Acute renal denervation produces a diuresis and natriuresis in young SHR but not WKY rats

1986 ◽  
Vol 251 (4) ◽  
pp. F655-F661 ◽  
Author(s):  
M. A. Rudd ◽  
R. S. Grippo ◽  
W. J. Arendshorst
Keyword(s):  
Sodium Excretion ◽  
Renal Denervation ◽  
Strain Differences ◽  
Urine Flow ◽  
Sprague Dawley ◽  
Renal Vasculature ◽  
Renal Nerve ◽  
Water Excretion ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

Clearance experiments were conducted to determine the effect of acute unilateral renal denervation (DNX) on renal hemodynamics and salt and water excretion in anesthetized 6-wk-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto genetic control rats (WKY). Before DNX, SHR had higher mean arterial pressure (33%) and renal vascular resistance (RVR) (57%) and lower glomerular filtration rate (GFR) (10%); urine flow and sodium excretion were similar. Following DNX in SHR, sodium and water excretion increased by 138 and 62%, respectively (P less than 0.001); GFR and RVR were unchanged. In contrast, DNX in WKY did not affect urine flow (0%) or sodium excretion (-21%). These strain differences were observed in Okamoto-Aoki rats from two sources. Effective DNX was indicated by 95% reduction of norepinephrine content 3 days after DNX in both strains. Six-week-old Sprague-Dawley and Munich-Wistar rats, in contrast to WKY, responded to DNX with a natriuresis (+182%) and diuresis (+95%) (P less than 0.001). Renal function was unaffected by sham DNX in SHR. Our results indicate that efferent renal nerve activity has little tonic influence on the renal vasculature in these young rats. Augmented neurotransmitter release and/or tubular responsiveness may be involved in fluid and electrolyte retention and the pathogenesis of hypertension in SHR. Conversely, blunted renal neuroeffector responses may prevent WKY from developing hypertension.

Attenuation of enhanced tubuloglomerular feedback activity in SHR by renal denervation

1990 ◽  
Vol 258 (4) ◽  
pp. F980-F985 ◽  
Author(s):  
T. Takabatake ◽  
Y. Ushiogi ◽  
K. Ohta ◽  
N. Hattori
Keyword(s):  
Sodium Excretion ◽  
Renal Denervation ◽  
Ringer Solution ◽  
Urine Flow ◽  
Tubuloglomerular Feedback ◽  
Renal Nerves ◽  
Renal Vasculature ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Renal Vascular

We evaluated the effect of acute unilateral renal denervation (DNX) on the tubuloglomerular feedback (TGF) mechanism in Inactin-anesthetized hydropenic male 8- to 10-wk-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). SHR had higher mean arterial pressure (MAP, 28%) and renal vascular resistance (RVR, 35%), whereas renal blood flow (RBF), glomerular filtration rate (GFR), urine flow, and sodium excretion were similar. DNX in SHR did not change MAP but decreased RVR (26%) and increased RBF (29%), GFR (16%), urine flow (52%), and sodium excretion (431%). DNX did not affect these in WKY. Loop of Henle perfusion with Ringer solution reduced early proximal flow rate (EPFR) in SHR more than in WKY; significantly different at a loop flow of 20 nl/min (9.8 +/- 0.7 vs. 6.5 +/- 0.7 nl/min). DNX in SHR increased the nonperfused EPFR from 25.6 +/- 1.1 to 31.7 +/- 1.3 nl/min and reduced TGF responses during perfusion at both 20 nl/min (9.8 +/- 0.7 vs. 4.4 +/- 0.7 nl/min) and 40 nl/min (14.2 +/- 1.1 vs. 10.4 +/- 0.7 nl/min). TGF sensitivity was attenuated by DNX, as indicated by reduced maximum reactivity (-0.89 +/- 0.14 to -0.36 +/- 0.07) and increased turning point (16.5 +/- 0.9 to 25.2 +/- 2.9 nl/min). TGF responses in WKY were not influenced by DNX. Sham denervation did not alter renal hemodynamics and TGF. These results indicate that renal nerves exert a tonic influence on the renal vasculature and the TGF system in SHR but not in WKY. Enhanced TGF responsiveness may be involved in volume retention and in the maintenance of hypertension in SHR.

Role of sodium and water excretion in the antihypertensive effect of vasopressin in the spontaneously hypertensive rat

1992 ◽  
Vol 70 (10) ◽  
pp. 1309-1314 ◽  
Author(s):  
E. K. Y. Chiu ◽  
H. Wang ◽  
J. R. McNeill
Keyword(s):  
Arterial Pressure ◽  
Sodium Excretion ◽  
Spontaneously Hypertensive Rat ◽  
Control Level ◽  
Sprague Dawley ◽  
Water Excretion ◽  
Spontaneously Hypertensive ◽  
Vasopressin Infusion ◽  
Hypertensive Rat ◽  
Wistar Kyoto

Mean arterial pressure (mmHg (1 mmHg = 133.322 Pa)), sodium excretion rate (μmol∙kg−1∙min−1), and urine flow (μL∙kg−1∙min−1) were measured in conscious unrestrained spontaneously hyptertensive rats (SHR) and normotensive Wistar–Kyoto rats (WKY) before, during, and after a 3-h intravenous infusion of arginine vasopressin (20 ng∙kg−1∙min−1), an equipressor dose of phenylephrine, or an infusion of the vehicle. Cessation of the phenylephrine infusion was associated with a return of arterial pressure to preinfusion control values in both SHR and WKY. Cessation of the vasopressin infusion was also associated with a return of arterial pressure to preinfusion values in WKY. In contrast, in the SHR, arterial pressure fell from a preinfusion control level of 164 ± 6.2 to 137 ± 4 mmHg within 1 h of stopping the vasopressin infusion. Five hours after stopping the infusion, pressure was 134 ± 3 mmHg (29 ± 5 mmHg below preinfusion levels). Similar to the WKY, cessation of a vasopressin infusion was associated with a return of arterial pressure to preinfusion values in Sprague–Dawley rats. Thus, the failure to observe a hypotensive response in normotensive rats was not a peculiarity of the WKY strain. Sodium excretion rates increased during the infusions of vasopressin to a greater extent in SHR than in WKY. However, the natriuresis induced by phenylephrine was not significantly different from that generated by vasopressin in SHR, and in WKY, the natriuresis was greater for phenylephrine than for vasopressin. Urine output increased to a greater extent during the infusions of phenylephrine in both SHR and WKY than during vasopressin infusion. Because the infusions of phenylephrine were associated with either a similar or greater natriuresis and diuresis than the infusions of vasopressin, it is unlikely that the large fall in arterial pressure that occurred following the withdrawal of the vasopressin infusion (the "withdrawal-induced antihypertensive phenomenon") was related to the preceding natriuresis and diuresis.Key words: vasopressin, spontaneously hypertensive rat, sodium excretion, water excretion, renal function, phenylephrine.

High-NaCl diets increase natriuretic and diuretic responses in salt-resistant but not salt-sensitive SHR

1991 ◽  
Vol 260 (6) ◽  
pp. F890-F897 ◽  
Author(s):  
M. S. Mozaffari ◽  
S. Jirakulsomchok ◽  
Z. H. Shao ◽  
J. M. Wyss
Keyword(s):  
Arterial Pressure ◽  
Renal Denervation ◽  
Isotonic Saline ◽  
Renal Nerves ◽  
Sprague Dawley ◽  
Volume Loading ◽  
Spontaneously Hypertensive ◽  
Volume Load ◽  
Sprague Dawley Rats ◽  
Wistar Kyoto

This study tested the hypothesis that NaCl-sensitive spontaneously hypertensive rats (SHR-S) display a defect in natriuretic and diuretic responses to acute volume loading that contributes to the rise in arterial pressure observed when the rats are fed a high-NaCl diet. Seven-week-old SHR-S and NaCl-resistant SHR rats (SHR-R) and normotensive (Wistar-Kyoto and Sprague-Dawley rats) were fed high- or basal NaCl diets. After 2.5 wk on the diets, preinstrumented conscious rats received an intravenous infusion (5% body wt; 0.5 ml/min) of isotonic saline, and urine was collected through a bladder catheter for 90 min. Control rats on the high-NaCl diet (compared with basal) excreted a significantly greater percentage of Na+ and volume load. In contrast, SHR-S on high-NaCl diet (compared with basal) had a very small increase in natriuretic response and no increase in diuretic response to volume expansion. The effect of renal denervation on natriuretic and diuretic responses to volume load was tested. In SHR-R on 1 and 8% NaCl diets, renal denervation had little or no effect on these responses, suggesting that renal nerves do not play a prominent role in the dietary NaCl-induced increases in the natriuretic and diuretic responses to volume load. These results demonstrate that NaCl-resistant rats rapidly adapt to diets high in NaCl content with increased natriuretic and diuretic responses to acute volume loading. The failure of SHR-S to adapt to the dietary challenge may result in volume loading and a secondary increase in arterial pressure after feeding.

Impaired renal D1-like and D2-like dopamine receptor interaction in the spontaneously hypertensive rat

2001 ◽  
Vol 281 (4) ◽  
pp. R1071-R1078 ◽  
Author(s):  
Cecilia A. Ladines ◽  
Chunyu Zeng ◽  
Laureano D. Asico ◽  
Xiaoguang Sun ◽  
Felice Pocchiari ◽  
...  
Keyword(s):  
Dopamine Receptor ◽  
Sodium Excretion ◽  
Spontaneously Hypertensive Rat ◽  
Rank Order ◽  
Urine Flow ◽  
Receptor Interaction ◽  
Dopamine Receptor Agonist ◽  
Renal Tubules ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

D1-like (D1, D5) and D2-like (D2, D3, D4) dopamine receptors interact in the kidney to produce a natriuresis and a diuresis. Disruption of D1 or D3 receptors in mice results in hypertension that is caused, in part, by a decreased ability to excrete an acute saline load. We studied D1-like and D2-like receptor interaction in anesthetized spontaneously hypertensive rats (SHR) by the intrarenal infusion of Z-1046 (a novel dopamine receptor agonist with rank order potency of D3≥D4>D2>D5>D1). Z-1046 increased glomerular filtration rate (GFR), urine flow, and sodium excretion in normotensive Wistar-Kyoto rats but not in SHRs. The lack of responsiveness to Z-1046 in SHRs was not an epiphenomenon, because intrarenal cholecystokinin infusion increased GFR, urine flow, and sodium excretion to a similar extent in the two rat strains. We conclude that renal D1-like and D2-like receptor interaction is impaired in SHRs. The impaired D1-like and D2-like receptor interaction in SHRs is not caused by alterations in the coding sequence of the D3 receptor, the D2-like receptor expressed in rat renal tubules that has been shown to be involved in sodium transport. Because the diuretic and natriuretic effects of D1-like receptors are, in part, caused by an interaction with D2-like receptors, it is possible that the decreased Z-1046 action in SHRs is secondary to the renal D1-like receptor dysfunction in this rat strain.

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)

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.

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.

scholarly journals Open-loop analysis on sympathetically mediated arterial pressure and urine output responses in spontaneously hypertensive rats: effect of renal denervation

2021 ◽  
Vol 71 (1) ◽  
Author(s):  
Toru Kawada ◽  
Takuya Nishikawa ◽  
Satoru Suehara ◽  
Satoshi Sawada ◽  
Tetsuo Tanaka ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Urine Output ◽  
Spontaneously Hypertensive Rats ◽  
Renal Denervation ◽  
Sympathetic Innervation ◽  
Urine Flow ◽  
Hypertensive Rats ◽  
Loop Analysis ◽  
Intact Side ◽  
Spontaneously Hypertensive

AbstractPrimary acute sympathetic activation (PASA) causes a subsequent arterial pressure (AP) elevation. In this case, an antidiuretic effect via the renal innervation and pressure diuresis can act antagonistically on the kidneys. We examined the effect of PASA on urine output in spontaneously hypertensive rats (SHR) 4–7 days after unilateral renal denervation (RDN) (n = 9). The slope of the plot of urine flow versus AP was positive (0.120 ± 0.031 μL min−1 kg−1 mmHg−1) on the intact side, but it was less than 1/3 of the slope observed previously in normotensive Wistar–Kyoto rats (WKY). RDN did not normalize the slope of urine flow versus AP (0.179 ± 0.025 μL min−1 kg−1 mmHg−1, P = 0.098 versus the intact side). The urine flow at the operating point of the AP tended to be greater on the denervated than the intact side (29.0 ± 1.8 vs. 25.3 ± 1.9 μL min−1 kg−1, P = 0.055). The percent increase (17.2 ± 7.2%) was not different from that observed previously in WKY. Although high-resting sympathetic nerve activity is prerequisite for maintaining hypertension in SHR, the effect of sympathetic innervation on the urine output function was not greater than that in WKY.

A rapid bioassay for quantification of atrial natriuretic polypeptides

1987 ◽  
Vol 252 (5) ◽  
pp. R1009-R1014 ◽  
Author(s):  
K. Matsui ◽  
T. Kimura ◽  
K. Ota ◽  
M. Shoji ◽  
M. Inoue ◽  
...  
Keyword(s):  
Sodium Excretion ◽  
Urine Volume ◽  
Good Tool ◽  
Spontaneously Hypertensive ◽  
Assay Procedure ◽  
Rapid Bioassay ◽  
Wistar Kyoto ◽  
Dose Dependent ◽  
Atrial Natriuretic

A quantitative bioassay for the detection and quantification of atrial natriuretic polypeptides (ANPs) was developed in a pentobarbital-anesthetized rat. Ten percent mannitol in 0.9% saline was infused to achieve stable diuresis. The conductivity of the urine, urine flow, and blood pressure were continuously recorded. A bolus injection of synthetic alpha-human atrial natriuretic polypeptide (alpha-hANP) elicited dose-dependent increases in the urine conductivity, sodium excretion, and urine volume. Changes in the urine conductivity correlated significantly with the increase in sodium excretion. By use of changes in urine conductivity, biological ANP activity of crude rat atrial extract was determined. Atrial contents of ANP in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) were 25.5 +/- 1.2 microgram per atrium (n = 4) and 25.1 +/- 0.8 (n = 5) in euhydration. They were increased to 27.0 +/- 1.1 micrograms (n = 4) and 29.3 +/- 1.3 (n = 5, P less than 0.05), after 5-day water deprivation, respectively. This assay procedure provides a good tool for rapid and quantitative determination of ANPs.

Sign in / Sign up

Export Citation Format

Share Document