• The Korean Journal of Physiology
• /
• v.23 no.1
• /
• pp.67-78
• /
• 1989

Since the atrial receptor was suggested to be involved in the control of extracellular fluid volume, it has been shown that the granularity of atrial cardiocytes can be changed by water and salt depletion, and that an extract of atrial tissue, when injected intravenously into anesthetized rats, causes a large and rapid increase in renal excretions of sodium and water. The immunoreactive atrial natriuretic peptide (ANP) has been found in the plasma of patients suffering from various cardiovascular diseases. A high level of ANP in the plasma has been reported in essential hypertension. Several studies on the effects of ANP on renal function and arterial blood pressure have presented contradictory results showing attenuated or accentuated responses. Thus, involvement of the ANP in the development of hypertension remains unresolved. Present study was undertaken to investigate whether the ANP is involved in the development of hypertension in two-kidney one-clip Goldblatt hypertensive rats. The plasma concentration of immunoreactive ANP appeared to be significantly elevated in hypertensive rats as compared with normotensive Goldblatt operated and sham-operated rats. Plasma renin concentration was higher in hypertensive rats than in normotensive rats, as observed in earlier experiments. Intravenous infusions of ANP resulted in increases of urine flow and urinary excretions of sodium and potassium in both hypertensive and normotensive rats. The renal response to ANP was markedly accentuated in Goldblatt hypertensive rats. The plasma concentration of ANP showed a linear relationship with the arterial blood pressure. Infusions of ANP reduced blood pressure both in hypertensive and normotensive rats. These results suggest that in Goldblatt hypertensive rats an elevation of ANP level in the plasma may not be a cause, but instead a consequence of hypertension, and that the renal responsiveness to the ANP is accentuated by some unknown mechanisms.

• The Korean Journal of Physiology and Pharmacology
• /
• v.2 no.1
• /
• pp.77-84
• /
• 1998

Ureteral obstruction causes increase in renal blood flow (RBF) and partial impairment of the autoregulation of RBF. Although increased renal prostaglandin production is responsible for the former, it is not clear whether or not it is also responsible for the latter. Therefore, we investigated the role which prostaglandins play in the autoregulation of RBF during an ureteral pressure elevation (40 $cmH_2O$). Since the major mechanism of RBF autoregulation is the tubuloglomerular feedback, studying the interaction between ureteral pressure and RBF autoregulation may reveal the role of prostaglandin in tubuloglomerular feedback. To pursue the purpose, six anesthetized dogs were prepared for the measurements of RBF, mean sytemic and renal arterial pressure (RAP) and the manipulation of ureteral pressure. The autoregulation curves were determined during both control and elevation of the ureteral pressure, before and after the pretreatment with indomethacin, a cyclooxygenase inhibitor. The desired ureteral pressure was achieved by vertically elevating the water-filled reservoir connected to the ureteral catheter to 40 cm above the kidney level. In response to the elevation of the ureteral pressure, RBF increased from $170{\pm}8 ml{\cdot}min^{-1}\;to\;189{\pm}8$, and the systemic arterial pressure didn't change significantly. During spontaneous urine flow, RBF autoregulation was abolished when RAP was reduced to $59{\pm}3$ mmHg. On the other hand, during the ureteral pressure elevation, the autoregulation curves shifted upward and rightward from control, and the pressure when RBF autoregulation was abolished was $74{\pm}3$ mmHg. The pretreatment of the dogs with indomethacin failed to affect the lower limit of RBF autoregulaion during both control ($63{\pm}5$ mmHg) and the elevated ureteral pressure ($77{\pm}5$ mmHg). Since RBF failed to increase in response to the elevated ureteral pressure, RBF autoregulation curves obtained during the elevated ureteral pressure shifted only rightward from indomethacin control. The results indicate that the increased intrarenal level of prostaglandin or prostaglandin-induced vasodilation does not appear to bear any relation to the reduction in the autoregulatory capacity during partial ureteral obstruction. It seems that the partial impairment of the autoregulation during acute ureteral obstruction is due to the consumption of tubuloglomerular feedback mechanism at spontaneous RAP and that prostaglandin is neither mediator nor effector of tubuloglomerular feedback mechanism.

• YAKHAK HOEJI
• /
• v.29 no.6
• /
• pp.362-366
• /
• 1985

These paper was attempted to investigate the mechanism of increased blood level of sulfisomidine by cimetidine pretreatment pharmacokinetically. Especially, effect of cimetidine pretreatment on both renal clearance and biliary clearance of sulfisomidine was studied in rabbits. The results are as follows. The blood level of sulfisomidine administered intravenously in dose of 25mg/kg was elevated significantly by cimetidine pretreatment. Relative bioavailability and biological half-life were increased significantly by cimetidine pretreatment. Overall elimination rate constant ($betha$) and distribution rate constant ($K_{13}$) of sulfisomidine were decreased significantly by cimetidine pretreatment. The renal and biliary clearance of sulfisomidine were decreased significantly compared with those of control rabbits by cimetidine pretreatment. The results may be also related to the inhibition of sulfisomidine metabolism enzyme activity or reduction of blood flow in the liver.

• Childhood Kidney Diseases
• /
• v.19 no.2
• /
• pp.71-78
• /
• 2015

The incidence of acute kidney injury (AKI) in critically ill pediatric patients has been reported as increasing to 25 %, depending on population characteristics. The etiology of AKI has changed over the last 10-20 years from primary renal disease to the renal conditions associated with systemic illness. The AKI in pediatric population is associated with increased mortality and morbidity, and prevention is needed to reduce the consequence of AKI. It is known that the most important risk factors for AKI in critically ill pediatric patients are clinical conditions to be associated with decreased renal blood flow, direct renal injury, and illness severity. Renal hypoperfusion leads to neurohormonal activation including renin-angiotensin-aldosterone system, sympathetic nervous system, antidiuretic hormone, and prostaglandins. Prolonged renal hypoperfusion can result in acute tubular necrosis. The direct renal injury can be predisposed under the condition of renal hypoperfusion, and appropriate treatment of volume depletion is important to prevent AKI. The preventable causes of AKI include contrast-induced nephropathy, hemodynamic instability, inappropriate mediation use, and multiple nephrotoxic insults. Given the evidence of preventable factors for AKI, several actions such as the use of protocol for prevention of contrast-induced nephropathy, appropriate treatment of volume depletion, vigorous treatment of sepsis, avoidance of combinations of nephrotoxic medications, and monitoring of levels of drugs should be recommended.

• The Korean Journal of Pharmacology
• /
• v.2 no.1 s.2
• /
• pp.13-16
• /
• 1966

The action of serotonin (5-Hydroxytryptamine) on the excretory function of the kidney was investigated in the dog, utilizing the clearance method and the stop-flow technique. It was shown that serotonin, $10{\mu}g/kg/min$, i. v., exerts a marked antidiuretic effects and elicits a marked hemodynamic changes in the kidney: a highly significant decrease of the glomerular filtration rate and a tendency of decrement in the renal plasma flow. Little change in the systemic blood pressure was noted, and the participation of the antidiuretic hormone in the antidiuretic action was ruled out by adding vasopressin to the infusion fluid. The stop-flow analysis showed that there is no evidence of altered activity in the tubules by serotonin. It was thus concluded that serotonin elicits anti diuresis in the dog by decreasing glomerular filtration rate, which results from the constriction of Vas afferens in the glomeruli.

• Asian-Australasian Journal of Animal Sciences
• /
• v.23 no.3
• /
• pp.355-365
• /
• 2010

The aim of this study was to investigate the effect of supplemental recombinant bovine somatotropin (rbST) and cooling with misters and fans on renal function in relation to regulation of body fluids in different stages of lactation in crossbred Holstein cattle. Ten, 87.5% crossbred Holstein cattle were divided into two groups of 5 animals each, housing in a normal shaded barn (NS) and in a shaded barn with a mister-fans cooling system (MF). The experiment in each group was divided into 3 phases, early- (Day 75 postpartum), mid- (Day 135 postpartum), and late stage of lactation (Day 195 postpartum). The pre-treatment study was conducted on the starting day of each stage of lactation and the treatment study was performed after the end of the pre-treatment, during which the animal was injected with 500 mg of rbST (POSILAC) every 14 days for three times. During the study, ambient temperature at the hottest period daily in the MF barn was significantly lower, while relative humidity was higher than that of the NS barn. The temperature humidity index (THI) in both barns ranged from 79-85 throughout the periods of study. Cows in the MF barn showed a lower rectal temperature and respiration rate as compared with cows in the NS barn. The effect of rbST administration increased both rectal temperature and respiration rates of cows housed in either the NS or MF barn. Milk yield significantly increased in cows treated with rbST in all stages of lactation. Increases in mammary blood flow, accompanied by increases of total body water (TBW), extracellular fluid (ECF), blood volume (BV) and plasma volume (PV), were observed in both groups of cows receiving rbST in all stages of lactation. No alterations of renal blood flow and glomerular filtration rate were observed in cows receiving rbST, but decreases in urinary excretion and fractional excretion of sodium, potassium and chloride ions appeared to correlate with reduction in the rate of urine flow and osmolar clearance during rbST administration. These results suggest that the effect of rbST supplementation to cows housed either in NS or MF barns on body fluid volume expansion is attributable to changes in the rate of electrolyte excretion by the kidney. The increased availability of renal tubular reabsorption of sodium, potassium and chloride ions during rbST treatment was a major factor in retaining body water through its colligative properties in exerting formation of an osmotic force mechanism.

• Asian-Australasian Journal of Animal Sciences
• /
• v.20 no.5
• /
• pp.742-747
• /
• 2007

In order to investigate the mechanism of adaptation to long-term heat stress, six female buffalo calves of about 7 to 8 months age, were exposed to the cool-comfort environment (THI 65) for 21 days to obtain normal values of blood acid-base. An adaptive response of acid-base regulation was determined to long term (21 days) exposure of buffalo calves to hot-dry (THI 80) and hot-humid (THI 84) conditions. Higher rectal temperature and respiratory rate was recorded under hot-humid exposure compared to hot-dry. Significant reduction in the rectal temperature and respiratory rate on day 21 of hot-dry exposure indicated early thermal adaptation compared to hot-humid. Decreasing rectal temperature and respiratory rate from day 1 to 21 was associated with concurrent decrease in blood pH and pCO2. Increased plasma chloride concentration with low base excess in blood and in extracellular fluid suggested compensatory response to respiratory alkalosis. Reduced fractional excretion of sodium with increased fractional excretion of potassium and urine flow rate indicated renal adaptive response to heat stress.

• YAKHAK HOEJI
• /
• v.35 no.1
• /
• pp.38-44
• /
• 1991

It has been reported that the pharmacokinetic behaviors of drugs which are mostly metabolized in the liver are significantly different in patients with renal failure. Theophylline(TP) is mainly metabolized in the liver (approximately 90%) and renal clearance of the drug is negligible (less than 10%). Therefore, we have investigated the changes in pharmacokinetics of theophylline in normal, G-ARF and U-ARF rats after an intravenous administration. The total body clearance of TP decreased approximately 40% in U-ARF rats. The reduced CL$_{T}$, value in U-ARF rats could be due to reduced hepatic intrinsic clearance by up to 40% since it has been published that plasma protein binding of TP and liver blood flow does not change in U-ARF rats.

• Journal of Korean Academy of Nursing
• /
• v.46 no.5
• /
• pp.642-652
• /
• 2016

Purpose: In this single repeated measures study, an examination was done on the effects of dialysate flow rate on dialysis adequacy and fatigue in patients receiving hemodialysis. Methods: This study was a prospective single center study in which repeated measures analysis of variance were used to compare Kt/V urea (Kt/V) and urea reduction ratio (URR) as dialysis adequacy measures and level of fatigue at different dialysate flow rates: twice as fast as the participant's own blood flow, 500 mL/min, and 700 mL/min. Thirty-seven hemodialysis patients received all three dialysate flow rates using counterbalancing. Results: The Kt/V ($M{\pm}SD$) was $1.40{\pm}0.25$ at twice the blood flow rate, $1.41{\pm}0.23$ at 500 mL/min, and $1.46{\pm}0.24$ at 700 mL/min. The URR ($M{\pm}SD$) was $68.20{\pm}5.90$ at twice the blood flow rate, $68.67{\pm}5.22$ at 500 mL/min, and $70.11{\pm}5.13$ at 700 mL/min. When dialysate flow rate was increased from twice the blood flow rate to 700 mL/min and from 500 mL/min to 700 mL/ min, Kt/V and URR showed relative gains. There was no difference in fatigue according to dialysate flow rate. Conclusion: Increasing the dialy-sate flow rate to 700 mL/min is associated with a significant increase in dialysis adequacy. Hemodialysis with a dialysate flow rate of 700 mL/min should be considered in selected patients not achieving adequacy despite extended treatment times and optimized blood flow rate.

• The Korean Journal of Physiology
• /
• v.23 no.2
• /
• pp.363-375
• /
• 1989

It has been well known that peripheral infusion of angiotensin II results in an increase of blood pressure, and an elevation of aldosterone secretion, and an inhibition of renin relase. However, the direct effect of angiotensin II on renal function has not been clearly established. In the present study, to investigate the effect of angiotensin II on renal function and renin release, angiotensin II (0.3, 3 and 10 ng/kg/min) was infused into a unilateral renal artery of the unanesthetized rabbit and changes in renal function and active and inactive renin secretion rate (ARSR, IRSR) were measured. In addition, to determine the relationship between the renal effect of angiotensin II and adenosine, the angiotensin II effect was evaluated in the presence of simultaneously infused 8-phenyltheophylline (8-PT, 30 nmole/min), adenosine A 1 receptor antagonist. Angiotensin II infusion at dose less than 10 ng/kg/min decreased urine flow, clearances of para-amino-hippuric acid and creatinine, and urinary excretion of electrolytes in dose-dependent manner. The changes in urine flow and sodium excretion were significantly correlated with the change in renal hemodynamics. Infusion of angiotensin II at 10 ng/kg/min also decreased ARSR, but it has no significant effect on IRSR. The change in ARSR was inversely correlated with the change in IRSR. The plasma concentration of catecholamine was not altered by an intarenal infusion of angiotensin II. In the presence of 8-PT in the infusate, the effect of angiotensin II on renal function was significantly attenuated, but that on renin secretion was not modified. These results suggest that the reduction in urine flow and Na excretion during intrarenal infusion of angiotensin II was not due to direct inhibitions of renal tubular transport systems, but to alterations of renal hemodynamics which may partly be mediated by the adenosine receptor.