Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In male Wistar rats, under osmotic diuresis, the effect of angiotensin II, noradrenaline, vasopressin and aldosterone on urinary kallikrein excretion were evaluated. Angiotensin II did not modify but all the others drugs used increased significantly the urinary kallikrein excretion. In all the groups studied the urinary sodium excretion increased. No modifications were observed in urine flow, glomerular filtration rate, urine osmolality and potassium excretion. The urinary kallikrein excretion was always positively correlated with the urinary flow and urinary sodium excretion. No correlation was observed with the other parameters studied. These findings suggest that noradrenaline, vasopressin and aldosterone are important stimulators of the urinary kallikrein excretion. Probably, kallikrein is one of the mechanisms involved in the regulation of urinary sodium excretion.
 ...
PMID:Effect of angiotensin, noradrenaline, vasopressin and aldosterone on urinary kallikrein excretion in the rat. 656 41

In an attempt to investigate a possible interaction between vasopressin and the renal kallikrein-kinin system, renal function and urinary kallikrein excretion were monitored in trained conscious dogs and in anesthetized rats in water diuresis and in vasopressin-induced antidiuresis. Vasopressin elevated urinary kallikrein excretion in a dose-dependent way in both species, with concomitant increases in urinary osmolality and electrolyte excretion. A significant increase in kallikrein excretion was observed with a dose of vasopressin as low as 2 mU . kg-1 . h-1 in the dog and 3 mU . kg-1 . h-1 in the rat without a change in renal hemodynamics. In the rat vasopressin-induced changes in kallikrein excretion were positively correlated with changes in sodium and potassium excretion and negatively correlated with changes in free water clearance. It is concluded that vasopressin over its normal physiological range of concentration stimulates renal kallikrein secretion.
 ...
PMID:Effect of vasopressin on renal kallikrein excretion. 690 27

This is a report about a 14-year old girl who, following chemotherapy for malignant teratoma, developed a clinical state of SIADH (syndrome of inappropriate secretion of antidiuretic hormone). The causative agent was most likely vincristine (VCR). The important feature in this case was that the urinary kallikrein activity was high when she was affected by SIADH and decreased when her hyponatremia improved. Sodium clearance was significantly correlated with the increase in urinary kallikrein activity. It is considered that the kallikrein-kinin system may in part participate in the excessive natriuresis of SIADH.
 ...
PMID:Increased renal kallikrein excretion in SIADH after vincristine therapy. 692 Feb 97

A strong inverse relationship was found between the excretion rates of the prostaglandins PGE2 and PGF2 alpha and urine flow (and osmolar excretion rate) over a range of urine flow rates from 1.5 to 40 microliters . min-1 . g kidney weight-1, covering spontaneous variations and isotonic saline diuresis. These results suggest the operation of a negative feedback mechanism by which the diuretic action of the prostaglandins, as part of a defence system, counteracts excessive oliguria. PGE2 excretion did not correlate with either urinary kallikrein excretion or plasma renin concentration. When the concentrating mechanism was interfered with by reducing renal perfusion pressure to, or below 65 mmHg, and vasopressin was given i.v. PGE2 excretion rate roughly parallelled urine--and probably medullary interstitial osmolar activity. However, in hydropenic rats there was no correlation between urine osmolality (Uosm) and PGE2 excretion over a range of osmolalities from 500 to 2 500 mOsm . kg-1, nor any relationship between delta Uosm and delta PGE2 excretion. Thus, a high interstitial osmolar activity appears to be a prerequisite for the activation of PG-synthesis in the renal medulla, but another (other) yet undefined factor(s) play the major role as (a) determinant(s) for PG-excretion in vivo.
 ...
PMID:On the relationship between urinary PGE2 and PGF2 alpha excretion rates and urine flow, osmolar excretion rate and urinary osmolality in anesthetized rats. 695 76

The activity of the renal kallikrein-kinin system was investigated in male Brattleboro rats homozygous for hypothalamic diabetes insipidus (DI); Long-Evans rats (LE) were taken as controls. In the rats with DI, urinary kallikrein excretion was lower (P less than 0.05) than in the LE rats. However, when related to total renal mass or to body weight, there was no difference between the two strains. Kallikrein activity in the renal cortex was similar in the Brattleboro and the LE rats. Antidiuretic hormone (vasopressin tannate) in a dose of 100 mU given once daily for 3 days had no effect on urinary kallikrein excretion in either of the strains. Water deprivation for 24 h resulted, also in both strains, in a similar reduction in urinary kallikrein excretion. The renal kallikrein-kinin system of LE rats and that of DI rats does not principally differ in basic activity, nor in response to the administration of vasopressin, nor to water deprivation.
 ...
PMID:The renal kallikrein-kinin system in Brattleboro rats with hereditary hypothalamic diabetes insipidus. Missing relationship between antidiuretic hormone and the renal kallikrein-kinin system. 702 43

Studies in humans have shown that cortisol administration (200 mg/day) increases cardiac output, renal vascular resistance, glomerular filtration rate, plasma volume, extracellular fluid volume, exchangeable sodium, plasma glucose, insulin, renin substrate and atrial natriuretic peptide concentrations as well as urinary kallikrein excretion. Cortisol treatment decreases renin and angiotensin II concentrations while catecholamines and vasopressin are decreased or unchanged. We have clear evidence from a number of studies that cortisol-induced hypertension is modulated by, but not dependent on, exogenous sodium. The increase in cardiac output normally seen with cortisol administration is not essential for the blood pressure rise. The role of the increase in renal vascular resistance in the genesis of the hypertension is unclear. Studies using measurements of noradrenaline spillover and assessment of reflex function have not shown any increase in sympathetic nervous system activity but changes in vascular responsiveness, particularly to phenylnephrine and noradrenaline are marked. Cortisol is known to have a variety of effects on brain, heart, kidneys, blood vessels and body fluid volumes. To what extent the observed changes are epiphenomena, amplifiers or modulators, or are causal is unclear. Cortisol hypertension may reflect a complex interplay of these factors varying with the steroid concentrations achieved, underlying genetic factors and the particular experimental circumstances.
 ...
PMID:Experimental studies on cortisol-induced hypertension in humans. 747 17

14 healthy subjects (8 males and 6 females), aged 25-40 years, were studied before and after oral administration of a single dose of 50 mg captopril as well as after 3 d treatment with 100 mg captopril daily per os. We found that in addition to the well-known effects on the renin-angiotensin-aldosterone system, captopril, after 3 d treatment, significantly increases plasma and urinary kallikrein activity, plasma vasopressin and urinary prostaglandin (PG) E2. Atrial natriuretic peptide did not change significantly after either the single dose or the short-term treatment. We conclude that the blood pressure lowering effect of captopril could be mediated by increasing activity of the kallikrein-kinin system and of PGE2 without any participation of atrial natriuretic peptide.
 ...
PMID:Effects of a single dose and short-term captopril treatment on some pressor and depressor humoral factors in healthy subjects. 859 78


<< Previous 1 2 3