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1.
Perry V. Halushka Harry S. Margolius Harry Allen Edward C. Conradi 《Prostaglandins & other lipid mediators》1979,18(3):359-368
In a controlled study of 11 women, 5 with mild essential hypertension and 6 normal volunteers, furosemide produced a significant natriuresis and diuresis without changes in the urinary excretion of prostaglandin E-like material and kallikrein. Therefore, although some evidence in man or animals suggests involvement of both of these substances in renal responses to furosemide, the present data suggest that the natriuretic and diuretic effects of this drug are not associated with an increased excretion of prostaglandin E like material or kallikrein. 相似文献
2.
L F Obika 《Archives internationales de physiologie et de biochimie》1987,95(1):13-18
The relationship of urinary kallikrein excretion to urine volume, and to urinary sodium and potassium excretions was studied in normal rats during furosemide diuresis and superimposed injection of amiloride, a K+-sparing diuretic. Continuous infusion of furosemide increased urinary kallikrein, sodium and potassium excretions and the urine volume. Amiloride injection during furosemide diuresis caused further increase in diuresis and natriuresis, but a prompt decrease in urinary kallikrein excretion to basal level, and potassium excretion to below the basal level. The significant correlation of urinary kallikrein excretion to urinary potassium excretion, but not to urine volume and urinary sodium excretion after amiloride injection suggests that the major determinant of urinary kallikrein excretion is renal potassium secretion through a mechanism that is affected by amiloride. 相似文献
3.
G Thibault R Garcia M Cantin J Genest 《Canadian journal of physiology and pharmacology》1984,62(6):645-649
The rat atrium contains a potent natriuretic factor which appears to inhibit the sodium reabsorption in the collecting tubules of the kidneys. We examined the effects of the injection of partially purified atrial natriuretic factor (ANF) and synthetic ANF (8-33) into rats with simultaneous infusions of dextrose or aprotinin. Aprotinin, an inhibitor of serine proteases, increases the natriuretic and diuretic effects of the atrial factor by 50%. Urinary kallikrein excretion is also slightly increased by ANF but is not affected by aprotinin. As a comparison, aprotinin has no effect on the diuretic or natriuretic responses of furosemide, although it inhibits by 50% the kallikrein excretion induced by furosemide. When ANF is incubated with purified rat urinary kallikrein, the natriuretic and diuretic effects are decreased by more than 50%. We conclude that glandular kallikrein or a similar serine protease may be involved in the catabolism of ANF. 相似文献
4.
Urinary excretion of sodium, potassium and some hormones influencing their transport was investigated before and after i.v. furosemide administration in 10 offsprings of normotensive subjects who had a normal Na(+)-K+ cotransport activity and in 26 normotensive men with a positive family history of essential hypertension. The latter group was divided into two subgroups with regard to the activity of red cell Na(+)-K+ cotransport. The Co[-] subjects with a decreased Na(+)-K+ cotransport activity had lower urinary excretion of sodium and vasodilators (kallikrein, dopamine, PGE2 and prostacyclin) after furosemide administration. The urinary excretion of vasopressor factors (PGF2 alpha, thromboxane) was unchanged as compared with that in the control group. There was a significant correlation between Na(+)-K+ cotransport activity and kallikrein excretion. These results suggest a deficit in the secretion of renal substances with vasodilating or natriuretic effects in Co[-] subjects. This could negatively affect their sodium excretion. 相似文献
5.
Géza Fejes-Tóth Anikó Náray-Fejes-Tóth Bart Rigter Jürgen C. Frölich 《Prostaglandins & other lipid mediators》1983,25(1):99-103
To study the relationship between urine flow, urinary prostaglandin (PG) and kallikrein excretion in the rat high urine flow was induced in hydropenic Long-Evans rats by either hypotonic volume expansion or with manniitol or with furosemide. PGE, excretion remained unchanged during hypotonic volume expansion (134.5 ± 29.7 before and 153.0 ± 48.9 pg/min after) while it decreased significantly with mannitol (from 166.3 ± 32.4 to 45.2 ± 8.2 pg/min, p<0.01) and with furosemide (from 170.0 ± 20.4 to 29.5 ± 5.3 pg/min, p<0.001). PGF2α excretion rates were slightly reduced following all three interventions. Urinary kallikrein excretion remained unchanged in all three groups of animals. It is concluded that, in contrast to human and dogs in the rat urine flow and urinary PG excretion are not interlinked. 相似文献
6.
《Prostaglandins and medicine》1981,6(6):549-556
Plasma renin activity, total renin, active renin, and aldosterone were measured as well as urinary prostaglandin E2 and kallikrein in a group of patients with hyperkalemia (6.1–7.7 mEq per liter) and hypo reninemic hypoaldosteronism. Plasma renin activity and aldosterone were low and the response was markedly blunted to upright posture, and furosemide. The rise in cortisol but not aldosterone was normal following ACTH stimulation. Active renin was depressed; however, total renin was normal. Urine PGE was variable including some low values, but the mean of the group was normal (p >0.1). Urine kallikrein excretion was markedly diminished and undetectable in most cases. Fludrocortisone normalized potassium but minimally increased kallikrein in the patients. The possibility exists that kallikrein deficiency in these patients may underlie the inability to generate active renin. 相似文献
7.
Urinary kallikrein excretion is reduced in patients with hypertension of unknown etiology. In addition, the excretion of this renal, kinin-forming enzyme was found to be elevated in hypertensive patients with primary aldosteronism. Aldosterone regulates kallikrein excretion, as normal subjects show increased kallikrein excretion in response to a low sodium intake, high potassium intake, or the synthetic mineralocorticoid, fludrocortisone, whereas kallikrein excretion falls during treatment with spironolactone. The relationship between kallikrein excretion and aldosterone activity may directly reflect the intrarenal activity of the kallikrein-kinin system, as determined by studies of kallikrein levels from isolated renal cells or of plasma kinin levels in man in response to postural changes or saline loads. Some patients with essential hypertension do not show a normal increase in kallikrein excretion in response to low dietary sodium intake despite an apparently normal aldosterone response, suggesting that there may be a defect in the renal kallikrein-kinin system in these patients. Whether these findings are of pathogenetic significance in human hypertensive disease remains to be determined. 相似文献
8.
A Martínez Seeber S B Vila O L Catanzaro 《Archives internationales de physiologie et de biochimie》1985,93(2):83-88
The purpose of this study was to investigate the effect of norepinephrine and vasopressin on urinary kallikrein excretion in the rat. Two studies were undertaken: (a) acute experiments in which the rats were infused with 30% dextrose in water with the addition of norepinephrine or vasopressin, (b) chronic experiments in which the drugs were infused during seven days through an osmotic minipump. In acute experiments, urinary kallikrein excretion increased without modification in urinary flow and glomerular filtration rate. In chronic experiments, urinary kallikrein excretion was not modified in norepinephrine-treated rats and decreased in vasopressin-infused animals. This decrease followed the modifications of the urine flow. In chronic experiments the dextrose infusion increased urinary kallikrein excretion. In all the groups studied a positive correlation between urine flow and urinary kallikrein excretion was observed. It is concluded that norepinephrine and vasopressin are important stimulators of the urinary kallikrein excretion only in those circumstances where it is necessary to eliminate an excess of water. 相似文献
9.
A Martinez Seeber S B Vila O L Catanzaro 《Archives internationales de physiologie et de biochimie》1984,92(2):89-91
Urinary kallikrein excretion was compared with urea excretion in the rat and the results showed that they were correlated. Like urea excretion is flow-dependent, we conclude that the principal mechanism regulating kallikrein excretion is a wash-out effect on renal kallikrein. 相似文献
10.
A Martínez Seeber C T Arranz S B Vila O L Catanzaro 《Archives internationales de physiologie et de biochimie》1985,93(3):209-213
In control rats urinary kallikrein excretion was positively correlated with inulin space and its both components, plasma volume and interstitial space. When the animals were infused with dextrose solution or dextrose albumin solution the distribution of water in extracellular space was altered and the correlations with urinary kallikrein excretion disappear. We conclude that the possible regulation of the components of the extracellular space on urinary kallikrein excretion has not the same importance when water distribution is altered, at least in acute situations. 相似文献
11.
Urinary kallikrein excretion was studied in a number of animal models of hypertension. Kallikrein excretion was subnormal in spontaneously hypertensive rats as compared to Wistar/Kyoto rats and in rats made hypertensive by a clip on one renal artery. Kallikrein excretion was supranormal in rats made hypertensive by desoxycorticosterone and salt and in rats receiving desoxycorticosterone alone. It was subnormal after bilateral adrenalectomy. Kallikrein excretion increased in normotensive rats fed a low-sodium diet but was unchanged by a high-sodium diet. Thus, kallikrein excretion responded to changes in activity of sodium-retaining steroids and was not correlated with excretion of salt or water. In studies in dogs with stenosis of one renal artery kallikrein excretion was decreased on the stenoic side and the decrease correlated highly with the reduction in renal blood flow. While the role of the kallikrein-kinin system is still unclear the data indicate that the kidney may modify the initiation or maintenance of hypertension via this potent vasodilator system. 相似文献
12.
Hypertension and its related increase in cardiovascular morbidity in postmenopausal women is a major public health problem. The hypotensive property of urinary kallikrein has been described since 1909. Despite the controversy surrounding the effects of hormone replacement therapy on blood pressure regulation, its mechanisms remain incompletely understood, and no evidence has yet been provided for its effects on renal kallikrein excretion in postmenopausal women. In a double-blind, randomized study we examined the effects of hormone replacement therapy in the form of 2 mg 17-beta estradiol (ERT) or 2 mg 17-beta estradiol combined with continuous 5 mg medroxyprogesterone acetate (HRT) on urinary kallikrein excretion in postmenopausal women. Thirty-nine postmenopausal women collected their urine for 24 hours on two separate occasions 3 months apart. During the 3 month period women were randomized to placebo, ERT, or HRT. Urine samples were assayed for kallikrein activity, normalized to urine creatinine and expressed as mU/gm creatinine. Urinary kallikrein excretion increased significantly after 3 months in the ERT (p < 0.001) and HRT (p < 0.01) groups, and decreased non-significantly in the placebo group (p > 0.06). There were no significant blood pressure changes after 3 months of therapy. The findings demonstrate that hormone replacement therapy in the form of estrogen or estrogen combined with continuous medroxyprogesterone is effective in increasing urinary kallikrein excretion. Given that a decrease in kallikrein excretion may mark risk for development of hypertension, the findings of this study are of value in demonstrating a novel mechanism underlying cardioprotective properties of postmenopausal hormone replacement therapy in women without pre-existing coronary disease. 相似文献
13.
The present experiment was undertaken to determine whether or not the effects of furosemide depend upon the administration time and, if so, to study the mechanism(s) for these variations. After administration of furosemide (5 mg/kg) in Wistar rats at 10:00 or at 22:00, urine volume and urinary excretion of sodium, furosemide, and prostaglandin E2 (PGE2) were measured. Urine volume and urinary excretion of sodium and furosemide, but not PGE2, were significantly greater when furosemide was administered at 10:00 than when it was administered at 22:00. There was a good correlation between the urinary output of furosemide and the urine volume, or the urinary sodium. It is concluded that the effects of furosemide vary with the administration time and these variations depend upon the amount of furosemide secreted in urine. 相似文献
14.
Our previous studies have suggested that the adrenergic nervous system is involved in the mechanism responsible for the time-dependent change in the urinary excretion of furosemide in rats. To examine a potential role of renal nerves in this phenomenon, renal denervation or sham operation was performed using unilaterally nephrectomized rats. Furosemide (30 mg/kg) was given orally at 12 am or 12 pm. Urine was collected for 8 hours after furosemide dosing, and urinary excretions of furosemide and sodium were determined. Urinary furosemide excretion and diuretic effects of the agent (urine volume and urinary sodium) were significantly greater at 12 am than at 12 pm in the sham-operated group of rats. However these administration time-dependent changes in urinary furosemide and its diuretic effects disappeared in the renal-denervated group of animals. These results suggest that the renal nerves contribute to the time-dependent changes in the urinary excretion of furosemide and its subsequent diuretic effects. 相似文献
15.
The distribution of kallikrein in dog kidneys was studied. It was found that kallikrein decreased from the outer to the inner cortex and that the medulla and papilla had very little kallikrein. The site of kallikrein secretion in the nephron was also studied by performing stop-flow techniques in dogs. The highest kallikrein concentration was found in the fractions with the lowest sodium concentration. It was concluded that kallikrein is secreted into the urine at the level of the distal tubule by either the tubule itself or by a structure related to this part of the nephron. In addition, the possible involvement of the kallikrein-kinin system in the regulation of sodium excretion was investigated. Circulating kinins and urinary kallikrein were increased in saline-loaded dogs. Urinary kallikrein also increased in dogs that have "escaped" the sodium-retaining effect of desoxycorticosterone. Experiments in rats with different sodium intake showed a relationship between water and sodium excretion and urinary kallikrein. These data suggest that the kallikrein-kinin system could participate in the regulation of the renal function at the level of the distal tubule or collecting duct. 相似文献
16.
A Martínez Seeber C T Arranz S B Vila O L Catanzaro 《Archives internationales de physiologie et de biochimie》1985,93(1):33-36
Urinary kallikrein excretion was positively correlated with urine flow and negatively with urinary osmolality, it was also positively correlated with inulin space and its both components, plasma volume and interstitial space. We postulate that increased extracellular fluid increases kallikrein excretion and kallikrein avoids water reabsorption leading to a decrease in the extracellular fluid. 相似文献
17.
J P Girolami B Corman 《Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.)》1990,193(2):149-154
The effect of aging on the intrarenal kallikrein-kinin system activity was investigated in normotensive 3-, 10-, 20-, and 30-month-old female Wistar rats. Urinary kallikrein excretion was measured by three independent assays (immunoreactive concentration, kininogenase, and amidolytic activities) and was found to decrease progressively from 10 to 30 months. In the 30-month-old rats the urinary immunoreactive kallikrein excretion represented 40-44% of the level detected in 3-month-old rats. Active and total kallikrein exhibited the same magnitude of reduction. Furthermore, the active to inactive kallikrein ratio remained unchanged throughout the life period studied. The level of urinary kallikrein inhibitor was studied by measuring the recovery of purified rat urinary kallikrein added in the samples; no change was observed with aging. None of the factors known at present to influence kallikrein excretion could be evoked to explain this age-related decrease. It is therefore suggested that this decrease may reflect a progressive impairment of the intrarenal endocrine function or an alteration in the secretion of the enzyme. 相似文献
18.
The role of the renal kallikrein-kinin system in the development of salt-sensitive hypertension was studied using mutant kininogen-deficient Brown-Norway Katholiek (BN-Ka) rats, which generate no kinin in their urine, and other hypertensive rat models. It was found that ingestion of a low sodium diet or infusion of NaCl in doses slightly above 0.15 M caused hypertension and sodium accumulation in erythrocytes and the cerebrospinal fluid of kininogen-deficient BN-Ka rats. Development of hypertension in the deoxycorticosterone-acetate-salt model was completely prevented by administration of a newly discovered inhibitor, ebelactone B, of carboxypeptidase Y-like exopeptidase (an urinary kininase). The urinary kallikrein excretion of spontaneously hypertensive rats was lower than that of Wistar Kyoto rats at 4 weeks of age and did not increase by administration of furosemide, a diuretic agent, although approximately 50% of the diuretic action of this agent was dependent upon the renal kallikrein-kinin system in normal rats. In conclusion, the renal kallikrein-kinin system works as a safety valve for excess sodium intake. 相似文献
19.
J P Girolami C Orfila C Pecher G Cabos-Boutot J L Bascands J P Moatti A Adam A Colle 《Biological chemistry Hoppe-Seyler》1989,370(12):1305-1313
Acute renal failure (ARF) was induced in rat following a single injection of sodium chromate. A transient polyuria and a 10-fold decrease in glomerular filtration rate was immediately observed after sodium chromate administration. Urinary sodium and potassium excretion were reduced within 24 h and remained decreased for 8 to 10 days. Progressive recovery of normal renal functions, mainly electrolyte excretion and filtration rate was observed 12 days after sodium chromate administration. Urinary kallikrein excretion (UKE) was decreased only 48 h after sodium chromate administration. However the proportion of the active and inactive form excreted was unchanged. UKE remained also at a reduced level for 8 to 10 days and returned progressively to base-line level. The kallikrein content in the tissue was significantly increased immediately after sodium chromate administration and recovered normal values 12 days later. The increase of kallikrein in the tissue is more likely unspecific due to impaired protein transport than a specific stimulation of renal kallikrein biosynthesis. The decreased UKE may indicate a distal tubular reversible dysfunction in this ARF model. These reductions in electrolyte excretion, glomerular filtration and UKE were associated with selective morphological lesions. Whereas the glomeruli were intact, important damages affected proximal tubule cells which appeared necrotic and showed presence of vacuoles, liquefaction of cytoplasmic material and lost of microvilli. Less marked lesions were however observed in distal tubules, particularly large vacuoles were present at the apical poles of the tubule cells, the sites of kallikrein secretion. These distal damages may be involved in the increase of tissue concentration and in the decrease of UKE.(ABSTRACT TRUNCATED AT 250 WORDS) 相似文献
20.
G Porcelli G Bianchi H R Croxatto 《Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.)》1975,149(4):983-986
Concentration and 24-hr excretion of urinary kallikrein in spontaneous hypertensive Wistar strain rats of both sexes obtained by selected inbreeding (25th generation) are significantly decreased as compared with the excretion in normotensive inbred rats (24th generation) descending from common ancestors. Apparently in these hypertensive rats there is an abnormal capacity of the kidneys to produce or release kallikrein, but more studies will be necessary to correlate this findings with blood pressure increase. 相似文献