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

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.
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PMID:Increased renal kallikrein excretion in SIADH after vincristine therapy. 692 Feb 97

The studies concerned age-dependent peculiarities of the vasopressin effect on the hemodynamics and tone of the coronary vessels in dogs, the contraction of the isolated vascular strip in rats, and the hemodynamic and ECG indices in rabbits and in rats. The data obtained indicate the great sensitivity of old vessels to vasopressin. In aging, both humans and animals show a rise of vasopressin concentration in the blood. Age-dependent differences of the vasopressin effect on the kallikrein-kinin system, adenosine metabolism, the contents of prostaglandins and cyclic AMP have been established. High sensitivity to vasopressin in combination with its increased concentration in the blood is an important factor that contributes to the development of arterial hypertension and ischemic heart disease.
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PMID:Vasopressin and cardiovascular system in aging. 692 18

The urinary excretion of PGE2, PGF2 alpha, arginine-vasopressin, and kallikrein was measured in 58 healthy subjects aged 2 days to 13 years. In contrast to the activity of the renin-angiotensin-aldosterone system, which is known to decrease from birth, urinary excretion of PGE2, PGF2 alpha, vasopressin, and kallikrein significantly increased with age. These changes were not correlated to urine volume, natruresis, or glomerular filtration rate. Correction of the values by body surface area obliterated the differences for PGs and vasopressin, but not for kallikrein.
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PMID:Urinary prostaglandins, vasopressin, and kallikrein excretion in healthy children from birth to adolescence. 695 20

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.
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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.
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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.
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PMID:Experimental studies on cortisol-induced hypertension in humans. 747 17

Bradykinin receptors on vascular smooth muscle may play an important role in regulating the endogenous effects of the vascular kallikrein-kinin system. The present study examined the effect of cyclic nucleotides on bradykinin-stimulated responses in cultured arterial smooth muscle cells. Short term stimulation (1 min) with cyclic AMP produced a variable inhibition of bradykinin-stimulated calcium mobilization which was lost in later passaged cells. However, long-term stimulation (24 h) produced a consistent increase in bradykinin-stimulated calcium mobilization in both early and late passaged cells. Further analysis demonstrated that chronic exposure to cAMP produced a twofold increase in both the number of cell surface bradykinin receptors and in bradykinin-stimulated phosphoinositide hydrolysis. The increase in bradykinin receptors was time dependent (> 7 h) and blocked by protein synthesis inhibitors, suggesting that cAMP enhanced the synthesis of new bradykinin receptors. The increase in bradykinin receptor binding and calcium mobilization was also stimulated by cholera toxin, forskolin, and isobutylmethylxanthine, but not isoproterenol or prostaglandin E2. Of considerable interest, prolonged exposure to cAMP inhibited both angiotensin II and arginine vasopressin-stimulated phosphoinositide hydrolysis and intracellular calcium mobilization. In summary, prolonged treatment with cAMP selectively stimulates the synthesis and expression of bradykinin receptors on arterial smooth muscle while decreasing the responsiveness to vasoconstrictor agonists such as angiotensin II and vasopressin.
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PMID:Cyclic AMP selectively enhances bradykinin receptor synthesis and expression in cultured arterial smooth muscle. Inhibition of angiotensin II and vasopressin response. 820 Sep 90

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.
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PMID:Effects of a single dose and short-term captopril treatment on some pressor and depressor humoral factors in healthy subjects. 859 78

Heart failure is a physiopathological condition, with an increasing incidence and prevalence, involving the action of a series of mechanisms known as 'compensators', which are phylogenetically ready to normalize minute volume and blood pressure. These mechanisms include the activation of a series of neurohormonal systems: the sympathetic nervous system, the aldosterone renin-angiotensin system, vasopressin arginine, endothelin, which are basically vasoconstrictors, with the counterpoint of other vasodilator systems, such as the endothelial relaxation factor, certain prostaglandins and the bradykinin-kallikrein system, which modulate global response. The authors review the physiopathology of each of these systems, as well as their significance in the diagnosis and prognostic evaluation of heart failure. We analyze the possible deleterious effects of neurohormonal activation, anatomically and at the cardiovascular function level, and try to determine if they are capable of explaining the evolution and progression of heart failure, in a truly vicious circle, up until the irreversible heart failure phase. We review the current importance of the inhibition of the aldosterone renin-angiotensin system in the prophylaxis and treatment of heart failure. Furthermore, we describe the present-day value of the inhibition of the sympathetic nervous system in some forms of heart failure. We also analyze the different pharmacological treatment for heart failure: diuretics, inotropic agents, vasodilators (in their different pharmacological types), paying particular attention to their action on neurohormonal systems and their implications in the prognosis and evolution of heart failure.
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PMID:[Neurohormonal factors in heart failure. I]. 865 Mar 99

The arcades are long, branched renal tubules which connect deep and mid-cortical nephrons to cortical collecting ducts in the renal cortex. Because they are inaccessible by standard physiological techniques, their functions are poorly understood. In this paper, we demonstrate that the arcades are a site of expression of two proteins, aquaporin-2 (the vasopressin-regulated water channel) and the V2 vasopressin receptor, that are important to regulated water transport in the kidney. Using a peptide-derived polyclonal antibody to aquaporin-2, quantitative ELISA in microdissected segments showed that aquaporin-2 is highly expressed in arcades and that the expression is increased in response to restriction of fluid intake. Immunocytochemistry revealed abundant aquaporin-2 labeling of structures in the cortical labyrinth in a pattern similar to that of the Na(+)-Ca2+ exchanger and kallikrein, marker proteins expressed in arcades but not in cortical collecting ducts. RT-PCR experiments demonstrated substantial aquaporin-2 and V2 receptor mRNA in microdissected arcades. In situ hybridization, using 35S-labeled antisense cRNA probes for the V2 receptor demonstrated strong labeling of both arcades and cortical collecting ducts. Thus, these results indicate that the arcades contain the specific proteins associated with vasopressin-regulated water transport, and may be a heretofore unrecognized site of free water absorption.
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PMID:Rat renal arcade segment expresses vasopressin-regulated water channel and vasopressin V2 receptor. 867 87


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