scholarly journals RENAL PLASMA FLOW AND SODIUM REABSORPTION AND EXCRETION IN CONGESTIVE HEART FAILURE 1

1948 ◽  
Vol 27 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Reuben Mokotoff ◽  
George Ross ◽  
Louis Leiter
1981 ◽  
Vol 6 (12) ◽  
Author(s):  
W.Newlon Tauxe ◽  
EvaV. Dubovsky ◽  
JohnA. Mantle ◽  
HarrietP. Dustan ◽  
JosephR. Logic

1991 ◽  
Vol 260 (6) ◽  
pp. F883-F889 ◽  
Author(s):  
H. Eiskjaer ◽  
J. P. Bagger ◽  
H. Danielsen ◽  
J. D. Jensen ◽  
B. Jespersen ◽  
...  

Renal plasma flow (RPF), glomerular filtration rate (GFR), renal proximal tubular delivery of sodium and water evaluated by lithium clearance, and hormonal parameters were measured in 12 patients with congestive heart failure NYHA class II-IV before and after captopril treatment for 4 wk and in 13 healthy control subjects. RPF and GFR were significantly decreased in heart failure, whereas the filtration fraction (FF) was increased. Treatment with captopril increased RPF and decreased FF, whereas GFR was unchanged. Total and fractional urinary excretion of sodium were reduced in the patients compared with the controls, but increased after captopril. Fractional excretion of lithium was normal in heart failure and was increased by captopril. Atrial natriuretic peptide, guanosine 3',5'-cyclic monophosphate, and aldosterone in plasma were significantly elevated in heart failure and were reduced by treatment with captopril. Plasma renin activity was increased in patients, correlated inversely with RPF, and increased further after captopril treatment. It is concluded that the reduced sodium excretion in heart failure was caused by a combination of diminished glomerular filtration and enhanced tubular reabsorption beyond the proximal tubule and that treatment with captopril increased urinary sodium excretion partly due to an attenuated sodium reabsorption in the proximal tubule. The present data in patients with congestive heart failure are consistent with an increased intrarenal angiotensin II generation and an elevated plasma level of aldosterone being involved in the pathogenesis of the glomerular hemodynamic changes and the enhanced distal tubular reabsorption, respectively.


1990 ◽  
Vol 79 (2) ◽  
pp. 123-129 ◽  
Author(s):  
Michael Allon ◽  
Charles B. Pasque ◽  
Mariano Rodriguez

1. Eight nephrotic patients were studied in order to evaluate the effects of acute changes in renal plasma flow and glomerular filtration rate on renal solute and water handling, in the absence of plasma volume expansion. 2. The subjects were studied first after the administration of captopril, a manoeuvre that increased renal plasma flow without a significant change in glomerular filtration rate, and a second time after receiving combined therapy with captopril and ibuprofen, a manoeuvre that decreased glomerular filtration rate without a significant change in renal plasma flow. 3. After captopril therapy, despite the increase in renal plasma flow, there was no significant change in proximal sodium reabsorption (as estimated from fractional lithium reabsorption), urine volume or urine osmolality. 4. The decrease in glomerular filtration rate observed after the administration of captopril plus ibuprofen was associated with decreases in fractional excretion of sodium and urine volume, and an increase in urine osmolality. The changes in these parameters of tubular function were proportionate to the changes in glomerular filtration rate. Fractional proximal sodium reabsorption increased substantially. 5. These observations suggest that, in the absence of plasma volume expansion, an increase in renal plasma flow does not increase sodium or water excretion by the nephrotic kidney. Moreover, during acute decreases in glomerular filtration rate, glomerulotubular balance appears to be disrupted, resulting in disproportionately high rates of proximal tubule sodium reabsorption.


2020 ◽  
Vol 25 ◽  
pp. 14-20
Author(s):  
Vitaliy Bondur ◽  
A.V. Klymenko

Introduction. Mineralocorticoids mainly affect the exchange of electrolytes, promote retention in the body of sodium, chlorides and water, and accelerate the excretion of potassium, calcium and magnesium. Their synthesis and blood supply are regulated mainly by angiotensin-II, which makes it possible to consider aldosterone as a part of renin-angiotensin-aldosteon system, which ensures the proper state of water-salt metabolism and hemodynamics. The purpose. Consider the relationship of dynamic balance of mineralocorticoids in patients with kidney and adrenal lesions. Material and methods. Review of contemporary and foreign literary sources; techniques - description, analysis, abstracting. Results. The pathogenesis of the development and progression of adrenal and kidney damage is closely associated with impaired synthesis, absorption of mineralocorticoids. The glucocorticoid activity of aldosterone roughly corresponds to 1/3 of cortisone. Main target organs of the hormone are salivary glands and kidneys. In the kidneys, aldosterone enhances sodium reabsorption. In pathological cases, the prolonged presence of chlorides and water in the body leads to the development of edema, hypernatremia, hypokalemia, hypervolemia, arterial hypertension, and sometimes, to the development of congestive heart failure. It poses particular danger in patients with impaired renal function. Deoxycorticosterone acetate (DOCSA) is a synthetic analogue of the Mineralocorticoids of the adrenal cortex. The drug is indicated for rapid-flowing adrenal hypofunction (addisonism), for myasthenia (increases muscle tone and performance), shock and trauma, for hypocorticism. Spironolactone is effective in swelling associated with increased aldosterone production, congestive heart failure, liver cirrhosis and nephrotic syndrome. Conclusions. Patients with kidney and adrenal lesions may have a violation of mineralocorticoid homeostasis, for the correction of which synthetic mineralocorticoids and their analogues, mineral and glucocorticoid antagonists, are used.


1981 ◽  
Vol 240 (5) ◽  
pp. F411-F422 ◽  
Author(s):  
J. Buerkert ◽  
D. Martin ◽  
J. Prasad ◽  
D. Trigg

Recollection micropuncture in Munich-Wistar rats was used to study the effects of intravenous hypertonic mannitol infusions on fluid reabsorption by surface nephrons, prior to the bend of Henle's loop of deep nephrons, and along the papillary collecting duct. During mannitol diuresis, single nephron glomerular filtration rate rose significantly in surface nephrons but fell in deep nephrons. Although mannitol increased the delivery of sodium and water to the end of the proximal tubule and to the first portion of the distal tubule of surface nephrons, water and sodium were reabsorbed between these two sites. In deep nephrons, water reabsorption prior to the bend of the loop of Henle was significantly decreased. Absolute sodium delivery to this site was reduced despite a marked decrease in fractional sodium reabsorption prior to the bend. Papillary osmolality was decreased. Renal plasma flow and inner medullary plasma flow (IMPF) increased proportionally. The reduced water extraction prior to the bend of deep nephrons and the decrease in papillary osmolality could have been partly due to a concomitant increase in IMPF and a decrease in sodium delivery to the medulla. The reabsorption of delivered sodium and water by the papillary collecting duct was reduced to a greater extent than could be expected from the increase in sodium delivery.


1990 ◽  
Vol 1 (6) ◽  
pp. 875-881
Author(s):  
C Baylis ◽  
P Harton ◽  
K Engels

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.


1999 ◽  
Vol 96 (1) ◽  
pp. 5-15 ◽  
Author(s):  
Kaare T. JENSEN ◽  
Hans EISKJÆR ◽  
Jan CARSTENS ◽  
Erling B. PEDERSEN

The effect of a continuous infusion of human brain natriuretic peptide, 2 ;pmol·min-1·kg-1, during 60 ;min was studied in nine patients with congestive heart failure and in 10 healthy control subjects. Brain natriuretic peptide increased from 1.6 to 101 ;pmol/l in control subjects and from 25 to 173 ;pmol/l in congestive heart failure during infusion. Urinary sodium excretion increased significantly in both congestive heart failure (60%) and control subjects (71%), but the absolute increase was significantly lower in congestive heart failure (27 ;μmol/min) than in control subjects (190 ;μmol/min). Urinary flow rate did not change. The lithium clearance technique was used to evaluate the segmental tubular function; the distal fractional reabsorption of sodium decreased significantly less in congestive heart failure (DFRNa: -0.8%) than in control subjects (DFRNa: -3.7%). Baseline values for glomerular filtration rate and renal plasma flow were reduced in congestive heart failure, but brain natriuretic peptide induced no significant changes between congestive heart failure and control subjects. Brain natriuretic peptide induced the same absolute increase in secondary messenger cGMP in plasma and urine in both patients and healthy subjects. It is concluded that the natriuretic response to brain natriuretic peptide infusion was impaired in patients with congestive heart failure compared with healthy subjects, and it is likely that the impaired natriuretic response was caused by a reduced responsiveness in the distal part of the nephron.


1973 ◽  
Vol 85 (1) ◽  
pp. 55-64 ◽  
Author(s):  
William M. Bennett ◽  
Grover C. Bagby ◽  
John N. Antonovic ◽  
George A. Porter

1998 ◽  
Vol 275 (3) ◽  
pp. R836-R843
Author(s):  
Norihisa Wada ◽  
M. Gore Ervin ◽  
Machiko Ikegami

Renal adaptive responses during the 24 h after delivery in term newborn lambs include marked increases in both glomerular filtration rate (GFR) and sodium reabsorption. This study investigated the effects of ventilation style on cardiovascular, renal, and endocrine adaptations in preterm newborn lambs. Lambs ( n = 62) were delivered by cesarean section at 131 days gestation (term = 150 days), treated with surfactant, and randomized to one of three ventilation strategies: high-frequency oscillation (12 Hz), high rate (50 breaths/min; tidal volume = 8 ml/kg), or low rate (15 breaths/min; tidal volume = 15 ml/kg). Lambs (5 or 6/group) were ventilated for 2, 5, 10, and 24 h to maintain arterial[Formula: see text] between 45 and 50 mmHg. Plasma vasopressin levels decreased to <25 pg/ml by 10 h, and fractional sodium excretion decreased to <1% by 16 h in all groups. However, cardiac output, renal plasma flow, and GFR values did not change over time for any of the groups. The style of ventilation employed had no measurable effects on overall cardiovascular, renal, or endocrine function. We conclude in ventilated preterm lambs that 1) the ventilation style does not affect the time course for postnatal adaptation, 2) adaptive changes in renal tubular sodium reabsorption are evident by 16 h after birth, and 3) changes in preterm newborn renal sodium reabsorption occur in the absence of postnatal changes in renal plasma flow or GFR.


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