• The Korean Journal of Physiology
• /
• v.23 no.1
• /
• pp.51-66
• /
• 1989

Mammalian cardiocytes secrete atrial natriuretic peptides (ANPs) into plasma, which cause marked natriuresis, diuresis, vasorelaxation and inhibition of hormone secretions. Aging influences the ability of the kidney both to conserve and to excrete sodium; i.e., in old animals, the excretory capacity of sodium is reduced and the time required to excrete sodium load is prolonged. Therefore, it is possible that animals differing in ages may respond differently to ANP. In the present study, we determined whether the renal, hormonal and vascular effects of ANP may be influenced by aging in conscious rabbits. The plasma renin concentration decreased with aging but plasma ANP concentration was significantly lower only in 24-month-old rabbits. Plasma aldosterone concentration and atrial ANP content did not change by aging. In 1-month-old rabbits, ANP (atriopeptin III, 3 ug/kg) administered intravenously caused hypotension and decreased in plasma renin and aldosterone concentrations, but did not cause diuresis and natriuresis. In 2 to 5 month-old rabbits, ANP caused hypotension, decreases in Plasma renin and aldosterone concentrations and marked renal effects. However, in 24-month-old rabbits, all the above effects of ANP was blunted. With hydration of physiological saline at a rate of 15 ml/kg/h for 2hr, urine volume and glomerular filtration rate did not change but the electrolyte excretion as well as fractional excretion of sodium significantly increased. The plasma concentrations of active renin and aldosterone were decreased but plasma inactive renin and ANP concentrations were increased. The changes in renal function and plasma level of hormone showed no differences in different ages. These results suggest that the peripheral vascular receptors to ANP may develop earlier than those in the kidney, and the attenuated vascular and renal responses to ANP in the old age may be due to age-related modifications in renal function and blood vessel.

• The Korean Journal of Pharmacology
• /
• v.21 no.1
• /
• pp.49-61
• /
• 1985

In view of the facts that dopamine (DA) when given directly into a lateral ventricle (i.c.v.) of the rabbit brain induces antidiuresis and that haloperidol, a non-specific antagonist of DA receptors, produces anti-diuresis in smaller doses and diuresis and natriuresis in larger doses, the present study was undertaken to delineate the roles of various DA receptors involved in the center-mediated regulation of renal function. Bromocriptine (BRC), a relatively specific agonist of D-2 receptors and at the same time a D-,1 antagonist, elicited natriuresis and diuresis when given i.c.v. in doses ranging from 20 to 600 {\mu}g/kg$, roughly in dose-related fashion, while the renal perfusion and glomerular filtration progressively decreased with doses, indicating that the diuretic, natriuretic action resides in the tubules, not related to the hemodynamic effects. These diuresis and natriuresis were most marked with 200 ${\mu}g/kg$, with the fractional sodium excretion reaching about 10%. With 600 ${\mu}g/kg$, however, the diuretic, natriuretic action was preceded by a transient oliguria resulting from severe reduction of renal perfusion, concomitant with marked but transient hypertension. When given intravenously, however, BRC produced antidiuresis and antinatriuresis along with decreases in renal hemodynamics associated with systemic hypotension, thus indicating that the renal effects produced by i.c.v. BRC is not caused by a direct renal effects of the agent which might have reached the systemic circulation. In experiments in which DA was given i.c.v. prior to BRC, 150 ${\mu}g/kg$ DA did not affect the effects of BRC (200 ${\mu}g/kg$), while 500 ${\mu}g/kg$ DA abolished the BRC effect. In rabbits treated with reserpine, 1 mg/kg i.v.,24 h prior to the experiment, i.c.v. BRC could unfold its renal effects not only undiminished but rather exaggerated and more promptly. In preparations in which one kidney is deprived of nervous connection, the denervated kidney responded with marked diuresis and natriuresis, whereas the innervated, control kidney exhibited antidiuresis. These observations suggest that i.c.v. BRC influences the renal function through release of some humoral natriuretic factor as well as by increasing sympathetic tone, and that various DA receptors might be involved with differential roles in the center-mediated regulation of the renal function.

• The Korean Journal of Pharmacology
• /
• v.13 no.2
• /
• pp.35-39
• /
• 1977

Cyclic adenosine monophosphate (cAMP), known as a versatile regulator of cellular processes and as a secondary messenger of various hormones and other biogenic agents, such as prostaglandins and histamine, induced prompt and transient antidiuresis followed by mild natriuresis and diuresis, when it was administered into the lateral ventricle of the rabbit in doses ranging from $100\;{\mu}g$ to 1 mg. The initial antidiuresis was brought about by the systemic hypotension, whereas the secondary diuresis seemed to be resulted from the decreased tubular reabsorption of sodium, suggestive of participation of certain endogenous natriuretic agent. This observation suggests that cAMP might be involved in the center-mediated renal action of prostaglandins.

• YAKHAK HOEJI
• /
• v.37 no.6
• /
• pp.561-570
• /
• 1993

Renal action of domperidone known as dopamine receptor blocker and effect of domperidone on renal function of dopamine were investigated in dog. Domperidone, when administered into vein, produced diuretic action by the improvement of renal hemodynamic state, when given into a renal artery, elicited diuretic action accompanied with natriuresis in only experimental kidney, whereas domperidone given into carotid artery exhibited antidiuretic action by the decrease of Na$^{+}$ excretion in urine. Diuretic action of dopamine was not influenced by domperidone given into vein or into a renal artery, was blocked by domperidone given into carotid artery. Above results suggest that domperidone produced both peripheral diuretic and central antidiuretic action, and domperidone do not block diuretic action by renal hemodynamic improvement of dopamine in kidney.

• The Korean Journal of Pharmacology
• /
• v.24 no.1
• /
• pp.135-145
• /
• 1988

Dopamine when given icv induces antidiuresis along with transient natriuretic tendency, and it has been suggested that both subtypes of central dopamine receptors may influence renal function differentially. This study was undertaken to delineate the role of central $D_2$ receptors employing domperidone (DOM), a selective $D_2$ antagonist. DOM icv elicited antidiuresis and antinatriuresis in doses ranging from 15 to $135{\mu}g/kg$. GFR and RPF as well as sodium excretion decreased. Systemic blood pressure increased slightly. Intravenous DOM did not elicit significant changes in sodium excretion. Denervation of the kidney abolished the hemodynamic change induced by icv DOM, but sodium excretion decreased on both innervated and denervated kidneys. No diuretic tendency was uncovered by the denervation. Dopamine, $150{\mu}g/kg$ icv, produced antidiuresis along with decreases in hemodynamics. These effects were not affected by DOM-pretreatment, and no natriuretic tendency was unveiled. Bromocriptine, a $D_2$ receptor agonist, $200{\mu}g/kg$ icv, elicited marked diuresis and natriuresis, which were completely abolished by DOM-pretreatment. Apomorphine, another prototype of $D_2$ agonist, $150{\mu}g/kg$ icv, produced diuresis and natrituresis with increases in renal hemdoynamics, followed by decreases in all parameters. DOM-pretreatment did not affect the renal hemodynamic effects, wherease the increases in urine flow and sodium excretion were markedly reduced by DOM, Present study suggests that central $200{\mu}g/kg$ receptors mediate natriuretic and diuretic influence to the kidney, possibly through mediation of natriuretic humoral factor, and provide further evidence supporting the hypothesis that central $200{\mu}g/kg$ receptors mediate antidiuretic influence via nerve pathway, whereas natriuresis are brought about through mediation of central $200{\mu}g/kg$ receptors.

• The Korean Journal of Physiology
• /
• v.24 no.1
• /
• pp.131-144
• /
• 1990

It is well known that the atrial natriuretic peptide (ANP) has a prepro-hormone of 151 amino-acids which loses their hydrophobic signal peptide to form 126 amino acid prohormone. The whole prohormone is released and then cleaved by proteases into more than one circulating forms. Recently, Winters et al. (1988a, b) reported that high concentrations of N-terminal fragments of prepro-ANP $(26{\sim}55),\;(56{\sim}92)\;and\;(104{\sim}123)$ were detected in human plasma. However, their physiological roles have not been established. The present study was conducted to determine whether the N-terminal fragments of pro-ANP have any effect on the renal function and to compare the effect with those of G-terminal fragments of pro-ANP The results indicate that intrarenal arterial infusions of prepro-ANP $(26{\sim}41),\;(26{\sim}55),\;(56{\sim}92)\;and\;(104{\sim}123)$ induced no significant changes in renal function. Whereas ${\alpha}-human$ ANP $(prepro-ANP,\;124{\sim}151)$ and pro-ANP caused a significant increase in urine volume, renal plasma flow, glomerular filtration rate, urinary excretions of sodium, chloride and potassium, and fractional excretion of sodium. These results suggest that the N-terminal fragments of pro-ANP are ineffective, while the C-terminal fragments retain the natriuretic and diuretic activities.

• The Korean Journal of Physiology and Pharmacology
• /
• v.1 no.4
• /
• pp.403-411
• /
• 1997

To elucidate the mechanism of gentamicin induced renal dysfunction, renal functions and activities of various proximal tubular transport systems were studied in gentamicin-treated rats (Fisher 344). Gentamicin nephrotoxicity was induced by injecting gentamicin sulfate subcutaneously at a dose of 100 $mg/kg{\cdot}day$ for 7 days. The gentamicin injection resulted in a marked polyuria, hyposthenuria, proteinuria, glycosuria, aminoaciduria, phosphaturia, natriuresis, and kaliuresis, characteristics of aminoglycoside nephropathy. Such renal functional changes occurred in the face of reduced GFR, thus tubular transport functions appeared to be impaired. The polyuria and hyposthenuria were partly associated with a mild osmotic diuresis, but mostly attributed to a reduction in free water reabsorption. In renal cortical brush-border membrane vesicles isolated from gentamicin-treated rats, the $Na^+$ gradient dependent transport of glucose, alanine, phosphate and succinate was significantly attenuated with no changes in $Na^+-independent$ transport and the membrane permeability to $Na^+$. These results indicate that gentamicin treatment induces a defect in free water reabsorption in the distal nephron and impairs various $Na^+-cotransport$ systems in the proximal tubular brush-border membranes, leading to polyuria, hyposthenuria, and increased urinary excretion of $Na^+$ and other solutes.

• Herbal Formula Science
• /
• v.24 no.3
• /
• pp.175-193
• /
• 2016

Objective : Diuretics are effective on the patients with hypertension and heart failure, as well as edema by regulating the function of kidney, which is key organ to maintain the balance of the different electrolytes in the body. The present review article is designed to review the diuretic effect of Korean medicinal prescription base on the experimental studies.Method : For this purpose, every article related to ‘diuresis’ and 'Korean medicinal prescription' were analysed from articles which published at domestic and international journals.Results : 1. Representative Korean medicine prescriptions showed diuretic effect along with electrolyte excretion were Oryeong-san, Paeryung-tang, Hwangryungbokryung-tang and Daeganghwal-tang. 2. Some Korean medicinal prescription including Oryeong-san, Jueryeong-tang, Sipcho-tang distribute diuresis through the inhibition of renin-angiotensin-system. 3. Oryeong-san, Bojungchiseup-tang had a diuretic effect on the down-regulation of aquaporin water channel in the renal collecting duct.Conclusion : Korean medicinal transcriptions have a diuretic effect through several types of mechanism such as along with electrolytes excretion, inhibition of renin-angiotensin system, and down-regulation of water channels.

• YAKHAK HOEJI
• /
• v.26 no.4
• /
• pp.197-208
• /
• 1982

In this study attemps were made to obtain evidence as to the action of Mori Radicis Cortex on the renal' function of anesthetized mongrel dogs. 1. A light brown powder isolated from Mori Radicis Cortex (MRC) by a slight modification of Tanemura's method, when given intravenously in doses ranging 0.5 to 5.0mg/kg, elicited diuresis with the increase of positive water clearance and amounts of $Na^{+}$ and $K^{+}$ excreted in the urine. At this time the glomerular filtration rate, renal plasma flow and osmolar clearance were not observed to have any significant changes. This diuresis was augmented in process of time and its maximum effect was exhibited about 30 minutes after administration of MRC. 2. The MRC, when administered into a intra carotid artery, responded promptly with diuresis and natriuresis at a level too small to effect renal functions when administered intravenously. In this experiment the patterns of changes of renal function were the patterns of changes of renal function were the same as those of the above intravenously administered experiment. 3. When infused directly into a renal artery, the MRC exhibited little effect on either kidney. 4. During water diuresis, the MRC did not elicit diuretic action or significant changes in renal functions. The above observations suggest that the diuresis of MRC is brought about by the inhibition of the release of antidiuretic hormone with the mechanism facilitating the excretion of $Na^{+/}$ and $K^{+}$ in urine.

• The Korean Journal of Pharmacology
• /
• v.26 no.2
• /
• pp.161-166
• /
• 1990

Infusion of bradykinin (BK) into the renal arteries increases sodium excretion. However, it is not clear whether natriuresis results from the renal hemodynamic effects or from the direct effect on renal tubular sodium transport. Therefore, we examined the effects of BK on the transport-dependent oxygen consumption in the distal tubule (DT) and cortical collecting tubule (CCT) of deoxycorticosterone-treated rats. BK inhibited oxygen consumption in a dose-dependent way with a maximal reduction at $0.1\;{\mu}M$ BK. The inhibitory effect of BK was not present in the absence of sodium or in the presence of ouabain (1 mM). These data imply that the inhibitory effect of BK is restricted to the sodium transport-dependent oxygen consumption. We also investigated the relationship between the effect of BK on oxygen consumption and arachidonic acid metabolism. Mepacrine $(10\;{\mu}M)$, an inhibitor of membrane phospholipases, prevented the inhibitory effect of BK, but indomethacin (0.5 mM) didn't. These results suggest that BK decreases the sodium transport-related oxygen consumption in the rat DT and/or CCT, and that it may be mediated by products of enzymes other than cyclooxygenase.