Possible contribution of impaired sodium excretion to the development and maintenance of hypertension: a study of the isolated kidneys of the Prague hypertensive rat

1997 ◽  
Vol 434 (5) ◽  
pp. 587-591 ◽  
Author(s):  
Ivana Vaněčková ◽  
Jiří Heller ◽  
Klaus Thurau
Keyword(s):  
Sodium Excretion ◽  
Hypertensive Rat ◽  
Prague Hypertensive Rat ◽  
Isolated Kidneys

Interactions between ADH and prostaglandins in isolated erythrocyte-perfused rat kidney

1987 ◽  
Vol 252 (2) ◽  
pp. F331-F337 ◽  
Author(s):  
W. Lieberthal ◽  
M. L. Vasilevsky ◽  
C. R. Valeri ◽  
N. G. Levinsky
Keyword(s):  
Sodium Excretion ◽  
Rat Kidney ◽  
Urine Osmolality ◽  
Sodium Reabsorption ◽  
Urinary Osmolality ◽  
Hemodynamic Characteristics ◽  
Urinary Concentrating Ability ◽  
Tubular Morphology ◽  
Isolated Kidneys

Interactions between antidiuretic hormone (ADH) and renal prostaglandins in the regulation of sodium reabsorption and urinary concentrating ability were studied in isolated erythrocyte-perfused rat kidneys (IEPK). In this model, hemodynamic characteristics are comparable to those found in vivo, and tubular morphology is preserved throughout the period of perfusion. [Deamino]-D-arginine vasopressin (dDAVP) markedly reduced fractional sodium excretion (FE Na) in the IEPK from 3.5 +/- 0.6 to 0.45 +/- 0.14%. After indomethacin, FE Na fell still further to 0.08 +/- 0.02%. In the absence of dDAVP indomethacin had no effect on sodium excretion; FE Na was 2.4 +/- 0.6% in control and 2.0 +/- 0.4% in indomethacin-treated groups. dDAVP increased urine osmolality in the IEPK to 741 +/- 26 mosmol/kg. When prostaglandin synthesis was blocked with indomethacin, urinary osmolality increased further to 1,180 +/- 94 mosmol/kg. In isolated kidneys perfused without erythrocytes (IPK), dDAVP decreased FENa from 14.5 +/- 1.8% to 9.6 +/- 1.2%; addition of indomethacin had no further effect. dDAVP increased urine osmolality only modestly to 350 +/- 12 mosmol/kg in the IPK and indomethacin did not increase concentrating ability further (342 +/- 7 mosmol/kg). Thus the IEPK (unlike the IPK) can excrete a markedly hypertonic urine in response to ADH. ADH also enhances tubular reabsorption of sodium in the IEPK. Prostaglandins inhibit both these actions of ADH but do not directly affect sodium excretion in the absence of the hormone.

The renal endothelin system in the Prague hypertensive rat, a new model of spontaneous hypertension

1999 ◽  
Vol 97 (1) ◽  
pp. 91 ◽  
Author(s):  
Volker VOGEL ◽  
Angela BÄCKER ◽  
Jiri HELLER ◽  
Herbert J. KRAMER
Keyword(s):  
Spontaneous Hypertension ◽  
New Model ◽  
Hypertensive Rat ◽  
Endothelin System ◽  
Prague Hypertensive Rat

The renal endothelin system in the Prague hypertensive rat, a new model of spontaneous hypertension

1999 ◽  
Vol 97 (1) ◽  
pp. 91-98 ◽  
Author(s):  
Volker VOGEL ◽  
Angela BÄCKER ◽  
Jiri HELLER ◽  
Herbert J. KRAMER
Keyword(s):  
Renal Cortex ◽  
Renal Tissue ◽  
Spontaneous Hypertension ◽  
Mrna Levels ◽  
New Model ◽  
Total Rna ◽  
Peptide Concentration ◽  
Hypertensive Rat ◽  
Mrna Content ◽  
Prague Hypertensive Rat

In a new model of spontaneous hypertension, namely the Prague hypertensive rat (PHR), hypertension is transferred with a kidney transplanted from the PHR to its normotensive counterpart (PNR) by an as yet unknown mechanism. One candidate may be endothelin (ET), since this potent vasoconstrictor affects vascular tone, renal haemodynamics and renal excretory function, and all members of this peptide family are located within the kidney and act in an autocrine/paracrine fashion. In the present study we investigated, in the renal tissue of PHRs and PNRs: (1) preproET-1 and preproET-3 mRNAs as well as ET-1 and ET-3 peptide distribution, (2) endothelin-converting enzyme (ECE)-1 mRNA expression, and (3) ET receptors and their characteristics in membranes of glomeruli and papillae. In addition, plasma ET concentration and urinary ET excretion were determined. Quantitative measurements by competitive reverse transcription-polymerase chain reaction revealed ET-1 mRNA levels in the renal cortex from PHRs and PNRs of 1.09±0.13 and 1.29±0.18 amol/µg of total RNA respectively, and in red medulla of 2.72±0.82 and 3.30±0.68 amol/µg respectively. In contrast, renal papilla from PHRs showed significantly lower levels of preproET-1 mRNA (1.81±0.64 amol/µg of total RNA, compared with 4.25±0.82 amol/µg in PNRs; each n = 5; P< 0.05). The ET-1 peptide concentration in papillary tissue was also significantly lower in PHRs than in PNRs (120.2±30.8 and 491.3±53.4 fmol/mg of protein respectively; n = 5; P< 0.01), whereas it was similar in cortex and medulla from PHRs and PNRs. The preproET-3 mRNA content in renal tissue was much lower than that of preproET-1 mRNA. It was significantly higher in red medulla from PHRs compared with that from PNRs (0.25±0.05 and 0.13±0.02 amol/µg of total RNA respectively; P< 0.05), but was similar in papillae of PHRs and PNRs (0.04±0.02 and 0.05±0.01 amol/µg respectively; n = 5). Cortical preproET-3 mRNA was at the lower limit of detection. Similarly, the ET-3 peptide concentration was slightly but significantly higher in the red medulla of PHRs compared with PNRs (15.4±2.0 and 8.8±0.8 fmol/mg of protein respectively; n = 5; P< 0.05), whereas no differences in ET-3 peptide concentration were found in papillae from PHRs and PNRs. ECE-1 mRNA levels were similar in the renal cortex, red medulla and papillae from PHRs and PNRs, ranging between 0.34±0.03 and 0.56±0.12 amol/µg of total RNA. Of the total ET receptors in glomerular membranes, 39% were ETA receptors, whereas papillary membranes contained exclusively ETB receptors. PHRs and PNRs showed similar Bmax and Kd values for ET-1 in renal glomerular membranes (Bmax, 6.5±1.3 and 4.9±1.2 pmol/mg of protein respectively; Kd, 0.69±0.10 and 0.56±0.10 nM respectively) and papillary membranes (Bmax, 9.7±1.1 and 11.3±1.6 pmol/mg of protein respectively; Kd, 0.30±0.04 and 0.42±0.07 nM respectively). Plasma ET-1/2 concentrations (10.4±1.3 and 12.2±1.2 fmol/ml in PHRs and PNRs respectively) and urinary ET-1 excretion (3.1±0.3 and 3.0±0.2 pmol/24 h in PHRs and PNRs respectively) were similar in hypertensive and normotensive rats. In summary, although tissue levels of preproET-3 mRNA were very low in the kidney, significantly greater amounts of preproET-3 mRNA and ET-3 peptide were found in medullary tissue from PHRs compared with PNRs, a finding that awaits further investigation. In contrast, the preproET-1 mRNA content and ET-1 peptide concentration were significantly lower in papillary tissue from PHRs compared with PNRs. Decreased synthesis of ET-1, which normally antagonizes the action of [Arg8]vasopressin, may allow increased water (and sodium) reabsorption at the level of the inner medullary collecting duct. This intrinsic defect of the kidney in the PHR may contribute to hypertension in this model, and may transmit high blood pressure on transplantation of the ‘hypertensive’ kidney into a normotensive rat.

Effect of potassium concentration and ouabain on the renal adaptation to potassium depletion in isolated perfused rat kidney

1986 ◽  
Vol 64 (11) ◽  
pp. 1427-1433 ◽  
Author(s):  
Daniel B. Ornt
Keyword(s):  
Sodium Excretion ◽  
Rat Kidney ◽  
Control Diet ◽  
Kidney Tissue ◽  
Renal Tissue ◽  
Renal Adaptation ◽  
Low K ◽  
K Depletion ◽  
Isolated Kidneys

Renal adaptation for potassium (K) conservation has been demonstrated in isolated perfused kidneys from rats within 3 days of K depletion and appears to be independent of aldosterone and sodium excretion. This study was designed to investigate whether the renal adaptation for K conservation is independent of ambient [K] and renal tissue levels of K and whether ouabain may have effects on K excretion, which are in constrast to the effects on K excretion in normal animals, in the first study, rats K depleted for 3 days received 2500 μequiv. KCl intraperitoneally, while other K-depleted rats and a group of control diet animals received intraperitoneal H2O alone to determine whether simple restoration of K deficits would reverse the renal adaptation for K conservation. Intraperitoneal KCl increased plasma [K] and kidney tissue K significantly within 3 h in the K-repleted group compared with the K-depleted rats. Isolated kidneys were perfused from the three groups of rats 3 h after intraperitoneal injection. Despite K repletion in vivo, perfused kidneys from the K-repleted group still had significantly decreased K excretion (1.28 ± 0.085 μequiv./min) compared with controls (2.05 ± 0.291 μequiv./min), and K excretion was still not different from the K-depleted group (0.57 ± 0.134 μequiv./min). However, fractional K excretion by the kidneys from K-repleted rats was increased above K-depleted kidneys (0.48 ± 0.051 vs. 0.18 ± 0.034, p < 0.01). Despite the increased renal tissue K in K-repleted kidneys at the start of perfusion (285 ± 5.1 vs. 257 ± 5.4 μequiv./g), by the end of the perfusion tissue K in perfused kidneys was identical in all three groups. In the second study, isolated kidneys were perfused from 3-day K-depleted or control rats with either 2 or 6 mM [K] in the perfusate. Isolated kidneys adapted to 3 days of K depletion excreted less K at both 2 and 6 mM [K] compared with controls at the same ambient [K]. The linear relationship of K excretion to perfusate [K] was significantly different in controls compared with low K adapted kidneys (p < 0.001). Finally, when 10−4 M ouabain was added after 60 min of perfusion in kidneys from control diet rats, there was a sodium diuresis and fractional K excretion decreased significantly (0.55 ± 0.043 to 0.32 ± 0.044, p < 0.01). However, in low K adapted kidneys, ouabain had no effect on fractional K excretion (0.020 ± 0.051 to 0.18 ± 0.038) despite a similar increase in sodium excretion. Perfusions of kidneys from 3-day K-depleted rats at 4 × 10−3 M ouabain gave similar results, showing no change in fractional K excretion. Low K adaptation to K depletion developed within 3 days and was not totally abolished by acute K repletion. Maneuvers that favored either a decrease in renal tissue K or an increase in tissue K did not reverse low K adaptation, although renal tissue K levels did alter the rate of K excretion in both controls and K-depleted kidneys. Therefore, a reduction in tissue K was clearly not the sole mediator of renal K conservation. Finally, the markedly different response of low K adapted kidneys to ouabain compared with controls strongly suggests a mechanism for K reabsorption that developed within 3 days of K depletion and is ouabain sensitive.

scholarly journals Glomerulus number and blood pressure in the Prague hypertensive rat

1998 ◽  
Vol 54 ◽  
pp. S211-S212 ◽  
Author(s):  
Helene Hellmann ◽  
John M. Davis ◽  
Klaus Thurau
Keyword(s):  
Blood Pressure ◽  
Hypertensive Rat ◽  
Prague Hypertensive Rat

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.

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