Impaired Transmission of Pressure to the Renal Interstitium in Spontaneous Hypertension

Physiology ◽  
1992 ◽  
Vol 7 (1) ◽  
pp. 23-26
Author(s):  
AA Khraibi
Keyword(s):  
Hydrostatic Pressure ◽  
Volume Expansion ◽  
Spontaneously Hypertensive Rats ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Renal Perfusion Pressure ◽  
Renal Interstitium ◽  
Wistar Kyoto

In Okamoto spontaneously hypertensive rats, compared with control Wistar-Kyoto rats, natriuretic and diuretic responses to increases in renal perfusion pressure are attenuated but with acute saline volume expansion they are exaggerated. The extent of elevations in renal interstitial hydrostatic pressure appears to determine the natriuretic and diuretic responses.

Abnormal pressure-diuresis-natriuresis response in spontaneously hypertensive rats

1985 ◽  
Vol 248 (2) ◽  
pp. F199-F205 ◽  
Author(s):  
R. J. Roman ◽  
A. W. Cowley
Keyword(s):  
Sodium Excretion ◽  
Spontaneously Hypertensive Rats ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Urine Flow ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Fourfold Increase ◽  
Renal Perfusion Pressure ◽  
Wistar Kyoto

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.

Implication of renal perfusion pressure in stroke of spontaneously hypertensive rats

1980 ◽  
Vol 238 (3) ◽  
pp. H317-H324 ◽  
Author(s):  
A. Nagaoka ◽  
A. Shino ◽  
M. Shibota
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Renal Cortex ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Hypertensive Rats ◽  
Cerebrovascular Lesions ◽  
Spontaneously Hypertensive ◽  
Renal Perfusion Pressure ◽  
Renal Changes ◽  
Renal Cortical Blood Flow

To elucidate the significance of hypertension associated with cerebrovascular lesions (CVL), renal perfusion pressure (RPP) was controlled by aortic clips of two different sizes in stroke-prone spontaneously hypertensive rats kept under normal or salt-loaded conditions. Tail and femoral arterial pressures (RPPs) in the mildly and severely clamped animals were reduced in proportion to the severity of the clamping. In contrast, carotid pressures in both clamped groups were significantly higher than that in the controls. Proteinuria and hyperreninemia accompanied by arteriolar changes in the renal cortex were observed in the controls prior to the onset of CVL. The renal changes were inhibited by both types of clamping. The onset of CVL was delayed by the mild clamping in salt-loaded animals, but accelerated by the severe clamping in both the normal and salt-loaded animals. Renal cortical blood flow was decreased only by the severe clamping. The results suggest that reduction in RPP and/or renal ischemia, which seems to be due to the hypertensive arteriolar changes in the renal cortex, may be related to the pathogenesis of CVL in the stroke-prone rats with or without hyperreninemia.

Mechanism of exaggerated diuresis in spontaneously hypertensive rats

1978 ◽  
Vol 235 (5) ◽  
pp. F409-F416 ◽  
Author(s):  
Gerald F. DiBona ◽  
Linda L. Rios
Keyword(s):  
Volume Expansion ◽  
Spontaneously Hypertensive Rats ◽  
Spontaneously Hypertensive Rat ◽  
Renal Perfusion ◽  
Sodium Reabsorption ◽  
Loop Of Henle ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Single Nephron ◽  
Wistar Kyoto

The mechanism of exaggerated diuresis and natriuresis was studied in spontaneously hypertensive rats (SHR) by renal clearance and micropuncture techniques. Control normotensive rats of the same age and sex [Wistar-Kyoto rats (WKY)] were also studied. During the hydropenic control and the volume-expansion experimental periods absolute and fractional water and sodium excretion were greater in SHR than in WKY. Although fractional and absolute water and sodium reabsorption were similar along the proximal convolution in SHR and WKY, fractional and absolute water reabsorption in Henle's loop was less in SHR than in WKY. Hydrostatic and colloid osmotic pressures in the cortical peritubular microvasculature were similar in WKY and SHR. Acute normalization of renal perfusion pressure by aortic constriction reversed the exaggerated diuresis and natriuresis in SHR by halving the filtered load of water and sodium; whole kidney and single nephron glomerular filtration rates and blood flows decreased by 50%. It is concluded that the exaggerated diuresis and natriuresis of the spontaneously hypertensive rat is caused by a decreased reabsorption in the loop of Henle. The mechanism of this decreased reabsorption in the loop of Henle cannot be explained by alterations in the measured physical forces in the renal cortical microvasculature. natriuresis; autoregulation; volume expansion Submitted on November 15, 1977 Accepted on June 7, 1978

Cerebral artery responses to pressure and flow in uremic hypertensive and spontaneously hypertensive rats

2003 ◽  
Vol 284 (4) ◽  
pp. H1212-H1216 ◽  
Author(s):  
D. I. New ◽  
A. M. S. Chesser ◽  
R. C. Thuraisingham ◽  
M. M. Yaqoob
Keyword(s):  
Blood Flow ◽  
Cerebral Artery ◽  
Spontaneously Hypertensive Rats ◽  
Perfusion Pressure ◽  
Hypertensive Rats ◽  
Independent Manner ◽  
Spontaneously Hypertensive ◽  
Cerebral Blood Flow Autoregulation ◽  
Wistar Kyoto ◽  
Normotensive Control

Impaired cerebral blood flow autoregulation is seen in uremic hypertension, whereas in nonuremic hypertension autoregulation is shifted toward higher perfusion pressure. The cerebral artery constricts in response to a rise in either lumen pressure or flow; we examined these responses in isolated middle cerebral artery segments from uremic Wistar-Kyoto rats (WKYU), normotensive control rats (WKYC), and spontaneously hypertensive rats (SHR). Pressure-induced (myogenic) constriction developed at 100 mmHg; lumen flow was then increased in steps from 0 to 98 μl/min. Some vessels were studied after endothelium ablation. Myogenic constriction was significantly lower in WKYU (28 ± 2.9%) compared with both WKYC (39 ± 2.5%, P = 0.035) and SHR (40 ± 3.1%, P = 0.018). Flow caused constriction of arteries from all groups in an endothelium-independent manner. The response to flow was similar in WKYU and WKYC, whereas SHR displayed increased constriction compared with WKYU ( P < 0.001) and WKYC ( P < 0.001). We conclude that cerebral myogenic constriction is decreased in WKYU, whereas flow-induced constriction is enhanced in SHR.

Altered muscle metabolism associated with vasoconstriction in spontaneously hypertensive rats

1998 ◽  
Vol 275 (6) ◽  
pp. E1007-E1015 ◽  
Author(s):  
Ji-Ming Ye ◽  
Eric Q. Colquhoun
Keyword(s):  
Glucose Uptake ◽  
Spontaneously Hypertensive Rats ◽  
Perfusion Pressure ◽  
Lactate Production ◽  
Ang Ii ◽  
Hypertensive Rats ◽  
Response Curves ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

In the rat muscle vascular bed, vasoconstrictors either increase or decrease oxygen consumption (V˙o 2). The present study compared the effects of norepinephrine (NE), angiotensin II (ANG II), and 5-hydroxytryptamine (5-HT) on vasoconstriction-associated metabolism in the constant-flow perfused hindlimb of spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) in the absence of insulin. Basal perfusion pressure,V˙o 2, glucose uptake, and lactate production were increased by 21.4, 11.9, 46.4, and 44.9% ( P < 0.05 for all), respectively, in SHR, which also had higher blood pressure and metabolic rate ( P < 0.05) in vivo. Dose-response curves for NE-induced perfusion pressure,V˙o 2, and lactate production in SHR were shifted to the left compared with WKY. Associated with the increased perfusion pressure, NE-inducedV˙o 2 and glucose uptake were both decreased ( P < 0.01), particularly at high concentrations. These differences were unaffected by 10 μM propranolol but were all diminished by further addition of prazosin (2.5 nM). ANG II stimulatedV˙o 2, glucose uptake, and lactate production in both strains, but the increased lactate production was smaller in SHR ( P < 0.05) with a proportional decrease ( P< 0.05) in glucose uptake. Conversely, 5-HT decreasedV˙o 2 in both strains ( P < 0.01), and this effect was greater in SHR ( P < 0.01). These data suggest that SHR muscle thermogenesis and glucose uptake are impaired during vasoconstriction, especially in response to NE.

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.

Abnormalities in kallikrein excretion in spontaneously hypertensive rats

1985 ◽  
Vol 248 (3) ◽  
pp. F396-F403 ◽  
Author(s):  
J. L. Ader ◽  
D. M. Pollock ◽  
M. I. Butterfield ◽  
W. J. Arendshorst
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Strain Differences ◽  
Renal Perfusion ◽  
Pressure Level ◽  
Urine Flow ◽  
Analysis Of Covariance ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Level Analysis

Experiments were conducted to examine kallikrein excretion in 12-wk-old anesthetized and conscious Okamoto-Aoki spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). Urinary excretion of active and total kallikrein was determined at spontaneous pressures and in response to acute decreases in renal perfusion pressure (RPP; suprarenal aortic constriction). Under basal conditions, active kallikrein excretion was lower in SHR compared with WKY whether conscious (4.4 +/- 1.7 vs. 9.4 +/- 1.3 pkat . min-1 . g kidney wt-1) or anesthetized (5.7 +/- 1.3 vs. 10.4 +/- 1.7). In both anesthetized SHR and WKY, excretion of active and total kallikrein was directly related to RPP after 20 mmHg decrements in RPP and was depressed in SHR at each pressure level. The slope of the relation between active kallikrein excretion and pressure was less in SHR (0.06 +/- 0.01 vs. 0.14 +/- 0.05 pkat . min-1 . g kidney wt-1 . mmHg-1). Thus kallikrein excretion is set at a lower level in SHR and is less responsive to changes in RPP. These strain differences are not related to urine flow, Na excretion, or glomerular filtration rate (GFR) since the values were the same in both strains at each pressure level. Analysis of covariance indicated a significant correlation between active kallikrein excretion and RPP in WKY and SHR, with RPP accounting for 92% of the variation in the kallikrein data. GFR, Na excretion, and urine flow rate were not significantly correlated to active kallikrein and were responsible for only 2% of the variation.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Enhanced myogenic response in the afferent arteriole of spontaneously hypertensive rats

2010 ◽  
Vol 298 (6) ◽  
pp. H1769-H1775 ◽  
Author(s):  
YiLin Ren ◽  
Martin A. D'Ambrosio ◽  
Ruisheng Liu ◽  
Patrick J. Pagano ◽  
Jeffrey L. Garvin ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Perfusion Pressure ◽  
Intraluminal Pressure ◽  
Myogenic Response ◽  
Afferent Arteriole ◽  
Hypertensive Rats ◽  
Luminal Diameter ◽  
Spontaneously Hypertensive ◽  
Before And After ◽  
Wistar Kyoto

Spontaneously hypertensive rats (SHRs) have normal glomerular capillary pressure even though renal perfusion pressure is higher, suggesting that preglomerular vessels exhibit abnormally high resistance. This may be due to increased superoxide (O2−) production, which contributes to the vasoconstriction in hypertension. We tested the hypothesis that the myogenic response of the afferent arteriole (Af-Art) is exaggerated in SHRs because of increased levels of reactive oxygen species (ROS). Single Af-Arts were microdissected from kidneys of SHRs and Wistar-Kyoto (WKY) rats and microperfused in vitro. When perfusion pressure in the Af-Art was increased stepwise from 60 to 140 mmHg, the luminal diameter decreased by 8.4 ± 2.9% in WKY Af-Arts but fell by 29.3 ± 5.6% in SHR Af-Arts. To test whether ROS production is enhanced during myogenic response in SHRs, we measured chloromethyl-dichlorodihydrofluorescein diacetate acetyl ester (CM-H2DCFDA) florescence before and after increasing intraluminal pressure from 60 to 140 mmHg. Pressure-induced increases in ROS were fourfold greater in SHR Af-Arts compared with WKY Af-Arts (SHR, 48.0 ± 2.2%; and WKY, 12.2 ± 0.3%). To test whether O2− contributes to the myogenic response in SHRs, either the membrane-permeant O2− scavenger Tempol or the nox2-based NADPH oxidase (NOX2) inhibitor gp91 ds-tat were added to the Af-Art lumen and bath and the myogenic response was tested before and after treatment. Both Tempol (10−4 M) and gp91 ds-tat (10−5 M) significantly attenuated the pressure-induced constriction in SHR Af-Arts but not in WKY Af-Arts. We conclude that 1) pressure-induced constriction is exaggerated in SHR Af-Arts, 2) NOX2-derived O2− may contribute to the enhanced myogenic response, and 3) O2− exerts little influence on the myogenic response under normotensive conditions.

Body fluid volumes in prehypertensive spontaneously hypertensive rats

1983 ◽  
Vol 244 (5) ◽  
pp. H652-H655 ◽  
Author(s):  
M. M. Mullins
Keyword(s):  
Volume Expansion ◽  
Body Fluid ◽  
Spontaneously Hypertensive Rats ◽  
Interstitial Fluid ◽  
Extracellular Fluid ◽  
Plasma Aldosterone ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Total Body

To ascertain the effect of aldosterone on body fluid volumes in neonatal, prehypertensive spontaneously hypertensive rats (SHR), we studied these animals at 12 days using age-matched Wistar-Kyoto (WKY) as normotensive controls. Some pups of each strain were treated with spironolactone (1.5 micrograms/g body wt) on days 10-12. Total body water (TBW, by dessication) and extracellular fluid (ECF, Na2 35SO4 space) volumes were significantly larger in SHR than in WKY, whereas plasma volumes (125I-serum albumin space) were not different. Thus the enlarged ECF was due to preferential expansion of the interstitial fluid (ISF) space. Treatment of SHR with spironolactone reduced TBW and ISF to values not different from untreated WKY and also reduced plasma volume to some extent. These results indicate 1) significant ISF volume expansion occurs in SHR prior to elevation of blood pressure, and 2) the previously observed elevation in plasma aldosterone in SHR at this age probably mediates the volume expansion.

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.

Sign in / Sign up

Export Citation Format

Share Document