Chronic treatment with losartan and carvedilol differentially modulates renal vascular responses to sympathomimetics compared to treatment with individual agents in normal Wistar Kyoto and spontaneously hypertensive rats

2009 ◽  
Vol 612 (1-3) ◽  
pp. 69-74 ◽  
Author(s):  
Mohammed H. Abdulla ◽  
Munavvar A. Sattar ◽  
Nor A. Abdullah ◽  
Md. Abdul H. Khan ◽  
H.H. AbdAllah ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Chronic Treatment ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Vascular Responses ◽  
Wistar Kyoto ◽  
Renal Vascular

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.

Resetting of renal blood flow autoregulation in spontaneously hypertensive rats

1987 ◽  
Vol 252 (3) ◽  
pp. F480-F486 ◽  
Author(s):  
B. M. Iversen ◽  
I. Sekse ◽  
J. Ofstad
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Spontaneously Hypertensive Rats ◽  
Lower Pressure ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Pressure Limit ◽  
Wistar Kyoto ◽  
Renal Vascular ◽  
Renal Blood Flow Autoregulation

Renal blood flow (RBF) autoregulation was examined in untreated 10- and 40-wk-old spontaneously hypertensive rats (SHR) [mean arterial pressure (MAP) 125 +/- 4 and 167 +/- 7 mmHg] and in captopril-treated (7 days) 10- and 40-wk-old SHR (88 +/- 7 and 112 +/- 5 mmHg). Age-matched Wistar-Kyoto rats (WKY) were used as controls (MAP 91 +/- 3 and 104 +/- 2 mmHg). The study was carried out in rats with and without acute uninephrectomy. In 10-wk-old acutely uninephrectomized animals, the lower pressure limit of autoregulation was 78 +/- 4 mmHg in WKY, 102 +/- 5 mmHg in SHR (P less than 0.02), and 78 +/- 7 mmHg in captopril-treated SHR (P greater than 0.10). The renal vascular resistance (RVR) was significantly elevated at the lower pressure limit of RBF autoregulation in untreated SHR (P less than 0.02) but became normal after treatment (P greater than 0.10). Neither uninephrectomy nor variation of RBF between different batches seemed to influence the lower pressure limit of RBF autoregulation. In 40-wk-old acutely nephrectomized animals, the lower pressure limit of RBF autoregulation in WKY was 85 +/- 4 mmHg, 128 +/- 3 mmHg in SHR (P less than 0.001), and 101 +/- 5 mmHg in captopril-treated SHR (P less than 0.01). RVR at the lower pressure limit was increased in untreated SHR (P less than 0.01), but fell to normal values during captopril treatment. Neither the uninephrectomy nor variation of RBF between different batches of rats seemed to influence the lower pressure limit of RBF autoregulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Renal hemodynamics and sodium excretion in stroke-prone spontaneously hypertensive rats

1981 ◽  
Vol 241 (3) ◽  
pp. F244-F249 ◽  
Author(s):  
A. Nagaoka ◽  
M. Kakihana ◽  
M. Suno ◽  
K. Hamajo
Keyword(s):  
Arterial Pressure ◽  
Sodium Excretion ◽  
Spontaneously Hypertensive Rats ◽  
Renal Perfusion ◽  
Renal Hemodynamics ◽  
Hypertensive Rats ◽  
Water Excretion ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Renal Vascular

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.

Spontaneously hypertensive rats demonstrate increased renal vascular alpha 1-adrenergic receptor responsiveness

1991 ◽  
Vol 260 (5) ◽  
pp. R889-R893 ◽  
Author(s):  
K. Uchino ◽  
E. D. Frohlich ◽  
T. Nishikimi ◽  
T. Isshiki ◽  
M. B. Kardon
Keyword(s):  
Arterial Pressure ◽  
Adrenergic Receptor ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Renal Vasculature ◽  
Spontaneously Hypertensive ◽  
Arteriolar Resistance ◽  
Proximal Tubular ◽  
Wistar Kyoto ◽  
Renal Vascular

To determine alpha 1-adrenergic receptor responsiveness of the renal vasculature in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR), phenylephrine (2.5 or 5.0 micrograms.kg-1.min-1 iv) or saline was infused. Effective renal blood flow (ERBF) and glomerular filtration rate were determined by p-aminohippuric acid and inulin clearances, respectively. Peritubular capillary, proximal tubular, and stop-flow pressures (SFP) were measured by micropuncture. Phenylephrine decreased ERBF (6.27 +/- 0.48 to 4.55 +/- 0.65 ml.min-1.g-1; P less than 0.05) and increased arterial pressure and SFP (31.5 +/- 0.9 to 34.2 +/- 1.0 mmHg) in SHR. It only increased arterial pressure and ERBF in WKY without changing SFP. Afferent arteriolar resistance (RA) and glomerular capillary pressure (PG) remained unchanged, whereas efferent resistance (RE) decreased in WKY; in contrast, RA, RE, and PG increased in SHR (RA 21.2 +/- 2.0 to 38.1 +/- 7.1 mmHg.ml-1.min.g, RE 6.9 +/- 0.6 to 13.9 +/- 3.8 mmHg.ml-1.min.g; and PG 49.6 +/- 0.9 to 53.7 +/- 1.1 mmHg; all P less than 0.05). These data demonstrated increased SHR afferent and efferent arteriolar responsiveness; WKY efferent arteriolar hyperresponsiveness was not observed. The findings support the concept of augmented intrarenal vascular alpha 1-adrenergic responsiveness in hypertension that may predispose to subsequent glomerular hypertension.

Membrane potential of vascular smooth muscle and hypertension in spontaneously hypertensive rats

1984 ◽  
Vol 62 (8) ◽  
pp. 957-960 ◽  
Author(s):  
D. W. Cheung
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Membrane Potential ◽  
Vascular Smooth Muscle ◽  
Spontaneously Hypertensive Rats ◽  
Chronic Treatment ◽  
Resting Membrane Potential ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

The resting membrane potential of tail arteries from spontaneously hypertensive rats (SHRs) and Wistar-Kyoto controls (WKYs) was compared. At 4–5 weeks old, the blood pressure and resting membrane potential of the SHRs was not significantly different from the WKYs. The blood pressure of 8- to 10-week-old SHRs increased significantly to 183 mmHg (1 mmHg = 133.322 Pa) from 127 mmHg at 4 weeks, and the membrane potential decreased from 60 to 51 mV. At 15 weeks of age, the blood pressure of the SHRs was 193 mmHg and the membrane potential was 49 mV. In WKYs, there was no significant change in membrane potential with age. The decrease in membrane potential in the SHRs is due to a decrease in the ouabain-sensitive electrogenic pumping. Chronic treatment of the SHRs with captopril (100 mg∙kg−1∙day−1) prevented the increase in blood pressure and the decrease in membrane potential.

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.

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