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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Blood pressure is controlled by both integrated neurogenic and humoral vasoactive mechanisms. 2. Both vasopressor (angiotensin and vasopressin) and vasodepressor (bradykinin) hormonal peptides have been identified. 3. In acute experimental renal hypertension in the rat plasma renin, angiotensin and vasopressin have all been shown to be elevated. 4. Associated with this increase in vasopressor hormonal peptides, urinary kallikrein excretion has been demonstrated to be reduced during the development of renal hypertension. 5. The level of blood pressure achieved in experimental renal hypertension is probably a summation of these vasoactive peptides as well as other factors.
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PMID:Vasoactive peptides in experimental renal hypertension. 73 55

Sodium excretion is correlated with kallikrein excretion in man, rabbits and rats on a free sodium and water intake, but not on a constant sodium or constant water intake. The correlation also exists during arterial infusion of angiotensin II, substance P and various vasodilators. During sodium depletion, the stimulation of the renin-angiotensin system causes increased drinking in rats and rabbits. The high angiotensin levels would stimulate kallikrein excretion. The excretion of water and dilution of urine are facilitated by the renal kallikrein-kinin system, even when antidiuretic hormone is high. This negative correlation between urinary osmolality and kallikrein excretion exists during arterial infusion of angiotensin or substance P and various vasodilators. During renal artery constriction, the kallikrein release per minute decreases, but over successive 10-minute periods, the kallikrein concentration in urine rises. This rise is correlated with some recovery in the clearance of rho-aminohippurate and inulin. Since kallikrein is released into renal lymph during saline infusion at a rate that correlates with its release into the urine, it is suggested that the renal kallikrein-kinin system protects the renal vasculature against the constricting action of the renin-angiotensin system. The decreased release of kallikrein (via the lymphatics into the circulation) during renal artery constriction, or decreased renal compliance, would potentiate the hypertensive effect of these procedures which cause increased renin release.
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PMID:The renal kallikrein-kinin system and the regulation of salt and water excretion. 76 62

1. The urinary excretion of active and inactive kallikrein was studied in volunteers during diuresis induced by water loading or oral frusemide and during antidiuresis induced by desamino-D-arginine-vasopressin. 2. During acute oral water loading, excretion of active kallikrein was unchanged, despite high urine flow rates and low urine osmolalities being achieved. Excretion of inactive kallikrein correlated with the urine flow rate. 3. After desamino-D-arginine-vasopressin in eight water-loaded and six normally hydrated subjects, excretion of inactive kallikrein also correlated with the urine flow rate. There were no significant changes in the excretion of active kallikrein. 4. After frusemide there was a small transient increase in excretion of active kallikrein 1-2 h after dosing which coincided with the maximum diuresis and natriuresis. Excretion of inactive kallikrein again correlated with urine flow rate but the regression relationship between the two variables was different for water-load-induced and frusemide-induced diuresis. 5. These studies do not support a role for urinary kallikrein in the modulation of the antidiuretic action of vasopressin, but suggest that it may contribute to the natriuretic action of frusemide.
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PMID:Active and inactive urinary kallikrein in man: effects of diuresis and antidiuresis. 216

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.
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PMID:Effect of norepinephrine and vasopressin on renal kallikrein excretion in rats. 241 15

We contrasted the renal effects of vasopressin in Brattleboro rats with and without pretreatment with aprotinin (20,000 KIU kg-1). In both treatment groups, vasopressin injected at 3 mU kg-1 sec caused in conscious rats elevation of urine osmolality and reduction of urine flow and urinary excretion of total solutes. However, these effects of vasopressin were significantly greater in aprotinin pretreated rats than in rats without aprotinin treatment. In ketamine-pentobarbital-anesthetized rats without aprotinin pretreatment, vasopressin infused at 2 mU kg-1 hr-1 elevated urinary kinin excretion but did not affect urine flow rate or osmolality; in contrast, in aprotinin-pretreated rats, the same dose of vasopressin did not increase urinary kinins but caused elevation of urinary osmolality and reduction of urine flow, solute excretion, and glomerular filtration rate. Aprotinin pretreatment in anesthetized rats also blunted the rise in kinin excretion elicited by vasopressin at a higher dosage, 5 mU kg-1 hr-1, but did not potentiate the vasopressin-induced antidiuresis. We conclude that aprotinin facilitates the expression of the antidiuretic effect of vasopressin at a low, but not at a high dosage. This effect of aprotinin may be a consequence of: renal kallikrein inhibition which prevents augmentation of renal kinins in response to increased vasopressin levels, or other unrecognized properties of aprotinin.
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PMID:Augmentation by aprotinin of the renal response to vasopressin. 243 37

The present review summarizes current and new knowledge concerning the major hormonal systems that directly or indirectly affect renal function during development. The role of the renin-angiotensin-aldosterone system in regulating renal function during fetal and postnatal life is reviewed. A summary of the role of this system during fetal and postnatal stresses is also provided. The physiological role of the renal kallikrein-kinin system in the control of renal blood flow, renin release and sodium excretion during development is examined. Possible influences of the prostaglandin system on regulation of renal function and renin secretion during fetal and postnatal maturation are explored. The effect of vasopressin on the ability of the fetal and postnatal kidney to concentrate urine and regulate body fluid homeostasis is reviewed in detail. The physiologic action of vasotocin on renal sodium and water homeostasis is described. New information regarding the role of the sympathetic system in the regulation of renal hemodynamics and in the control of renal function during development is presented. Finally, recent studies demonstrating the effect of atrial natriuretic factor and corticosteroids on the developing kidney are discussed.
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PMID:Hormonal regulation of renal function during development. 297 Aug 68

Kallikrein excretion and renal function were studied on 37 one-day-old newborn infants (14 fullterm and 23 preterm infants). Preterm infants excreted less kallikrein (p less than 0.001), had lower creatinine clearance (p less than 0.02) and urinary osmolality (p less than 0.01). They had higher values on urinary volume (p less than 0.001), FENa (p less than 0.001), FEK (p less than 0.02), and free water clearance (p less than 0.01) than fullterm infants. The excretion of kallikrein correlated directly with gestational age (p less than 0.01) and body weight (p less than 0.01). No correlations were found with FENa, urinary volume, FEK or free water clearance. The values of kallikrein excretion were very low when compared with a young adult population. As kallikrein is synthesized in the distal nephron we advance as an hypothesis that the low levels of kallikrein excretion observed in newborns could be a reflection of immature distal tubular mass, and to the relative unresponsiveness of the distal nephron to hormones known to stimulate renal kallikrein such as aldosterone and antidiuretic hormone.
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PMID:Kallikrein excretion: relationship with maturation and renal function in human neonates at different gestational ages. 365 20

To investigate the interaction between arginine-vasopressin (AVP) and the renal kallikrein-kinin system (KKS), urinary excretion rates of bradykinin (BK) and lysyl-bradykinin (LBK) were monitored in humans following water-loading, and in conscious diabetes insipidus (DI) rats during the infusion of AVP. In humans, the excretion rate of both BK and LBK decreased markedly 90 min after the water load. There was a close positive correlation between plasma AVP levels and urinary BK excretion, while urine flow was correlated negatively with the excretion rates of both kinins. In DI rats infusion of AVP caused a significant, reversible increase (from 14 +/- 2.8 to 35 +/- 5.1 fmol/min) in BK excretion. These results further implicate AVP in the regulation of the activity of the renal KKS.
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PMID:Urinary kinin excretion following alterations of vasopressin levels in man and rat. 380 18

To assess possible interactions of circulating vasopressin with the synthesis or activation of renal kallikrein, we studied the effect of chronic infusion of vasopressin (7.2 U/kg/day i.p.) for 6 days on the urinary excretion of total and active kallikrein in conscious rats. We determined urinary total, active and inactive kallikrein by measuring kallikrein activity using a kininogenase assay before and after the treatment with trypsin (200 micrograms/ml). Chronic infusion of vasopressin induced sustained decreases in urinary total, active and inactive kallikrein excretion, but did not affect the ratio of active to total kallikrein. The infusion of vasopressin induced significant increases in circulating levels of vasopressin (248.1 +/- 35.2 pg/ml in vasopressin-infused rats (n = 7) compared to 95.5 +/- 14.6 pg/ml in vehicle-infused rats (n = 7), p less than 0.001) and in weight gain (39.6 +/- 1.3 g in vasopressin-infused rats (n = 7) compared to 29.1 +/- 3.3 g in vehicle-infused rats (n = 7), p less than 0.05), and also sustained decreases in water intake and urine volume, but it did not induce any change in urinary sodium excretion. Circulating levels of angiotensin II was decreased by chronic infusion of vasopressin. Thus, the present study suggests that the elevation of circulating vasopressin levels induces a decrease in the synthesis of renal kallikrein.
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PMID:Decreased urinary active and inactive kallikrein by chronic infusion of vasopressin in conscious rats. 384 7

The 24-hour urinary excretion of kallikrein (K) and prostaglandin E2 (PGE2), which reflects their intrarenal synthesis, was measured in 7 normal women (NW), 10 women with essential hypertension (EH), 26 normal pregnant women (NP), 12 women with hypertension in pregnancy (HP), and 4 women with toxemia. All pregnant women were in the last trimester of their pregnancy (week 24-40). K was raised in NP (99.6 +/- 8.1 KU/24 h) and HP (106.5 +/- 8 KU/24 h) compared to NW (57 +/- 8.23 KU/24 h) (p less than 0.05). PGE2 excretion was decreased in EH (403.25 +/- 90.6 ng/24 h) compared to NW (508.6 +/- 80.26 ng/24 h). During pregnancy PGE2 was increased to 1,088 +/- 93.2 ng/24 h in NP and significantly more in HP, 1,885 +/- 40 ng/24 h (p less than 0.002). In this regard it differed from K. These data may suggest that, in addition to K, other factors (as angiotensin II and/or antidiuretic hormone) possibly activate renal PGE2 production in HP. In toxemia, K (23 +/- 6.1 KU/24 h) and PGE2 (583 +/- 172.83 ng/24 h) were markedly decreased. The above results suggest that the renal kallikrein-kinin and prostaglandin systems may play a role in sodium homeostasis during pregnancy. Their exact influence on the pathogenesis of hypertension in nonpregnant, pregnant, and toxemic subjects awaits further investigation.
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PMID:Urinary kallikrein in normal pregnancy, pregnancy with hypertension, and toxemia. 385


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