Stress and sodium intake in neural control of renal function in hypertension.

Hypertension ◽  
1991 ◽  
Vol 17 (4_Suppl) ◽  
pp. III2-III2 ◽  
Author(s):  
G. F. DiBona
Keyword(s):  
Renal Function ◽  
Neural Control ◽  
Sodium Intake

Neural Control of Renal Function

1985 ◽  
Vol 7 (Supplement) ◽  
pp. S24 ◽  
Author(s):  
DiBona
Keyword(s):  
Renal Function ◽  
Neural Control

Intrarenal renin inhibition increases renal function by an angiotensin II-dependent mechanism

1988 ◽  
Vol 255 (4) ◽  
pp. F749-F754 ◽  
Author(s):  
H. M. Siragy ◽  
N. E. Lamb ◽  
C. E. Rose ◽  
M. J. Peach ◽  
R. M. Carey
Keyword(s):  
Renal Function ◽  
Angiotensin Ii ◽  
Sodium Intake ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Competitive Inhibitor ◽  
Urinary Flow ◽  
Renin Substrate ◽  
Plasma Aldosterone Concentration ◽  
Renin Inhibition

ACRIP is a competitive inhibitor of renin in which an analogue of statine, (3R,4S)-4-amino-3-hydroxy-6-methylheptanoic acid, is incorporated into analogues of porcine renin substrate. ACRIP inhibits the enzymatic activity of renin, thus blocking the initiation of the angiotensin cascade. We studied the intrarenal action of ACRIP in small quantities without measurable systemic effects on renal function. In the first experiment, ACRIP was administered intrarenally at 0.02, 0.2, and 2 micrograms.kg-1.min-1 to uninephrectomized conscious dogs (n = 6) in metabolic balance at sodium intake of 10 meq/day. ACRIP, in doses of 0.02 and 0.2 micrograms.kg-1.min-1, markedly increased urine sodium excretion (UNaV) from 5.8 +/- 1.4 to 15.1 +/- 5.1 and 19.9 +/- 3.2 mu eq/min, respectively. Urinary flow rate (UV) underwent a similar increase and glomerular filtration rate (GFR) increased from 25.7 +/- 2.5 to 35.6 +/- 2.5 at 0.02 micrograms.kg-1.min-1 of ACRIP. Renal plasma flow (RPF), plasma renin activity (PRA), and plasma aldosterone concentration (PAC) were not affected. At 2 micrograms.kg-1.min-1, ACRIP traversed the kidney in quantities large enough to produce a reduction in systemic PRA and mean arterial pressure and caused natriuresis, diuresis, and increased GFR. In a second experiment, ACRIP was administered intrarenally at 0.2 micrograms.kg-1.min-1 in a separate group (n = 4) under identical conditions. ACRIP-induced increases in UV and UNaV were completely blocked by concurrent intrarenal administration of angiotensin II. The results indicate that intrarenal angiotensin II acts as a physiological regulator of renal sodium and fluid homeostasis.

scholarly journals Role of the endothelium-dependent relaxing factor nitric oxide on renal function.

1992 ◽  
Vol 2 (9) ◽  
pp. 1371-1387 ◽  
Author(s):  
J C Romero ◽  
V Lahera ◽  
M G Salom ◽  
M L Biondi
Keyword(s):  
Nitric Oxide ◽  
Renal Function ◽  
Perfusion Pressure ◽  
Sodium Intake ◽  
Systemic Circulation ◽  
Renal Perfusion ◽  
Renin Release ◽  
High Sodium ◽  
Renal Perfusion Pressure

The role of nitric oxide in renal function has been assessed with pharmacologic and physiologic interventions. Pharmacologically, the renal vasodilation and, to some extent, the natriuresis produced by endothelium-dependent vasodilators such as acetylcholine and bradykinin are mediated by nitric oxide and also by prostaglandins. However, prostaglandins and nitric oxide do not participate in the renal effects produced by endothelium-independent vasodilators such as atrial natriuretic peptide, prostaglandin I2, and nitroprusside. Physiologically, nitric oxide and prostaglandins exert a strong regulation on the effects produced by changes in renal perfusion pressure. Increments in renal perfusion pressure within the range of RBF autoregulation appear to inhibit prostaglandin synthesis while simultaneously enhancing the formation of nitric oxide. Nitric oxide modulates autoregulatory vasoconstriction and at the same time inhibits renin release. Conversely, a decrease of renal perfusion pressure to the limit of or below RBF autoregulation may inhibit the synthesis of nitric oxide but may trigger the release of prostaglandins, whose vasodilator action ameliorates the fall in RBF and stimulates renin release. Nitric oxide and prostaglandins are also largely responsible for mediating pressure-induced natriuresis. However, unlike prostaglandins, mild impairment of the synthesis of nitric oxide in systemic circulation produces a sustained decrease in sodium excretion, which renders blood pressure susceptible to be increased during high-sodium intake. This effect suggests that a deficiency in the synthesis of nitric oxide could constitute the most effective single disturbance to foster the development of a syndrome similar to that seen in salt-sensitive hypertension.

scholarly journals Enhanced Responses of Blood Pressure, Renal Function, and Aldosterone to Angiotensin I in the DD Genotype Are Blunted by Low Sodium Intake

2002 ◽  
Vol 13 (4) ◽  
pp. 1025-1033
Author(s):  
Frank G. H. van der Kleij ◽  
Paul E. de Jong ◽  
Rob H. Henning ◽  
Dick de Zeeuw ◽  
Gerjan Navis
Keyword(s):  
Renal Function ◽  
Vascular Resistance ◽  
Sodium Intake ◽  
Renal Vascular Resistance ◽  
Hemodynamic Parameters ◽  
Angiotensin I ◽  
Low Sodium ◽  
Renal Hemodynamic ◽  
Intake Level ◽  
Renal Vascular

ABSTRACT. Angiotensin-converting enzyme (ACE) activity is increased in the DD genotype, but the functional significance for renal function is unknown. Blunted responses of BP and proteinuria to ACE inhibition among DD renal patients during periods of high sodium intake were reported. It was therefore hypothesized that sodium status affects the phenotype in the ACE I/D polymorphism. The effects of angiotensin I (AngI) and AngII among 27 healthy subjects, with both low (50 mmol sodium/d) and liberal (200 mmol sodium/d) sodium intakes, were studied. Baseline mean arterial pressure (MAP) values, renal hemodynamic parameters, and renin-angiotensin system parameters were similar for all genotypes with either sodium intake level. With liberal sodium intake, the increases in MAP, renal vascular resistance, and aldosterone levels during AngI infusion (8 ng/kg per min) were significantly higher for the DD genotype, compared with the ID and II genotypes (all parameters presented as percent changes ± 95% confidence intervals), with mean MAP increases of 22 ± 2% (DD genotype), 13 ± 5% (ID genotype), and 12 ± 6% (II genotype) (P < 0.05), mean increases in renal vascular resistance of 100.1 ± 19.7% (DD genotype), 73.0 ± 16.3% (ID genotype), and 63.2 ± 16.9% (II genotype) (P < 0.05), and increases in aldosterone levels of 650 ± 189% (DD genotype), 343 ± 71% (ID genotype), and 254 ± 99% (II genotype) (P < 0.05). Also, the decrease in GFR was more pronounced for the DD genotype, with mean decreases of 17.9 ± 4.7% (DD genotype), 8.8 ± 3.4% (ID genotype), and 6.4 ± 5.9% (II genotype) (P < 0.05). The effective renal plasma flow, plasma AngII concentration, and plasma renin activity values were similar for the genotypes. In contrast, with low sodium intake, the responses to AngI were similar for all genotypes. The responses to AngII were also similar for all genotypes, with either sodium intake level. In conclusion, the responses of MAP, renal hemodynamic parameters, and aldosterone concentrations to AngI are enhanced for the DD genotype with liberal but not low sodium intake. These results support the presence of gene-environment interactions between ACE genotypes and dietary sodium intake.

THE USE AND MODE OF ACTION OF ETHACRYNIC ACID IN NEPHROGENIC DIABETES INSIPIDUS

PEDIATRICS ◽  
1966 ◽  
Vol 37 (3) ◽  
pp. 447-455
Author(s):  
David M. Brown ◽  
John W. Reynolds ◽  
Alfred F. Michael ◽  
Robert A. Ulstrom
Keyword(s):  
Renal Function ◽  
Diabetes Insipidus ◽  
Nephrogenic Diabetes Insipidus ◽  
Acid Metabolism ◽  
Ethacrynic Acid ◽  
Sodium Intake ◽  
Urine Volume ◽  
Free Water ◽  
Chloride Excretion ◽  
Diuretic Agents

The use of diuretic agents in the treatment of nephrogenic diabetes insipidus had been reported to result in decreased urine volume and decreased clearance of free water. A study of the use of ethacrynic acid, a potent saluretic agent, was instituted in patients with nephrogenic diabetes insipidus in an attempt to achieve a significant antidiuretic response while allowing a liberal sodium diet. Intravenous ethacrynic acid resulted in decreased urine volume, decreased clearance of free water and decreased RPF and GFR. Prolonged oral administration of ethacrynic acid promoted a significant antidiuretic response when the daily sodium intake was limited to 60 mEq. The effect of ethacrynic acid on renal function, potassium and chloride. excretion, and uric acid metabolism are discussed.

Steady-state arterial pressure-urinary output relationships during ovine pregnancy

1992 ◽  
Vol 263 (5) ◽  
pp. R1141-R1146
Author(s):  
E. W. Quillen ◽  
B. S. Nuwayhid
Keyword(s):  
Renal Function ◽  
Steady State ◽  
Arterial Pressure ◽  
Sodium Intake ◽  
Control Level ◽  
Urine Volume ◽  
Urinary Sodium Excretion ◽  
Pregnant Sheep ◽  
Plasma Angiotensin ◽  
Steady State Levels

To determine the effects of long-term changes in sodium intake on mean arterial pressure (MAP) regulation during pregnancy, nonpregnant (n = 16) and 110- to 140-day pregnant (n = 13) ewes received total daily sodium intakes of 10, 30, 100, 400, and 1,200 mmol for 7 days. The sheep were housed in metabolism cages and MAP was monitored 24 h/day. Urinary sodium excretion (UNaV) followed changes in sodium intake, with steady-state levels being achieved with similar degrees of rapidity (2-3 days) in nonpregnant and pregnant sheep. At 10 mmol/day sodium intake, MAP was lower (79 +/- 1 vs. 82 +/- 2 mmHg; P < 0.01) and water intake (2,275 +/- 494 vs. 3,286 +/- 725 ml/day; P < 0.001) and 24-h urine volume (1,454 +/- 279 vs. 2,299 +/- 496 ml/day; P < 0.01) were greater in pregnant sheep. All of these variables exhibited direct relationships with increases in sodium intake. Plasma angiotensin II (pANG II) was increased in pregnancy (10.6 +/- 1.6 vs. 24.5 +/- 6.3 pg/ml; P < 0.001) at 10 mmol/day. Elevation of sodium intake suppressed pANG II to minimal levels in nonpregnant sheep, but to only 25% of the control level in pregnant sheep. During pregnancy, the renal function curve representing the steady-state MAP-UNaV relationship was shifted to lower MAP setpoint, but the sodium sensitivity of MAP was unchanged. Also, the inverse relationship of sodium intake and pANG II was blunted, suggesting a reduced role for ANG II in the maintenance of renal function during pregnancy.

Physiology in perspective: The Wisdom of the Body. Neural control of the kidney

2005 ◽  
Vol 289 (3) ◽  
pp. R633-R641 ◽  
Author(s):  
Gerald F. DiBona
Keyword(s):  
Nervous System ◽  
Renal Function ◽  
Autonomic Nervous System ◽  
Neural Control ◽  
Sympathetic Nerves ◽  
The Body ◽  
Regulatory Agencies ◽  
Internal Environment ◽  
Renal Sympathetic

Cannon equated the fluid matrix of the body with Bernard’s concept of the internal environment and emphasized the importance of “the safe-guarding of an effective fluid matrix.” He further emphasized the important role of the autonomic nervous system in the establishment and maintenance of homeostasis in the internal environment. This year’s Cannon Lecture discusses the important role of the renal sympathetic nerves to regulate various aspects of overall renal function and to serve as one of the major “self-regulatory agencies which operate to preserve the constancy of the fluid matrix.”

Neural control of renal function in health and disease

1994 ◽  
Vol 4 (1-2) ◽  
pp. 69-74 ◽  
Author(s):  
Gerald F. DiBona
Keyword(s):  
Renal Function ◽  
Neural Control ◽  
Health And Disease

Rhythmic changes in renal function in the rat

1965 ◽  
Vol 209 (6) ◽  
pp. 1187-1192 ◽  
Author(s):  
George A. Bray
Keyword(s):  
Renal Function ◽  
Cold Exposure ◽  
Sodium Excretion ◽  
Urine Output ◽  
Sodium Intake ◽  
Urine Volume ◽  
Potassium Excretion ◽  
Electrolyte Excretion ◽  
Threefold Increase ◽  
Electrolyte Intake

Cold exposure causes rats to increase their urine output. This increase in urine output was found to occur in 5- to 8-day cycles with peak urine volumes three or more times the volumes prior to exposure to the cold. Cycles in urine volume occurred on a constant electrolyte intake and in animals receiving exogenous Pitressin. The peaks in urine volume were accompanied by a threefold increase in the variability of sodium excretion but not potassium excretion. The increase in urine volume which occurred at the same time in all rats in a group began at night and continued through the following day. These data have been discussed in the light of a possible mechanism controlling sodium intake with water intake and electrolyte excretion.

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