scholarly journals Endothelial derived relaxing factor controls renal hemodynamics in the normal rat kidney.

1990 ◽  
Vol 1 (6) ◽  
pp. 875-881
Author(s):  
C Baylis ◽  
P Harton ◽  
K Engels
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Plasma Flow ◽  
Rat Kidney ◽  
Renal Plasma Flow ◽  
Significant Rise ◽  
Sodium Reabsorption ◽  
Slight Reduction ◽  
Relaxing Factor ◽  
Basal Blood Pressure

These studies were conducted in the conscious, chronically catheterized rat to determine whether the endothelial derived relaxing factor (EDRF) controls renal function in the normal state. Administration of the EDRF synthesis inhibitors N-monomethyl-L-arginine (NMA; 100 mg/kg body weight) or N-nitro-L-arginine methylester (NAME; 10 mg/kg body wt) led to a large, sustained rise in blood pressure, a large rise in renal vascular resistance, a fall in renal plasma flow, a relatively slight reduction in glomerular filtration rate, and a consequent rise in filtration fraction. In addition, a marked natriuresis occurred because of a reduction in the fractional reabsorption of sodium. In separate studies, a continuous infusion of excess L-arginine (300 mg/kg body wt bolus followed by 50 mg/kg body wt per min) attenuated the NMA- or NAME-induced rise in blood pressure and reversed the renal hemodynamic effects such that a significant rise in renal plasma flow was seen. L-Arginine alone produced a selective renal vasodilation and large increases in sodium excretion. These observations support earlier suggestions that tonic release of EDRF controls the basal blood pressure and also show that renal function in the normal unstressed rat is markedly influenced by EDRF. These studies suggest that, in addition to controlling renal plasma flow, EDRF may have other, complex actions at the glomerulus. The natriuresis seen after acute inhibition of EDRF with NMA or NAME was probably the result of a pressure natriuretic response to the abrupt rise in blood pressure and also, perhaps, reflects removal of an EDRF influence to directly enhance sodium reabsorption somewhere in the nephron.

Renal Effects of Angiotensin I-Receptor Blockade and Angiotensin Convertase Inhibition in Man

1996 ◽  
Vol 90 (3) ◽  
pp. 205-213 ◽  
Author(s):  
Francois Schmitt ◽  
Svetlozar Natov ◽  
Frank Martinez ◽  
Bernard Lacour ◽  
Thierry P. Hannedouche
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Plasma Renin Activity ◽  
Plasma Flow ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Renin Activity ◽  
Angiotensin Converting Enzyme Inhibition ◽  
Converting Enzyme ◽  
Converting Enzyme Inhibition

1. The objective was to compare two means of inhibition of the renin—angiotensin system [angiotensin-converting enzyme inhibition and selective antagonism of angiotensin II subtype 1 (AT1) receptor] on renal function in 10 healthy normotensive volunteers on a normal sodium diet. Since mechanisms of action may differ between both drugs, a synergistic action was further studied by combining the two drugs. 2. The design was a double-blind randomized acute administration of either placebo or a single oral dose of enalapril, 20 mg, followed in each case by administration of the AT1 selective antagonist losartan potassium, 50 mg orally. 3. The methods included measurements of hormones (plasma renin activity, plasma aldosterone), blood pressure and renal function from 45 to 135 min after administration of placebo or enalapril, and from 45 to 135 min after losartan and placebo or losartan and enalapril. Renal function was studied using clearance of sodium, lithium, uric acid, inulin and para-aminohippuric acid. To examine further the determinants of glomerular filtration at the microcirculation level, fractional clearance of neutral dextran was determined and sieving curves were applied on a hydrodynamic model of ultrafiltration. 4. Losartan did not change plasma renin activity, blood pressure or glomerular filtration rate, but increased significantly renal plasma flow and urinary excretion of sodium and uric acid. Enalapril increased plasma renin activity and renal plasma flow, and decreased blood pressure without natriuretic, lithiuretic or uricosuric effects. The renal vasodilatation was potentiated when losartan and enalapril were combined, despite a further rise in plasma renin. In contrast to enalapril, losartan either alone or in combination with enalapril significantly depressed fractional clearances of dextran of small radii (34–42 Å). These changes in fractional clearances of dextran were presumably related to the rise in glomerular plasma flow since the other major determinants of filtration, i.e. transcapillary glomerular pressure gradient, ultrafiltration coefficient and membrane property, were computed as unchanged by either losartan, enalapril or a combination of both. 5. In conclusion, these findings suggest that in normal sodium-repleted man the renal, hormonal and blood pressure effects of AT1 antagonism and angiotensin-converting enzyme inhibition are not strictly similar and could be synergistic.

EFFECTS OF HYDRAZINOPHTHALAZINE (APRESOLINE®) ON BLOOD PRESSURE AND RENAL FUNCTION IN CHILDREN WITH ACUTE NEPHRITIS

PEDIATRICS ◽  
1953 ◽  
Vol 12 (1) ◽  
pp. 29-37
Author(s):  
W. W. MCCRORY ◽  
M. RAPOPORT
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Plasma Flow ◽  
Chronic Renal Disease ◽  
Renal Plasma Flow ◽  
Systemic Blood Pressure ◽  
Urine Flow ◽  
Systemic Blood ◽  
Excretory Function ◽  
Made In

The response of hypertension occurring in acute nephritis in children to apresoline® has been studied. Significant temporary reductions in elevated blood pressure were produced by parenteral and oral apresoline® in 5 of 7 children with acute nephritis. The effect of this agent in two patients with hypertension and chronic renal disease was less impressive. Studies of changes in renal function following parenteral administration of apresoline® were made in seven children with acute nephritis. Significant temporary depressions of the glomerular filtration rate and urine flow were observed in every instance in which apresoline® induced a fall in systemic blood pressure. Apresoline® did not regularly induce an increase in renal plasma flow in these subjects. Changes in renal plasma flow were variable, and even decreases were observed. Even though apresoline® can induce a fall in blood pressure in children with hypertension and acute nephritis, this response may be associated with a temporary depression in renal excretory function.

Inhibition of platelet-activating factor induced renal hemodynamic and tubular dysfunctions with L-655,240, a new thromboxane–prostaglandin endoperoxide antagonist

1989 ◽  
Vol 67 (4) ◽  
pp. 304-308 ◽  
Author(s):  
R. L. Hébert ◽  
P. Sirois ◽  
G. E. Plante
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Glomerular Filtration ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Platelet Activating Factor ◽  
Urinary Sodium ◽  
Dependent Manner ◽  
Prostaglandin Endoperoxide

The continuous infusion or bolus injection of the platelet-activating factor (PAF) is associated with profound hypotension, marked reductions of renal plasma flow, glomerular filtration, and urinary sodium excretion. All these effects are inhibited by blocking PAF receptors. To examine further the potential mediators of PAF on renal function, we utilized L-655,240 (6 mg/kg, intravenously), a thromboxane–prostaglandin endoperoxide antagonist, to study the systemic and renal response to PAF (0.8 μg/kg, intravenously) in the anesthetized dog, using clearance methodology. PAF decreased blood pressure from 115 ± 7 to 54 ± 4 mmHg (1 mmHg = 133.3 Pa), renal plasma flow from 105 ± 6 to 74 ± 56 mL/min, and glomerular filtration from 43 ± 3 to 32 ± 1 mL/min. PAF also reduced urine volume from 1.1 ± 0.2 to 0.4 ± 0.1 mL/min, and urinary sodium from 158 ± 7 to 86 ± 7 μequiv./min. L-655,240 alone had no significant effect on blood pressure, renal plasma flow, and filtration rate, at any dose. However, the 6-mg/kg dose resulted in a slight elevation of diuresis, from 1.1 ± 0.2 to 1.9 ± 0.1 mL/min, and urinary sodium, from 134 ± 13 to 212 ± 19 μequiv./min. All doses of L-655,240 blocked the effect of PAF on blood pressure. However, the two lower doses of this antagonist (1 and 3 mg/kg) failed to prevent the PAF-induced fall of renal plasma flow and filtration rate, and attenuated the effect on urinary sodium in a dose-dependent manner. These results indicate that the renal vasoconstriction and antinatriuretic effects of PAF are probably mediated by thromboxane A2 and (or) prostaglandin endoperoxides in the dog. L-655,240 represents therefore a potent inhibitor of PAF-induced renal dysfunctions, and may be of significant interest to explore further the physiology and pathophysiology of PAF.Key words: platelet-activating factor, renal function, lipid mediators, thromboxane antagonist, shock.

Clinical Renal Function Testing by External Double Isotope Monitoring Technique

1971 ◽  
Vol 10 (01) ◽  
pp. 16-24
Author(s):  
J. Fog Pedersen ◽  
M. Fog Pedersen ◽  
Paul Madsen
Keyword(s):  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Correlation Coefficients ◽  
Feedback System ◽  
Effective Renal Plasma Flow ◽  
Advantages And Disadvantages

SummaryAn accurate catheter-free technique for clinical determination simultaneouslyof glomerular filtration rate and effective renal plasma flow by means of radioisotopes has been developed. The renal function is estimated by the amount of radioisotopes necessary to maintain a constant concentration in the patient’s blood. The infusion pumps are steered by a feedback system, the pumps being automatically turned on when the radiation measured over the patient’s head falls below a certain preset level and turned off when this level is again readied. 131I-iodopyracet was used for the estimation of effective renal plasma flow and125I-iothalamate estimation of the glomerular filtration rate. These clearances were compared to the conventional bladder clearances and good correlation was found between these two clearance methods (correlation coefficients 0.97 and.90 respectively). The advantages and disadvantages of this new clearance technique are discussed.

RENAL FUNCTION AND KIDNEY SIZE FOLLOWING HYPOPHYSECTOMY IN MAN

1965 ◽  
Vol 48 (3) ◽  
pp. 348-354 ◽  
Author(s):  
Thomas Falkheden ◽  
Ingmar Wickbom
Keyword(s):  
Renal Function ◽  
Diabetic Retinopathy ◽  
Glomerular Filtration Rate ◽  
Plasma Flow ◽  
Mammary Carcinoma ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Kidney Weight ◽  
Kidney Size ◽  
Before And After

ABSTRACT Measurements of glomerular filtration rate (GFR) and renal plasma flow (RPF) were performed in close connection with roentgenographic estimation of kidney size, before and after hypophysectomy, in 10 patients (four cases of metastatic mammary carcinoma, five cases of diabetic retinopathy and one case of acromegaly). Hypophysectomy was regularly followed by a decrease in GFR and RPF. In most cases, a reduction in the roentgenographic kidney size was also observed. However, the changes in the roentgenographic kidney size and calculated kidney weight after hypophysectomy were smaller and occurred at a slower rate than the alterations in GFR and RPF. The results favour the view that, primarily, the decrease in GFR and RPF following hypophysectomy is essentially functional rather than due to a reduced kidney mass.

scholarly journals Metabolic Syndrome and Salt-Sensitive Hypertension in Polygenic Obese TALLYHO/JngJ Mice: Role of Na/K-ATPase Signaling

2019 ◽  
Vol 20 (14) ◽  
pp. 3495 ◽  
Author(s):  
Yanling Yan ◽  
Jiayan Wang ◽  
Muhammad A. Chaudhry ◽  
Ying Nie ◽  
Shuyan Sun ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Significant Rise ◽  
Protein Carbonylation ◽  
High Salt ◽  
Kidney Cortex ◽  
High Salt Diet ◽  
Salt Diet ◽  
Salt Sensitive Hypertension

We have demonstrated that Na/K-ATPase acts as a receptor for reactive oxygen species (ROS), regulating renal Na+ handling and blood pressure. TALLYHO/JngJ (TH) mice are believed to mimic the state of obesity in humans with a polygenic background of type 2 diabetes. This present work is to investigate the role of Na/K-ATPase signaling in TH mice, focusing on susceptibility to hypertension due to chronic excess salt ingestion. Age-matched male TH and the control C57BL/6J (B6) mice were fed either normal diet or high salt diet (HS: 2, 4, and 8% NaCl) to construct the renal function curve. Na/K-ATPase signaling including c-Src and ERK1/2 phosphorylation, as well as protein carbonylation (a commonly used marker for enhanced ROS production), were assessed in the kidney cortex tissues by Western blot. Urinary and plasma Na+ levels were measured by flame photometry. When compared to B6 mice, TH mice developed salt-sensitive hypertension and responded to a high salt diet with a significant rise in systolic blood pressure indicative of a blunted pressure-natriuresis relationship. These findings were evidenced by a decrease in total and fractional Na+ excretion and a right-shifted renal function curve with a reduced slope. This salt-sensitive hypertension correlated with changes in the Na/K-ATPase signaling. Specifically, Na/K-ATPase signaling was not able to be stimulated by HS due to the activated baseline protein carbonylation, phosphorylation of c-Src and ERK1/2. These findings support the emerging view that Na/K-ATPase signaling contributes to metabolic disease and suggest that malfunction of the Na/K-ATPase signaling may promote the development of salt-sensitive hypertension in obesity. The increased basal level of renal Na/K-ATPase-dependent redox signaling may be responsible for the development of salt-sensitive hypertension in polygenic obese TH mice.

Effects of NG-nitro-L-arginine methyl ester on renal function and blood pressure

1991 ◽  
Vol 261 (6) ◽  
pp. F1033-F1037 ◽  
Author(s):  
V. Lahera ◽  
M. G. Salom ◽  
F. Miranda-Guardiola ◽  
S. Moncada ◽  
J. C. Romero
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Renal Function ◽  
Methyl Ester ◽  
Renal Plasma Flow ◽  
Urinary Sodium Excretion ◽  
Systemic Blood Pressure ◽  
Synthesis Inhibitor ◽  
Renal Changes ◽  
Dose Dependent

The dose-dependent effects of intravenous infusions of nitric oxide (NO) synthesis inhibitor, NG-nitro-L-arginine methyl ester (L-NAME; 0.1, 1, 10, and 50 micrograms.kg-1.min-1), were studied in anesthetized rats to determine whether the inhibitory actions of L-NAME are manifested primarily in alterations of renal function or whether they are the consequences of the increase in systemic blood pressure. Mean arterial pressure (MAP) was not altered by the intravenous L-NAME infusions of 0.1 and 1.0 microgram.kg-1.min-1. However, 0.1 microgram.kg-1.min-1 L-NAME induced a 30% decrease in urine flow rate (UV). The administration of 1.0 microgram.kg-1.min-1 L-NAME, in addition to decreasing UV, also decreased urinary sodium excretion (UNaV) and renal plasma flow (RPF). The intravenous L-NAME infusions of 10.0 and 50.0 microgram.kg-1.min-1 intravenous L-NAME infusions of 10.0 and 50.0 microgram.kg-1.min-1 produced significant increases in MAP that reversed the initial fall in UV and UNaV, despite decreasing RPF and glomerular filtration rate (GFR). The administration of L-arginine alone (10 micrograms.kg-1.min-1) did not modify any of the parameters measured, but it effectively prevented all the hemodynamic and renal changes induced by the infusion of 50 micrograms.kg-1.min-1 L-NAME. These results suggest that the decrease in nitric oxide production induced by the intravenous infusion of L-NAME affects renal excretion of sodium and water in the absence of any significant change in blood pressure. At larger doses, L-NAME also produces hypertension that overrides the initial antinatriuretic effect.

Salt loading produces severe renal hemodynamic dysfunction independent of arterial pressure in spontaneously hypertensive rats

2007 ◽  
Vol 292 (2) ◽  
pp. H814-H819 ◽  
Author(s):  
Luis C. Matavelli ◽  
Xiaoyan Zhou ◽  
Jasmina Varagic ◽  
Dinko Susic ◽  
Edward D. Frohlich
Keyword(s):  
Renal Function ◽  
Arterial Pressure ◽  
Plasma Flow ◽  
Spontaneously Hypertensive Rats ◽  
Renal Plasma Flow ◽  
Renal Hemodynamics ◽  
Dietary Salt ◽  
Hypertensive Rats ◽  
Salt Loading ◽  
Spontaneously Hypertensive

We have previously shown that salt excess has adverse cardiac effects in spontaneously hypertensive rats (SHR), independent of its increased arterial pressure; however, the renal effects have not been reported. In the present study we evaluated the role of three levels of salt loading in SHR on renal function, systemic and renal hemodynamics, and glomerular dynamics. At 8 wk of age, rats were given a 4% ( n = 11), 6% ( n = 9), or 8% ( n = 11) salt-load diet for the ensuing 8 wk; control rats ( n = 11) received standard chow (0.6% NaCl). Rats had weekly 24-h proteinuria and albuminuria quantified. At the end of salt loading, all rats had systemic and renal hemodynamics measured; glomerular dynamics were specially studied by renal micropuncture in the control, 4% and 6% salt-loaded rats. Proteinuria and albuminuria progressively increased by the second week of salt loading in the 6% and 8% salt-loaded rats. Mean arterial pressure increased minimally, and glomerular filtration rate decreased in all salt-loaded rats. The 6% and 8% salt-loaded rats demonstrated decreased renal plasma flow and increased renal vascular resistance and serum creatinine concentration. Furthermore, 4% and 6% salt-loaded rats had diminished single-nephron plasma flow and increased afferent and efferent arteriolar resistances; glomerular hydrostatic pressure also increased in the 6% salt-loaded rats. In conclusion, dietary salt loading as low as 4% dramatically deteriorated renal function, renal hemodynamics, and glomerular dynamics in SHR independent of a minimal further increase in arterial pressure. These findings support the concept of a strong independent causal relationship between salt excess and cardiovascular and renal injury.

Dynamics of ascites formation in rats with experimental cirrhosis

1980 ◽  
Vol 238 (5) ◽  
pp. F353-F357 ◽  
Author(s):  
J. M. Lopez-Novoa ◽  
M. A. Rengel ◽  
L. Hernando
Keyword(s):  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Hepatic Cirrhosis ◽  
Renal Plasma Flow ◽  
Sodium Balance ◽  
Partial Removal ◽  
Experimental Cirrhosis ◽  
Ascites Formation

Renal function, sodium balance, and ascites formation were observed during induction in rats of experimental cirrhosis. The same variables were studied after partial removal of the ascites in rats with experimental cirrhosis. Glomerular filtration rate (GFR) and effective renal plasma flow (RPF) did not change during hepatic cirrhosis development. Positive sodium balance significantly higher than that observed in controls preceded the appearance of ascites for a period of about 2 wk. When the ascites was removed, GFR, RPF and positive Na balance did not change if Na intake remained constant. Ascites reformation rate was largely dependent on sodium balance. These data strongly support the "overflow" theory of ascites formation and are difficult to reconcile with the classical "underfilling" theory.

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