scholarly journals THE EFFECT OF DESOXYCORTICOSTERONE ACETATE ON BLOOD PRESSURE, RENAL FUNCTION, AND ELECTROLYTE PATTERN IN THE INTACT RAT

1948 ◽  
Vol 87 (4) ◽  
pp. 329-338 ◽  
Author(s):  
Sydney M. Friedman ◽  
John R. Polley ◽  
Constance L. Friedman
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
No Reduction ◽  
Renal Plasma Flow ◽  
Excretory Function ◽  
Small Doses ◽  
Cent Saline ◽  
Electrolyte Change ◽  
Desoxycorticosterone Acetate ◽  
Pellet Form

Small doses of DCA administered at intervals in pellet form are capable of raising the blood pressure, altering renal function, and changing the electrolyte pattern in the intact rat. The concomitant feeding of 1 per cent saline intensifies the process. The elevation in blood pressure occurs prior to demonstrable changes in renal excretory function. The alteration in renal function consists first of a reduction in CPAH with the maintenance of a normal filtration rate. Filtration fraction is elevated while there is no reduction in renal plasma flow per unit of tubular excretory tissue. Later, filtration is interfered with and renal ischemia occurs. The electrolyte change is characterized by a sustained fall in plasma K and Cl, a rise in plasma Na, an increase in the Na/Cl ratio, and finally an elevation of Na plus K. Plasma Ca is unaffected. These observations suggest the possible etiological significance of the adrenal cortex in some types of hypertension.

scholarly journals OBSERVATIONS ON THE RÔLE OF THE RAT KIDNEY IN HYPERTENSION CAUSED BY DESOXYCORTICOSTERONE ACETATE

1949 ◽  
Vol 89 (6) ◽  
pp. 631-641 ◽  
Author(s):  
Sydney M. Friedman ◽  
Constance L. Friedman
Keyword(s):  
Blood Pressure ◽  
Drinking Water ◽  
Renal Mass ◽  
Rat Kidney ◽  
Drinking Water Treatment ◽  
Albino Rats ◽  
Cent Saline ◽  
Renal Changes ◽  
Desoxycorticosterone Acetate ◽  
Pellet Form

Desoxycorticosterone acetate in pellet form was administered for 51 days to albino rats of the Sherman strain which also received 1 per cent saline as drinking water. Treatment was stopped in representative groups at 25, 37, and 51 days so that the regression of blood pressure and renal changes could be observed. It was noted that both the elevation in blood pressure during treatment and its reversal when treatment was stopped were closely correlated with corresponding changes in renal mass. In the time for which the process was studied it did not become irreversible. Removal of both kidneys from DCA-treated animals aggravated the hypertension, suggesting that the kidneys are actively concerned with the excretion and possible inactivation of the steroid.

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.

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.

Renin content and excretory function of the kidney in rats with experimental hypertension

1962 ◽  
Vol 202 (4) ◽  
pp. 795-799 ◽  
Author(s):  
H. Brunner ◽  
P. A. Desaulles ◽  
D. Regoli ◽  
F. Gross
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Renal Hypertension ◽  
Experimental Hypertension ◽  
Elevated Blood ◽  
Hypertensive Rats ◽  
Excretory Function ◽  
Contralateral Kidney ◽  
Ligation Of The Ureter ◽  
Renin Content

To determine relationship between kidney renin content and excretory function, rats with renal hypertension induced by unilateral clamping of the renal artery were given an oral load of 3 ml of 0.9% saline/100 g body wt. Excretion of the saline load was accelerated in rats with renal hypertension as well as in animals with hypertension due to overdosage with cortexone and salt, provided that the loading experiment was made 3–4 weeks after hypertension was established, but not when animals had been hypertensive for 11–14 weeks. Renin concentration was markedly reduced in the unclamped kidney and also in the kidney of the rats overdosed with cortexone and salt. Excreting capacity of the clamped kidney was compared with that of the unclamped kidney, after removal or after functional elimination of the contralateral kidney, by ligation of the ureter, 3, 24, and 48 hr after the operation. In all experiments excretion of saline load by the unclamped kidney was more rapid than by the clamped kidney, but the highest values were reached in the presence of a functional clamped kidney. Only in rats with elevated blood pressure was the load more rapidly excreted than in normal rats, but hypertension alone cannot be the only factor responsible, the excretion not being accelerated in unilaterally nephrectomized hypertensive rats. Although these hint at a connection between the renin concentration and renal function the nature of this relationship remains uncertain.

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.

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.

Chronic intrarenal hyperinsulinemia does not cause hypertension

1991 ◽  
Vol 260 (5) ◽  
pp. F663-F669 ◽  
Author(s):  
J. E. Hall ◽  
M. W. Brands ◽  
H. L. Mizelle ◽  
C. A. Gaillard ◽  
D. A. Hildebrandt
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Mean Arterial Pressure ◽  
Sodium Excretion ◽  
Insulin Infusion ◽  
Sodium Intake ◽  
Renal Plasma Flow ◽  
Systemic Effects ◽  
Potassium Excretion ◽  
Renal Vascular

Hyperinsulinemia has been postulated to link obesity and hypertension via the antinatriuretic actions of insulin. The main goal of this study was to quantitate the importance of the direct intrarenal actions of insulin, independent of systemic effects, in altering blood pressure and renal function. This was accomplished by determining the responses to chronic intrarenal insulin infusion in uninephrectomized, chronically instrumented conscious dogs maintained on a 74 meq/day sodium intake. Insulin was infused at rates calculated to raise intrarenal, but not systemic, insulin to levels similar to those observed in obese hypertensive dogs. Intrarenal insulin infusion (0.6 mU.kg-1.min-1) for 7 days caused transient decreases in sodium excretion but no significant changes in potassium excretion. Mean arterial pressure did not change during 7 days of insulin infusion, averaging 93 +/- 4 mmHg during control and 93 +/- 3 mmHg during insulin infusion. Intrarenal insulin caused small increases in GFR but no significant changes in effective renal plasma flow or renal vascular resistance. These results demonstrate that insulin causes transient decreases in sodium excretion, but chronic intrarenal hyperinsulinemia does not elevate blood pressure in normal dogs. Additional factors other than the direct sodium-retaining effects of insulin may be important in raising blood pressure in obesity-associated hypertension.

Perinatal ANG II programs adult blood pressure, glomerular number, and renal function in rats

1998 ◽  
Vol 275 (5) ◽  
pp. R1593-R1599 ◽  
Author(s):  
Lori L. Woods ◽  
Ruth Rasch
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Arterial Pressure ◽  
Renal Plasma Flow ◽  
Postnatal Life ◽  
Renal Development ◽  
Ang Ii ◽  
Body Weights ◽  
Long Term Consequences

ANG II is known to be important in normal renal development, but the long-term consequences of a suppressed renin-angiotensin system (RAS) during the developmental period are not completely understood. This study tested the hypothesis that the RAS in the developing animal is important in long-term regulation of renal function and arterial pressure. Newborn Sprague-Dawley rat pups were given the ANG II AT1receptor antagonist losartan (25 mg ⋅ kg−1⋅ day−1sc) for the first 12 days of postnatal life (Los). Body weights at weaning (22 days) were significantly reduced in Los (53.4 ± 3.2 vs. 64.5 ± 3.6 g in controls); however, at the time of study (∼22 wk), body weights and the kidney-to-body weight ratios were not different. In chronically instrumented conscious animals, glomerular filtration rate and effective renal plasma flow were reduced by 27 and 20%, respectively, in Los; the filtration fraction was not different. Maximal urine concentrating ability was also reduced in Los (1,351 ± 45 vs. 2,393 ± 52 mosmol/kg in controls). Mean arterial pressure was significantly higher in Los (134 ± 3 vs. 120 ± 1 mmHg). The number of glomeruli per kidney was reduced by 42% in Los, but the total glomerular volume was unchanged. Thus perinatal blockade of ANG II AT1receptors results in fewer but enlarged glomeruli, reduced renal function, and an increased arterial pressure in adulthood. These data indicate that perinatal ANG II, acting via AT1receptors, plays an important role in renal development and long-term control of renal function and arterial pressure. Physiological conditions that cause suppression of the RAS in the developing animal may have long-term consequences for renal function and blood pressure.

Kidney cross transplants in Dahl salt-sensitive and salt-resistant rats

1992 ◽  
Vol 262 (6) ◽  
pp. H1809-H1817 ◽  
Author(s):  
P. C. Churchill ◽  
M. C. Churchill ◽  
A. K. Bidani
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Fractional Excretion ◽  
Transplanted Kidney ◽  
Native Kidney ◽  
Clearance Studies ◽  
Genetically Determined

Previous kidney cross-transplant studies have demonstrated that the genotype of the kidney plays a role in determining the blood pressure of the recipient in Dahl salt-sensitive (S) and salt-resistant (R) rats. The present studies were designed to elucidate this role. Kidney cross transplants were performed in unilaterally nephrectomized male recipients (John Rapp strains), such that each rat had a native kidney and a transplanted kidney of the opposite genotype. S and R rats with a native kidney and a transplanted kidney of the same genotype served as controls. After 4 wk on a 7.8% NaCl diet, rats were anesthetized and renal clearance studies were performed. S kidneys had lower glomerular filtration rate (GFR) and renal plasma flow (RPF) than R kidneys, and these differences were determined by the kidney's genotype rather than the recipient's, since S kidneys in R recipients tended to have lower GFR and RPF than R kidneys in S recipients. In contrast, independent of the kidney's genotype, the kidneys in S rats tended to have higher fractional excretion of H2O and Na (FEH2O and FENa) than the kidneys in R rats. Thus there were genetically determined differences in renal function between S and R rats; some (RPF and GFR) were intrinsic to the kidney, whereas others (FEH2O and FENa) were intrinsic to the host.(ABSTRACT TRUNCATED AT 250 WORDS)

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