Effect of plasma from patients with essential hypertension on vascular resistance in the isolated perfused rat kidney

1991 ◽  
Vol 80 (1) ◽  
pp. 17-23 ◽  
Author(s):  
Jürgen Bachmann ◽  
Hartmut Schlüter ◽  
Walter Storkebaum ◽  
Herbert Witzel ◽  
Franz Wessels ◽  
...  
Keyword(s):  
Perfusion Pressure ◽  
Direct Action ◽  
Rat Kidney ◽  
Gel Filtration ◽  
Hypertensive Patients ◽  
Vasopressor Agent ◽  
Resistance Vessels ◽  
Plasma Fractions ◽  
Normotensive Subjects ◽  
Rat Kidneys

1. Isolated perfused rat kidneys were used to study the effects of plasma fractions obtained by gel filtration from essential hypertensive patients (n = 40) and from normotensive subjects (n = 36) on resistance vessels. Perfusion pressure was recorded at a constant flow. 2. Plasma fractions were obtained by gel filtration and contained substances with a molecular mass in the range 1000–1500 Da. The plasma fractions from hypertensive patients used in this study had been shown to increase blood pressure after intravenous injection in rats. 3. In the isolated rat kidneys, the hypertensive fractions increased perfusion pressure by 20 ± 17 mmHg (mean ± SD, range 5–58 mmHg, n = 40). The analogous fractions from normotensive subjects did not change perfusion pressure significantly. 4. In Ca2+-free medium containing 2 mmol/l ethyleneglycol bis-(aminoethyl ether)tetra-acetate, the change in perfusion pressure induced by active plasma fractions was reduced by 95.2 ± 6.3%. Addition of nifedipine to the perfusion medium reduced, but did not abolish, the pressure response of the kidneys. 5. In solutions containing phentolamine or saralasin, vasoconstriction was not reduced. 6. Thus in the active fractions from hypertensive plasma, a vasopressor agent with direct action on resistance vessels can be demonstrated. This substance probably acts by increasing Ca2+ influx in vascular smooth muscle cells.

Inhibition of Renin Secretion in the Isolated Rat Kidney by Antidiuretic Hormone

1975 ◽  
Vol 49 (1) ◽  
pp. 73-76 ◽  
Author(s):  
R. Vandongen
Keyword(s):  
Antidiuretic Hormone ◽  
Calcium Ions ◽  
Perfusion Pressure ◽  
Direct Action ◽  
Rat Kidney ◽  
Renal Perfusion ◽  
Renin Secretion ◽  
Renal Perfusion Pressure ◽  
Isolated Rat Kidney ◽  
Isolated Rat

1. The effect of antidiuretic hormone (ADH) on isoprenaline-stimulated renin secretion was examined in the isolated rat kidney perfused with modified Krebs-Ringer saline. 2. Intrarenal infusion of ADH effectively prevented stimulation of renin secretion by isoprenaline whilst increasing renal perfusion pressure. 3. The exclusion of calcium ions from the perfusion medium abolished the vasoconstrictor effect of ADH and attenuated the inhibitory effect of ADH on isoprenaline-stimulated renin secretion. However, significant suppression of renin secretion was still apparent compared with experiments where isoprenaline was infused alone. 4. These observations indicate that ADH inhibits renin secretion and that this is effected by a direct action on the kidney. Although this may be partly mediated by the rise in renal perfusion pressure, an additional direct effect of ADH on the renin-producing cell, which is dependent on the availability of calcium ions, is proposed.

Effect of plasma from hypertensive subjects on Ca2+ transport in permeabilized human neutrophils

1988 ◽  
Vol 74 (1) ◽  
pp. 53-56 ◽  
Author(s):  
Walter Zidek ◽  
Agapios Sachinidis ◽  
Claus Spieker ◽  
Walter Storkebaum
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Gel Filtration ◽  
Human Neutrophils ◽  
Increase Blood Pressure ◽  
Selective Electrode ◽  
Control Value ◽  
Plasma Fraction ◽  
Plasma Fractions ◽  
Normotensive Subjects

1. The effects of plasma fractions from essential hypertensive subjects (n = 14) and normotensive subjects (n = 14) on Ca2+ transport in permeabilized human neutrophils was studied using an ion-selective electrode. 2. Plasma fractions were obtained by gel filtration and contained substances with a molecular mass in the range 1000–1500 daltons. This fraction isolated from essential hypertensive subjects has been shown to increase blood pressure after intravenous injection in the rat. 3. The rate of Ca2+ uptake by permeabilized neutrophils after addition of extracellular Ca2+ was significantly accelerated during incubation of the cells with the hypertensive fraction (1049.3 ±807.7% vs 242.5 ±320.9% of the control value, mean ± sd, P < 0.05). 4. It is concluded that the hypertensive plasma fraction increases Ca2+ accumulation in subcellular particles, so that under excitatory conditions Ca2+ release in arterial smooth muscle might be enhanced.

Kinetics of bumetanide-sensitive Na+-K+ co-transport in erythrocytes of essential hypertensive patients

1985 ◽  
Vol 69 (5) ◽  
pp. 607-611 ◽  
Author(s):  
Pietro Delva ◽  
Mario De Gasperi ◽  
Maurizio Degan ◽  
Grazia Covi ◽  
Alessandro Lechi
Keyword(s):  
Kinetic Parameters ◽  
Transport System ◽  
Clinical Data ◽  
Laboratory Data ◽  
Cation Transport ◽  
Hypertensive Patients ◽  
Apparent Affinity ◽  
Normotensive Subjects ◽  
Kinetics Of

1. Outward bumetanide-sensitive Na+-K+ co-transport was studied in the erythrocytes of 51 subjects, 24 normotensive subjects and 27 hypertensive patients, matched for sex and age. 2. Three kinetic parameters of this cation transport system were considered: velocity of efflux at saturating internal sodium (Nai) concentrations (Vmax.), apparent affinity for sodium (K50%) and index of co-operativity among Nai sites (Hill's n). 3. We correlated these values with clinical and laboratory data determined routinely in hypertension. 4. There were no significant differences between normotensive and hypertensive subjects for the values considered and we did not find any significant correlations between co-transport and clinical data.

Basal Activity of the Natriuretic Factor Extracted from the Rat Kidney as a Function of the Diet and its Role in the Regulation of the Acute Sodium Balance

1980 ◽  
Vol 58 (5) ◽  
pp. 385-391 ◽  
Author(s):  
F. Louis ◽  
H. Favre
Keyword(s):  
Sodium Intake ◽  
Rat Kidney ◽  
Extracellular Volume ◽  
Gel Filtration ◽  
Kidney Tissue ◽  
Weight Fraction ◽  
Sodium Content ◽  
Sodium Balance ◽  
Low Molecular Weight ◽  
Extracellular Volume Expansion

1. The effect of the sodium content of the diet on the natriuretic activity of an extract from the kidneys was studied in non-expanded and volume-expanded rats. 2. The kidney tissue was homogenized and the supernatant fractionated by gel filtration on Sephadex G-25. A single low-molecular-weight fraction eluted after the salt possessed the natriuretic activity and was tested on a rat bioassay. 3. The natriuretic activity of the fraction obtained from the kidneys of non-expanded rats was related to the sodium intake. 4. After an acute extracellular volume expansion, the natriuretic activity obtained from the fraction extracted from the kidneys was much greater than before expansion and was related to the dietary intake of sodium.

Abstract P274: Fruit Extract (blueberry, Cranberry, And Promegranate) Improved Insulin Resistance In Overweight Hypertensive And Normotensive Subjects

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Ludmila N Novaes ◽  
Mariele Moraes ◽  
Keyla Katayama ◽  
Carine Sangaleti ◽  
Maria Claudia Irigoyen ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Lipid Metabolism ◽  
Repeated Measures ◽  
Hdl Cholesterol ◽  
Biochemical Tests ◽  
Fruit Extract ◽  
Hypertensive Patients ◽  
Glucose And Lipid Metabolism ◽  
Normotensive Subjects ◽  
Group B

Arterial hypertension is frequently associated to glucose and lipid metabolism abnormalities. The purpose of this study was to determine if antioxidants (fruit extract) supplementation interfere with glucose and lipid metabolism in overweight hypertensive patients. A randomized clinical trial was conducted with 30 individuals, 23 hypertensive patients (group A) and 7 normotensive controls (group B). They were randomized to take 3 capsules of different fruits extract a day (blueberry, cranberry and pomegranate) or placebo for 4 weeks. This is a crossover study, which started with placebo changed to capsules and vice versa. Blood samples were collected after 12 hours fasting for biochemical tests (glucose, insulin, total cholesterol, LDL-cholesterol, HDL-cholesterol, triglycerides), anthropometric assessment (weight, height, and body mass index), systolic BP, diastolic BP and heart rate were evaluated at baseline, after 4, and 8 weeks. The comparisons between groups were held with the GLM repeated measures. Twenty three hypertensive patients (age 47 years, 14 females) and 7 normotensive controls (age 40 years, 7 females) were evaluated. BMI, blood pressure, heart and lipid profile did not differ between groups. HOMAir decreased significantly in both groups. See results in table 1. Values are expressed as medians (±SD) In these preliminary results a 4-weeks supplementation of antioxidants (fruit extract) improved insulin resistance in overweight hypertensive and normotensive subjects. Financial support: FAPESP 2014/25808-3

Membrane potential measurements in renal afferent and efferent arterioles: actions of angiotensin II

1997 ◽  
Vol 273 (2) ◽  
pp. F307-F314 ◽  
Author(s):  
R. Loutzenhiser ◽  
L. Chilton ◽  
G. Trottier
Keyword(s):  
Angiotensin Ii ◽  
Perfusion Pressure ◽  
Rat Kidney ◽  
Renal Perfusion ◽  
Membrane Potentials ◽  
Ang Ii ◽  
Ca Channels ◽  
Renal Perfusion Pressure

An adaptation of the in vitro perfused hydronephrotic rat kidney model allowing in situ measurement of arteriolar membrane potentials is described. At a renal perfusion pressure of 80 mmHg, resting membrane potentials of interlobular arteries (22 +/- 2 microns) and afferent (14 +/- 1 microns) and efferent arterioles (12 +/- 1 microns) were -40 +/- 2 (n = 8), -40 +/- 1 (n = 45), and -38 +/- 2 mV (n = 22), respectively (P = 0.75). Using a dual-pipette system to stabilize the impalement site, we measured afferent and efferent arteriolar membrane potentials during angiotensin II (ANG II)-induced vasoconstriction. ANG II (0.1 nM) reduced afferent arteriolar diameters from 13 +/- 1 to 8 +/- 1 microns (n = 8, P = 0.005) and membrane potentials from -40 +/- 2 to -29 +/- mV (P = 0.012). ANG II elicited a similar vasoconstriction in efferent arterioles, decreasing diameters from 13 +/- 1 to 8 +/- 1 microns (n = 8, P = 0.004), but failed to elicit a significant depolarization (-39 +/- 2 for control; -36 +/- 3 mV for ANG II; P = 0.27). Our findings thus indicate that resting membrane potentials of pre- and postglomerular arterioles are similar and lie near the threshold activation potential for L-type Ca channels. ANG II-induced vasoconstriction appears to be closely coupled to membrane depolarization in the afferent arteriole, whereas mechanical and electrical responses appear to be dissociated in the efferent arteriole.

Direct action of aldosterone on bicarbonate reabsorption in in vivo cortical proximal tubule

2009 ◽  
Vol 296 (5) ◽  
pp. F1185-F1193 ◽  
Author(s):  
Patricia Silva Pergher ◽  
Deise Leite-Dellova ◽  
Margarida de Mello-Aires
Keyword(s):  
Proximal Tubule ◽  
Direct Action ◽  
Rat Kidney ◽  
Free Calcium ◽  
Mineralocorticoid Receptor Antagonist ◽  
Control Value ◽  
Bicarbonate Reabsorption ◽  
Peritubular Capillaries ◽  
Inhibitor Of Protein Synthesis

The direct action of aldosterone (10−12 M) on net bicarbonate reabsorption ( JHCO3−) was evaluated by stationary microperfusion of an in vivo middle proximal tubule (S2) of rat kidney, using H ion-sensitive microelectrodes. Aldosterone in luminally perfused tubules caused a significant increase in JHCO3− from a mean control value of 2.84 ± 0.08 [49/19 ( n° of measurements/ n° of tubules)] to 4.20 ± 0.15 nmol·cm−2·s−1 (58/10). Aldosterone perfused into peritubular capillaries also increased JHCO3−, compared with basal levels during intact capillary perfusion with blood. In addition, in isolated perfused tubules aldosterone causes a transient increase of cytosolic free calcium ([Ca2+]i), monitored fluorometrically. In the presence of ethanol (in similar concentration used to prepare the hormonal solution), spironolactone (10−6 M, a mineralocorticoid receptor antagonist), actinomycin D (10−6 M, an inhibitor of gene transcription), or cycloheximide (40 mM, an inhibitor of protein synthesis), the JHCO3− and the [Ca2+]i were not different from the control value; these drugs also did not prevent the stimulatory effect of aldosterone on JHCO3− and on [Ca2+]i. However, in the presence of RU 486 alone [10−6 M, a classic glucocorticoid receptor (GR) antagonist], a significant decrease on JHCO3− and on [Ca2+]i was observed; this antagonist also inhibited the stimulatory effect of aldosterone on JHCO3− and on [Ca2+]i. These studies indicate that luminal or peritubular aldosterone (10−12 M) has a direct nongenomic stimulatory effect on JHCO3− and on [Ca2+]i in proximal tubule and that probably GR participates in this process. The data also indicate that endogenous aldosterone stimulates JHCO3− in middle proximal tubule.

Ca-dependent hemodynamic and natriuretic effects of atrial extract in isolated rat kidney

1984 ◽  
Vol 246 (4) ◽  
pp. F447-F456 ◽  
Author(s):  
M. J. Camargo ◽  
H. D. Kleinert ◽  
S. A. Atlas ◽  
J. E. Sealey ◽  
J. H. Laragh ◽  
...  
Keyword(s):  
Perfusion Pressure ◽  
Rat Kidney ◽  
Fractional Excretion ◽  
Electrolyte Excretion ◽  
Renal Vasculature ◽  
Filtration Fraction ◽  
Perfused Rat Kidney ◽  
Site Of Action ◽  
Initial Control ◽  
Renal Vascular

The effects of rat atrial tissue extract on renal hemodynamics and fluid and electrolyte excretion were investigated in the isolated perfused rat kidney (IK). IK were perfused at a constant effective perfusion pressure of about 90 mmHg. After control clearance periods (C), extracts of rat atria (AE) or ventricles (VE) were added to the perfusate and three 10-min experimental periods followed. AE, but not VE, significantly increased (P less than 0.001) renal vascular resistance (RVR) to 133 +/- 8% of C, GFR to 201 +/- 34%, filtration fraction to 245 +/- 41%, urine flow (V) to 675 +/- 131%, fractional excretion (FE) of H2O to 336 +/- 29%, absolute Na excretion (UNaV) to 1,259 +/- 290%, FENa to 642 +/- 129%, UKV to 2,226 +/- 1,237%, and FEK to 542 +/- 119%. Despite the marked natriuresis, since GFR doubled, Na reabsorption rose from 78.3 +/- 36.3 in C to 132 +/- 36.3 mueq/min after AE. The effects of AE were immediate and lasted to the end of the perfusion. The lower the initial control GFR, the larger was the AE-induced increase in GFR. Perfusion with low [Ca] (0.2 mM) or verapamil (10(-5) M) severely blunted the hemodynamic, diuretic, kaliuretic, and natriuretic effects of AE. AE decreased rather than increased the RVR when IK were perfused with vasoconstrictors such as angiotensin II, norepinephrine, or vasopressin. The results demonstrate that AE acts directly on the kidney, eliciting powerful Ca-dependent hemodynamic and natriuretic responses. The natriuresis induced by AE can be accounted for, at least in part, by its renal hemodynamic effects rather than by the presence of a putative tubular natriuretic factor. The hypothesis is advanced that AE contains a substance(s) which behaves as a functional agonist/antagonist of endogenous vasoconstrictors with a preferential site of action on the efferent arterioles of the renal vasculature.

scholarly journals Metabolism of glycine- and hydroxyproline-containing peptides by the isolated perfused rat kidney

1985 ◽  
Vol 229 (2) ◽  
pp. 545-549 ◽  
Author(s):  
M Lowry ◽  
D E Hall ◽  
J T Brosnan
Keyword(s):  
Amino Acids ◽  
Rat Kidney ◽  
Isolated Perfused Rat Kidney ◽  
Perfused Rat Kidney ◽  
Rat Kidneys

Isolated perfused rat kidneys removed considerable quantities of glycyltyrosine, glycylhydroxyproline, tetraglycine and prolylhydroxyproline from the perfusate. The component amino acids are released into the perfusate and, in the case of the glycine-containing peptides, there is increased synthesis of serine. Removal of peptides was more than could be accounted for on the basis of filtration, so antiluminal metabolism is indicated. Metabolism of such peptides by the kidney may contribute to renal serine synthesis in vivo.

scholarly journals Metabolism of parathyroid hormone. Degradation of 125I-labelled hormone by kidney enzyme

1969 ◽  
Vol 111 (4) ◽  
pp. 509-514 ◽  
Author(s):  
T. J. Martin ◽  
R. A. Melick ◽  
M. de Luise
Keyword(s):  
Parathyroid Hormone ◽  
Trichloroacetic Acid ◽  
Rat Kidney ◽  
Gel Filtration ◽  
Void Volume ◽  
Control Medium ◽  
Ph Values ◽  
Kidney Enzyme ◽  
Rapid Destruction ◽  
Kidney Microsomes

A study was made of the enzymic degradation of 125I-labelled parathyroid hormone by rat kidney microsomes. Incubation with microsomes resulted in rapid destruction of the labelled hormone. The microsomal factor was not separable by dialysis, and the reaction was favoured by pH values in the physiological range. Velocity of the reaction varied directly as the substrate concentration, and additional crude parathyroid hormone (trichloroacetic acid-precipitated, 3·68mg./ml.) inhibited destruction of labelled hormone. There was much less inhibition with added trichloroacetic acid-precipitated calcitonin (3·92mg./ml.) and virtually none with added pig insulin (3·80mg./ml.). Gel filtration of control medium on P6 (Bio-Gel) yielded one radioactive peak at the void volume. After incubation with microsomes three further peaks were obtained on gel filtration. Only the void-volume peak contained intact 125I-labelled parathyroid hormone, indicating that the microsomal enzyme degraded labelled hormone to a number of smaller fragments.

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