affect BP of normal-Na SHR but attenuated the increase in BP with Na load. Correspondingly, Na load in SHR significantly increased renal vascular resistance (RVR), and K supplementation attenuated the increased RVR of Na-loaded SHR. Moreover, Na space of SHR was increased compared with that of WKY, and although Na load did not affect Na space, K supplementation tended to decrease Na space in SHR. These results indicate that 9-wk-old SHR is relatively volume-expanded compared with age-matched WKY, and K supplementation could improve the lowered slope of the pressure-Na excretion relationship in SHR, resulting in maintenance of Na balance. Thus the data suggest that changes in RVR, which might be intimately related to renal function for Na excretion, contribute to both salt sensitivity of SHR and antihypertensive action of K supplementation in Na-loaded SHR.

scholarly journals D-α-tocopherol reduces renal damage in hypertensive rats

2012 ◽  
Vol 48 (2) ◽  
pp. 291-298 ◽  
Author(s):  
Thaís Maria da Fonseca Pletiskaitz ◽  
Guiomar Nascimento Gomes
Keyword(s):  
Renal Damage ◽  
Thiobarbituric Acid ◽  
Thiobarbituric Acid Reactive Substances ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Functional Changes ◽  
Beneficial Effects ◽  
Renal Vascular ◽  
Volume Retention ◽  
Normotensive Control

This study investigated the beneficial effects of D-α-tocopherol supplementation in protecting against the renal morphological and functional changes caused by hypertension. Spontaneously hypertensive (SHR) and normotensive control (WKY) rats received D-α-tocopherol (80 mg/kg by gavage) or vehicle (mineral oil) every other day for 60 days, from the age of 2 months. After this treatment period, all animals were assessed for renal morphological and functional parameters. The glomerular hypertrophy, increased interlobular wall thickness and enlarged renal vascular resistance found in SHR were reduced by D-α-tocopherol treatment. Sodium and volume retention observed in SHR were also decreased by D-α-tocopherol treatment. Moreover, D-α-tocopherol supplementation significantly reduced arterial pressure in SHR but not in WKY. D-α-tocopherol also reduced the excretion of thiobarbituric acid-reactive substances (TBARS), a marker of oxidative stress, in SHR. These results suggest that D-α-tocopherol supplementation can reduce kidney damage induced by hypertension.

scholarly journals Chronic recurrent dehydration associated with periodic water intake exacerbates hypertension and promotes renal damage in male spontaneously hypertensive rats

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Lucinda M. Hilliard ◽  
Katrina M. Mirabito Colafella ◽  
Louise L. Bulmer ◽  
Victor G. Puelles ◽  
Reetu R. Singh ◽  
...  
Keyword(s):  
Water Intake ◽  
Spontaneously Hypertensive Rats ◽  
Renal Damage ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive
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