Aberrant regulation of renal dopamine D3 receptor on sodium excretion in salt-loaded Wistar–Kyoto and spontaneously hypertensive rats

2009 ◽  
Vol 137 ◽  
pp. S70
Author(s):  
C.Q. YU ◽  
W.B. SHI ◽  
J. YANG ◽  
C.J. FU ◽  
D.F. HEN ◽  
...  
1993 ◽  
Vol 264 (4) ◽  
pp. R726-R732 ◽  
Author(s):  
R. A. Felder ◽  
S. Kinoshita ◽  
K. Ohbu ◽  
M. M. Mouradian ◽  
D. R. Sibley ◽  
...  

The coupling between the dopamine1 (DA1) receptor and the G protein/adenylyl cyclase (AC) enzyme complex is defective in the proximal convoluted tubule (PCT) of 20-wk-old spontaneously hypertensive rats (SHRs). Because this coupling defect could have been due to desensitization secondary to elevated renal dopamine levels in the adult animal, we studied the interaction between DA1 receptors and AC in PCT of rats as early as 3 wk of age, a time when renal dopamine levels are similar in SHRs and their normotensive controls (Wistar-Kyoto rats, WKYs). Maximum receptor density did not change with age and was similar in WKYs and SHRs in all the age groups studied (3, 8, and 20 wk). Basal-, forskolin-, and guanyl nucleotide-stimulated AC activities were also similar in WKYs and SHRs and did not change with age. However, the DA1 agonist-stimulated AC activity was greater in WKYs than in SHRs and increased with age in WKYs but not in SHRs. Moreover, the ability of a nonhydrolyzable analogue of GTP, Gpp(NH)p, to enhance DA1 agonist (SND-919-C12, 1 microM)-stimulated AC activity increased with age in WKY but not in SHRs. To determine if the defect noted in the PCT of SHRs is due to a defective D1A receptor gene, parallel studies were performed in the striatum, since this receptor is expressed predominantly in the latter tissue. In contrast to the results in PCT, radioligand binding and AC studies in striatum revealed no differences between WKYs and SHRs.(ABSTRACT TRUNCATED AT 250 WORDS)


1981 ◽  
Vol 241 (3) ◽  
pp. F244-F249 ◽  
Author(s):  
A. Nagaoka ◽  
M. Kakihana ◽  
M. Suno ◽  
K. Hamajo

Renal blood flow (RBF), renal vascular resistance (RVR), glomerular filtration rate (GFR), and sodium and water excretion were measured in anesthetized stroke-prone spontaneously hypertensive rats (SHRSP), spontaneously hypertensive rats (SHR), and control Wistar-Kyoto rats (WKY) at 9 wk of age. Mean arterial pressure in SHRSP and SHR was significantly higher than that in WKY. RBF was slightly increased in SHR and decreased in SHRSP. RVR was markedly elevated only in SHRSP. In both strains of SHR, GFR was significantly increased but water and sodium excretion were similar. When renal perfusion pressure in both strains of SHR was reduced to a level similar to that of WKY by aortic constriction, RBF was slightly but significantly reduced in both SHRSP and SHR, and GFR only in SHRSP. RVR in SHRSP was still higher. Sodium and water excretion were markedly decreased in both SHR and SHRSP. The data suggest that SHRSP are characterized by an alteration in renal hemodynamics at a young age and support the hypothesis that kidneys of SHR require a higher arterial pressure than kidneys of WKY to excrete a given amount of salt and water.


1985 ◽  
Vol 248 (2) ◽  
pp. F199-F205 ◽  
Author(s):  
R. J. Roman ◽  
A. W. Cowley

The renal responses to changes in perfusion pressure (RPP) were studied in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) to determine whether an abnormality in the pressure-diuresis phenomenon could be involved in the resetting of kidney function in hypertension. Differences in the neural and endocrine background to the kidneys were minimized by denervating the kidney and by holding plasma vasopressin, aldosterone, corticosterone, and norepinephrine levels constant by intravenous infusion. In WKY, increasing renal perfusion pressure 54 mmHg, from 103 to 157 mmHg, produced a ninefold increase in urine flow and sodium excretion with no measurable change in renal blood flow (RBF) or glomerular filtration rate (GFR). In SHR, increasing renal perfusion pressure 54 mmHg, from 133 to 187 mmHg, produced only a fourfold increase in urine flow and sodium excretion. GFR, RBF, and peritubular capillary pressures were well autoregulated and were similar in the SHR and WKY at pressures above 110 mmHg. These results indicate the presence of intrinsic changes in the kidney of SHR that enhance fractional tubular reabsorption and impair the pressure-diuresis response. This blunting of the renal pressure-diuresis phenomenon in SHR may represent the functional resetting of the kidney that is necessary for sustained hypertension.


1995 ◽  
Vol 78 (1) ◽  
pp. 101-111 ◽  
Author(s):  
J. M. Lash ◽  
H. G. Bohlen

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.


Biomedicines ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 676
Author(s):  
Kunanya Masodsai ◽  
Yi-Yuan Lin ◽  
Sih-Yin Lin ◽  
Chia-Ting Su ◽  
Shin-Da Lee ◽  
...  

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.


1991 ◽  
Vol 81 (1) ◽  
pp. 107-112 ◽  
Author(s):  
K. Fujito ◽  
M. Yokomatsu ◽  
N. Ishiguro ◽  
H. Numahata ◽  
Y. Tomino ◽  
...  

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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