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)

1. The renal effects of angiotensin II were investigated (a) with and without acute blockade of the effects of aldosterone and (b) with and without concomitant infusion of vasopressin. Angiotensin II (2 ng min-1 kg-1) and/or vasopressin (5 pg min-1 kg-1) was infused intravenously into conscious water-diuretic dogs and the effects were quantified by measurements of renal excretion of water, Na+ and K+, as well as determination of plasma renin activity and plasma levels of atrial natriuretic peptide and catecholamines. 2. Angiotensin II alone increased blood pressure by 7% (P < 0.05), decreased effective renal blood flow markedly and reduced urine flow and osmolar and free water clearances. Na+ and K+ excretion did not change significantly. Aldosterone blockade with canrenoate increased Na+ excretion by a factor of 10; subsequent infusion of angiotensin II decreased Na+ excretion by about 50%, the other renal effects being qualitatively similar to those seen without blockade. As expected, vasopressin also decreased diuresis and free water clearance substantially; however, the effect of combined infusion of angiotensin II and vasopressin was not compatible with the notion of additive effects of the two peptides. 3. Angiotensin II alone or in combination with vasopressin did not change the plasma concentrations of atrial natriuretic peptide, adrenaline, noradrenaline, or dopamine. Vasopressin alone exerted its antidiuretic effect without affecting plasma renin activity, plasma aldosterone concentration or renal excretion of Na+ and K+.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vasopressin and angiotensin II in the conscious dog: synergistic effects on renal excretory parameters? 133 Apr 10

The thermal dehydration test was performed in 12 patients with renal transplant and in 20 healthy subjects. The study was aimed at the evaluation of the effect of volume regulating hormones on electrolyte composition of thermal sweat in patients with renal transplant. Blood plasma renin activity (PRA) as well as plasma concentrations of aldosterone (ALD), vasopressin (AVP) and atrial natriuretic peptide (ANP) were determined before and after thermal dehydration in all the subjects studied. In all the subjects sweat was also collected after 15 and 45 minutes of exposition to heat and the concentrations of sodium, potassium and chloride were determined in all sweat samples. Significantly elevated PRA and ANP concentrations and significantly lowered plasma AVP concentrations but normal ALD levels were found before thermal dehydration test in all the patients with renal transplant. After the exposition to heat lasting 1 hour the direction of changes was similar, their magnitude was, however, different in renal transplant patients than in healthy subjects. In addition, lower concentrations of sodium and chloride in thermal sweat and lower total concentration of sweat solids were found in renal transplant patients than in healthy controls. No significant correlation was found between the plasma concentrations of the hormones determined and the electrolyte concentrations of thermal sweat both in the renal transplant patients and in healthy subjects. The results suggest that the volume regulating hormones have no effect on the electrolyte composition of thermal sweat induced by short exposition to heat both in renal transplant patients and in healthy subjects.
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PMID:[Effect of thermal dehydration on blood levels of hormones regulating volume and electrolyte content of sweat in patients with kidney transplantation]. 134 26

Urinary vasopressin (VP), aldosterone (ALDO), osmotic substances, sodium excretion, and plasma volume were assessed in 4 healthy male divers during 2 predive control days, 2 compression days, 6 days at 46 atm abs, and 26 days of decompression with stops at 37 and 27 atm abs. At pressure the ambient gas was trimix (0.5 atm abs O2:5% N2:remainder He). All urine was collected throughout the dive. Samples were divided into daytime (0700-1900) and nighttime (1900-0700). Indocyanine green dye dilution was used to determine plasma volume at predive 1, 46, and 24 atm abs. In agreement with previous dives at 31 atm abs, there was a decrease in VP excretion during compression lasting until return to 1 atm abs (P less than 0.05). Also similar to the shallower dives at 31 atm abs, the normal diurnal pattern of VP excretion, daytime higher than nighttime (P less than 0.05), disappeared at pressure. Urine osmolality showed alterations compatible with responses to VP. In contrast to previous studies at 31 atm abs, but in agreement with a previous study at 49.5 atm abs, there was no sustained increase in urinary ALDO excretion and only a transient natriuresis during the compression phase, followed by a reduced sodium excretion. In confirmation of earlier conclusions from indirect evidence, direct measurements of plasma volume indicated a reduction of about 20% (P less than 0.05) at 46 atm abs which remained reduced after decompression to 24 atm abs.
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PMID:Urinary vasopressin and aldosterone and plasma volume during a saturation dive to 450 m. 135 29

Myocardial pump deficiency is regarded to be the hemodynamic hallmark of congestive heart failure. A decline of arterial pressure in the systemic circulation is counter-regulated by vasoconstriction in the arteriolar vascular bed; the compensatory vasoconstriction, however, results in an increased afterload that in turn aggravates myocardial pump deficiency. As part of the counterregulatory systems the sympathetic nervous system is activated (increase of neuronal activity, increased plasma norepinephrine) and the renin-angiotensin-aldosterone system is stimulated as well (increased plasma renin activity, elevated angiotensin II serum levels, hyperaldosteronism). In parallel, serum levels of antidiuretic hormone (ADH) is despite a serum hypoosmolarity increased and only poorly compensated by release of the atrial natriuretic peptide. On the cellular level, congestive heart failure leads to a shift of the expression of contractile proteins towards to fetal forms (for instance myosin-isoenzymes). Although the counterregulatory activation of the neuroendocrine systems vasoconstricts the peripheral arteries thereby maintaining perfusion of vital organs, the rise in afterload ultimately leads to a progression of congestive heart failure. Consequently, vasodilators (such as ACE-inhibitors) that not only induce vasodilation in the peripheral arteries, but also inhibit progressive neuroendocrine stimulation evolved as excellent compounds for treating congestive heart failure.
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PMID:[Pathophysiology of left heart failure with reference to hemodynamic and neurohumoral changes]. 135 6

To investigate the renal effects of somatostatin in cirrhosis, renal function and plasma and urinary levels of endogenous neurohumoral vasoactive substances were measured in conditions of intravenous water overload (20 mL/kg body wt with 5% glucose) before and during the intravenous infusion of somatostatin (250-500 micrograms/h) in 6 cirrhotic patients without ascites and 17 nonazotemic cirrhotic patients with ascites. Somatostatin induced a significant reduction of renal plasma flow, glomerular filtration rate, and free water clearance in both groups of patients. In patients with ascites, somatostatin also reduced urinary sodium excretion. Changes in renal function were significantly more marked in patients with ascites than in those without ascites and occurred in the absence of changes in mean arterial pressure and plasma levels of renin, aldosterone, norepinephrine, antidiuretic hormone, and atrial natriuretic peptide. Somatostatin induced a significant reduction in the plasma concentration of glucagon and urinary excretion of prostaglandin E2 that was not related to changes in renal function. These findings indicate that somatostatin administration induces renal vasoconstriction and impairs glomerular filtration rate, free water clearance, and sodium excretion in cirrhosis by a mechanism unrelated to systemic hemodynamics and endogenous neurohumoral vasoactive systems.
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PMID:Effects of somatostatin on renal function in cirrhosis. 809 52

Diuretics have long been used to lower blood pressure in hypertensive patients or to control body fluid and electrolyte homeostasis in diseases such as congestive heart failure, chronic renal failure or cirrhosis. The initial response to diuretics is a negative sodium and fluid balance. The diuretic-induced loss of salt and water activates several hormonal systems such as vasopressin, the renin-angiotensin-aldosterone system or the sympathetic nervous system which tend to compensate for the changes in sodium and water balance. This neurohormonal response may have important clinical implications. Thus, the activation of the renin-angiotensin-aldosterone cascade appears to be partially responsible for the flat dose-blood pressure response curve of thiazides in hypertensive patients. It may also be responsible for the difference between responders and non-responders to diuretic therapy and for the development of side-effects such as hypokalaemia, metabolic alkalosis or hyponatraemia. There are several ways to prevent the undesirable consequences of the neurohormonal responses to diuretics. The first is to use low doses of these agents. It is also possible to combine them with agents that block the activity of the renin-angiotensin-aldosterone system such as ACE inhibitors or in combination with drugs that reduce aldosterone secretion such as calcium antagonists. The development of drugs able to enhance urinary sodium excretion and to reduce simultaneously the activity of the renin-angiotensin-aldosterone system may offer a new interesting alternative. This might perhaps be achieved in the future with the administration of neutral endopeptidase inhibitors which interfere with the enzymatic degradation of atrial natriuretic peptide.
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PMID:Neurohormonal consequences of diuretics in different cardiovascular syndromes. 136 43

Several studies implicate galanin as a central neuromodulator with an ability to influence hypothalamic and pituitary secretion. Central galanin content is also sensitive to the state of body hydration. Cardiovascular, renal and peripheral endocrine changes evoked by intracerebroventricular administration of galanin have been examined in the anaesthetized rat. Central galanin infusion consistently induced a transitory diuresis, the increase in urine flow being associated with a reduction in urine osmolality. There was no demonstrable change in plasma vasopressin concentration at the end of a 40 min galanin infusion. However, plasma aldosterone and corticosterone concentrations were significantly reduced by comparison with time-matched vehicle infused controls. There were no clear changes in renal electrolyte excretion or in heart rate or mean arterial blood pressure during the study period. The findings of this study support a participatory role for galanin in body fluid homeostasis, though the mechanisms responsible for mediating its central action on urine production remain unclear.
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PMID:Renal, cardiovascular and endocrine effects of centrally administered galanin in the anaesthetised rat. 137 92

We studied the effects of nifedipine on blood pressure and on clinical and analytical parameters in hypertensive patients. Seven male and eight female subjects (mean age of 46.27 +/- 5.38 years, range of 41-56 years) with essential arterial hypertension were given nifedipine (20 mg b.i.d.) for 3 months. Before and after treatment, history, blood pressure, and biochemical values were recorded [blood: Na, K, Ca, creatinine, uric acid, triglycerides, cholesterol, HDL cholesterol, antidiuretic hormone (ADH), and aldosterone; urine: Na, K, Ca, creatinine, ADH, aldosterone, and percentage fraction of Na, K, and Ca excreted]. After 3 months of treatment, we found (a) significant decreases in systolic (147 +/- 18 vs. 166 +/- 16 mm Hg, p less than 0.001) and diastolic blood pressure (90 +/- 8 vs. 107 +/- 8 mm Hg, p less than 0.0007), triglycerides (107 +/- 47 vs. 120 +/- 49 mg/dl, p less than 0.0007), and cholesterol (236 +/- 4 vs. 257 +/- 44 mg/dl, p less than 0.00075) in blood, and in K excretion (50 +/- 19 vs. 46 +/- 19 mEq/g of creatinine, p less than 0.0007) and excreted fraction of K (49 +/- 6% vs. 8 +/- 5%, p less than 0.0012) in urine; (b) significant increases in HDL cholesterol (65 +/- 13 vs. 58 +/- 13 mg/dl, p less than 0.001) in blood, and in Na (115 +/- 73 vs. 109 +/- 69 mEq/g of creatinine, p less than 0.0007) in urine; and (c) no significant change in the remaining biochemical parameters, or in heart rate. Secondary effects included flushing (34%), headache (20%), ankle swelling (17%), dizziness (13%), palpitations (4%), and pruritus (4%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Metabolic and antihypertensive effects of nifedipine in hypertensive patients. 137 8

In the guinea-pig, perindopril inhibited plasma angiotensin converting enzyme (ACE) by 90% when given orally at 2 mg/kg/day during 10 days. Mean blood pressure and plasma aldosterone, cortisol and vasopressin concentrations were not modified by this treatment, while plasma renin activity (PRA) and plasma angiotensin I concentrations increased significantly. The same parameters were studied using a constant intravenous 30 min-infusion of atrial natriuretic peptide (ANP) (0.1 micrograms.kg-1min-1). This dose of ANP infused to anesthetized guinea-pigs induced a significant decrease in mean blood pressure (about -20%) in control and in perindopril treated animals. In ANP infused animals, plasma aldosterone and cortisol concentrations decreased similarly in both groups by about -50%, whereas plasma vasopressin concentrations increased in controls (+169%) but not in perindopril treated guinea-pigs. An increase in PRA and plasma angiotensin I concentrations was observed in both groups after the infusion of ANP. Thus, when ANP demonstrated an potent hypotensive effect a concomitant increase in PRA occurred. The rise observed in vasopressin concentration in control animals was probably mediated by angiotensin II. The fall in plasma aldosterone and cortisol concentrations observed after ANP infusion demonstrated a direct potent action of ANP at the adrenal levels.
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PMID:Cardiovascular and hormonal responses to ANP infusion in the guinea-pig: effects of angiotensin-converting enzyme inhibition with perindopril. 137 87

Endothelins (ET-1, ET-2 and ET-3) are a family of 21 amino acid peptides produced by endothelial cells. They are thought to regulate the local vasomotor tone with endothelium-derived relaxing factors. ETs are the most potent vasoconstrictor substances yet identified and veins and renal vasculature are the most sensitive targets. They reduce cardiac output and have positive inotropic and chronotropic effects. ETs increase the secretion of atrial natriuretic peptide (ANP), aldosterone and catecholamines but reduce renal blood flow and glomerular filtration and they also have mitogenic properties. ETs bind to receptors (ETA and ETB), activate phospholipase C, modulate intracellular Ca2+ concentration and open Ca2+ channels. Vasoactive agents (adrenaline, angiotensin, vasopressin, thrombin, endotoxins) and hypoxia stimulate the release of ET and also ET gene expression. Raised concentrations of plasma ET have been found to occur in several clinical conditions such as hypertension, myocardial infarction, cardiogenic shock, pregnancy induced hypertension, arteriosclerosis, Raynaud's disease, subarachnoid haemorrhage, uraemia, ulcerative colitis, Crohn's disease and surgical operations suggesting that ETs have a role in several patophysiological processes.
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PMID:Endothelin peptides: biological activities, cellular signalling and clinical significance. 138 14


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