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)

A 77-year-old man developed syncope after meals at the age of 75. He had been treated with anti-Parkinson's drugs such as levodopa for 18 years as a patient with idiopathic Parkinson's disease (PD). The medications had been very effective to his parkinsonism. Ambulatory blood pressure was recorded every 20 minutes throughout one day by indirect measurement using a Colin medical instrument monitor (ABPM-630). The subsequent data disclosed that postprandial hypotension (PPH) was associated with the frequent after-meal syncope. It was also found that oral ingestion of a solution containing 50 grams of glucose caused a marked and prolonged hypotension during the resting supine position. Plasma norepinephrine failed to show any increment. Plasma vasopressin slightly increased while pulse rate, plasma renin activity, osmolality, and hematocrit did not change despite the production of severe hypotension of a relative acute onset. Signs of glucose intolerance and hyperinsulinemic response were observed. Indications of systemic autonomic nervous dysfunctions were revealed in various autonomic nervous function tests. Physical treatment combined with medication such as droxidopa, midodrine and especially caffeine and fludrocortisone proved to be effective on PPH. The authors confirmed the existence of PD with symptomatic PPH. In addition, we considered this present case as an example of "progressive autonomic failure with PD" (Bannister, 1988).
 ...
PMID:[Parkinson's disease with syncope as a chief complaint induced by prominent postprandial hypotension]. 130 Feb 58

Water deprivation induces the production of the transcription factor Fos in neurons of the neurohypophysial system. These neurons, which are located primarily in the hypothalamic paraventricular (PVN) and supraoptic nuclei (SON), produce the antidiuretic hormone vasopressin. The present immunocytochemical study has analyzed the distribution of Fos in brain regions involved in osmoregulation and compared the extent of Fos immunoreactivity (Fos-IR) in vasopressin-deficient Brattleboro and normal Long-Evans rats under stimulated and non-stimulated conditions. Rats were osmotically challenged by means of a single intraperitoneal injection of 1.5 M/L NaCl. Since Fos may be induced by the stress of handling of animals, non-injected and isotonic saline-injected rats were used as controls. Faint nuclear Fos immunostaining was found in the organum vasculosum of the lamina terminalis (OVLT), the median preoptic nucleus (MnPO), subfornical organ (SFO), and SON of non-injected and isotonic saline-injected Brattleboro but not Long-Evans rats. Hypertonic saline injection specifically induced Fos-IR in neurons located in the SFO, OVLT, MnPO, PVN, SON, hypothalamic accessory nuclei (including the nucleus circularis), and arcuate hypothalamic nucleus (Arc) in both Long Evans and Brattleboro rats. No differences in distribution of the induced immunostaining were found between the strains. Stress of handling and (isotonic saline) injection induced Fos-IR in the lateral septal nuclei, central amygdaloid nuclei, medial amygdaloid nucleus, medial preoptic area, the bed nucleus of the stria terminalis, cingulate- and piriform cortex, the lateral hypothalamic area, ventromedial hypothalamic nucleus, and the habenular nucleus. The data are consistent with a role for Fos in the regulation of vasopressin gene expression during acute hyperosmotic stimulation. In addition, this study demonstrated that during chronic osmotic stimulation, as experienced by homozygous Brattleboro rats, Fos-IR is limited but apparently present constantly and that it increased in these animals following acute osmotic challenge. Our observations suggest that c-fos regulatory controls in homozygous Brattleboro rats are different from those in Long-Evans rats.
 ...
PMID:Fos-like immunoreactivity in the brain of homozygous diabetes insipidus Brattleboro and normal Long-Evans rats. 151 86

To investigate whether activation of afferent and central baroreceptor pathways could differentiate between pure autonomic failure (PAF) and multiple system atrophy with autonomic failure (MSA), we determined the effect of upright tilt on circulating levels of vasopressin in patients with PAF and patients with MSA. We also studied 14 normal subjects, nine of whom developed acute hypotension due to vasovagal syncope. In patients with PAF and in normal subjects with vasovagal syncope, upright tilt induced marked hypotension and a pronounced increase in the plasma concentration of vasopressin (1.1 +/- 0.3 to 38.0 +/- 8.0 pmol/l in PAF and 1.0 +/- 0.2 to 27.4 +/- 7.2 pmol/l in vasovagal syncope, p less than 0.005 for both). In patients with MSA, upright tilt also elicited profound hypotension but circulating levels of vasopressin increased little (0.5 +/- 0.1 to 1.5 +/- 0.3 pmol/l, p less than 0.05). During upright tilt, the plasma concentration of norepinephrine significantly increased in normal subjects but did not increase in patients with autonomic failure. Our results indicate that afferent and central baroreceptor pathways involved in vasopressin release are normal in patients with PAF but are impaired in patients with MSA. Thus, measurement of baroreceptor-mediated vasopressin release appears to provide a clear marker to differentiate between patients with PAF and patients with MSA.
 ...
PMID:Hypotension-induced vasopressin release distinguishes between pure autonomic failure and multiple system atrophy with autonomic failure. 154 19

We report a 52-year-old male patient with Shy-Drager syndrome (SDS) complicated by an occurrence of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). The patient first developed impotence at the age of 48, accompanied by urinary incontinence, and episodes of dizziness while standing. The following year, the patient had developed a staggering gait and speech became monotonous. At age 52, the patient was admitted to the hospital after experiencing frequent episodes of syncope associated with complete loss of consciousness. Upon examination, blood pressure was 100/70 in a recumbent position, and 80/60 when standing. The pulse rate varied from 60 per minute to 62. The patient was alert. The alternating Horner sign was observed, and a paucity of facial movements was visible. His speech was slow and monotonous. Muscle tone was increased bilaterally. There was incoordination. A laboratory examination revealed reduced serum sodium levels of 127 mEq/L and increased sodium excretion with plasma hypoosmolality (262 mOsm/kg/H), urine hyperosmolality and low serum renin activity (0.2 ng/ml/h). Renal functions were normal and the levels of adrenocortical and thyroid hormones were normal. There were no abnormalities observed in the chest roentgenogram taken. The level of antidiuretic hormone (ADH) was unreasonably high (5.74 pg/ml). A water-load test demonstrated failure of both water diuresis and inhibition of ADH secretion. These data suggested that hyponatremia in this case was caused by SIADH. The correlation between plasma osmolality and the concentration of ADH suggested that osmolality that initiates ADH release appeared to have been reset to around 230 mOsm/kg lower than normal.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Shy-Drager syndrome and the syndrome of inappropriate secretion of antidiuretic hormone]. 161 76

Since plasma endothelin concentration increases with upright posture and decreases with volume expansion, a study was conducted to test whether activation of the baroreceptor reflex releases endothelin into plasma. The effect of passive upright tilt on the plasma concentrations of endothelin and vasopressin was examined in: (1) normal subjects; (2) patients with impaired baroreceptor reflex due to primary autonomic failure; (3) patients with normal afferent baroreceptor function but acute inhibition of vasoconstrictor sympathetic outflow (ie, with vasovagal syncope); and (4) patients with hypophysial diabetes insipidus. In normal subjects, upright tilt did not change arterial pressure and significantly increased the plasma concentrations of endothelin and vasopressin. In patients with autonomic failure, upright tilt induced a considerable fall in arterial pressure, no rise in plasma endothelin, and a slight increase in plasma vasopressin. In subjects with vasovagal syncope, arterial pressure dropped and the plasma concentrations of endothelin and vasopressin rose. In the subjects with diabetes insipidus, arterial pressure fell slightly, without change in plasma concentration of endothelin. The results suggest that activation of the baroreceptor reflex induces the release of endothelin into plasma, probably from the neurohypophysis, and they raise the possibility that impaired endothelin release contributes to the orthostatic hypotension of patients with primary autonomic failure.
 ...
PMID:Plasma endothelin during upright tilt: relevance for orthostatic hypotension? 168 70

After a short introduction into the general topic, the catecholamine-induced increase of leukocytes in which the granulocytes are predominant after short-term exercise is discussed. The reduction of lymphocytes is associated with work-dependent cortisol increase after long-term exercise or 1 h after strenous work. The catecholamine-stimulated lymphocytes increase could be explained by the liberation of the cells from the endothelial vessel wall after catecholamine interaction with the beta-adrenoceptors and by mobilization from lymph nodes and spleen after beta-adrenergic stimulation. Catecholamines reduce the proliferation of lymphocytes and the degranulation of mast cells, preventing hypersensitivity reaction due to inhibited mediator liberation. The influence of cortisol and cytokines and vice versa is discussed. The hormonal changes after runs of different intensities and duration are demonstrated; they show an interaction with immunological regulation. The neuroimmune modulation after physical and psychological stress also has to be considered in immune regulation since under this condition the secretion of encephalins, endorphins, ACTH, and cortisol is increased. The significance of enhanced vasopressin secretion causing postural fainting by vagovasal reaction indicates also the effect of a neuropeptide which is related to immunological reactions. In the changes of lymphocyte subclasses, the homing effect of these cells should be regarded. Advices which can improve the immunologic behaviour, avoiding susceptibility to infections by well-conducted training regimens and adequate periods of regeneration time, are necessary.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Interaction between hormones and the immune system. 189 95

1. Syncopal or near syncopal episodes have been observed in five subjects who stood or were tilted and in whom blood samples were being taken. 2. In all subjects bradycardia and hypotension developed before the onset of symptoms. Increases in plasma adrenaline concentrations occurred in all subjects, beginning before the faint. Changes in plasma noradrenaline concentrations were variable: in three subjects there was a marked fall and in the other two subjects an increase. Plasma vasopressin increased in all subjects. 3. Increase in plasma adrenaline may be contributing to the vasodilatation and arterial hypotension which occur during syncope.
 ...
PMID:Why does vasodilatation occur during syncope? 335 8

Although nursing homes are potentially important sites for geriatric research, previous reports have identified impediments to subject recruitment in this setting. We are conducting five simultaneous clinical studies in a 725-bed nursing home. Utilizing a systematic subject recruitment methodology designed to minimize patient and staff burden, we have recruited over 100 subjects. The average recruitment rate over two years from nursing home residents meeting study entry criteria was 43%. The rate was highest (81%) for a study of urinary incontinence offering direct benefit to participants, and lowest (28% and 14% respectively) for physiologic studies of vasopressin regulation and dermal vitamin D production, offering no direct benefit. Studies of syncope and dementia which benefitted groups affected by these problems but not controls, had intermediate recruitment rates (46 and 44%, respectively, P less than .002 compared to incontinence). Thus, clinically relevant projects, sensitive to the needs of the patient and institution, can recruit subjects from the nursing home.
 ...
PMID:Biomedical research in the nursing home: methodological issues and subject recruitment results. 358 66

The concept of depressor reflexes originating in the heart was introduced by von Bezold in 1867 and was later revived by Jarisch. The Bezold-Jarisch reflex originates in cardiac sensory receptors with nonmyelinated vagal afferent pathways. The left ventricle, particularly the inferoposterior wall, is a principal location for these sensory receptors. Stimulation of these inhibitory cardiac receptors by stretch, chemical substances or drugs increases parasympathetic activity and inhibits sympathetic activity. These effects promote reflex bradycardia, vasodilation and hypotension (Bezold-Jarisch reflex) and also modulate renin release and vasopressin secretion. Conversely, decreases in the activity of these inhibitory sensory receptors reflexly increase sympathetic activity, vascular resistance, plasma renin activity and vasopressin. Long regarded as pharmacologic curiosities, it is now clear that reflexes originating in these inhibitory cardiac sensory receptors are important to the pathophysiology of many cardiovascular disorders. This paper reviews the role of inhibitory cardiac sensory receptors in several clinical states including 1) bradycardia, hypotension and gastrointestinal disorders with inferoposterior myocardial ischemia and infarction, 2) bradycardia and hypotension during coronary arteriography, 3) exertional syncope in aortic stenosis, 4) vasovagal syncope, 5) neurohumoral excitation in chronic heart failure, and 6) the therapeutic effects of digitalis.
 ...
PMID:The Bezold-Jarisch reflex revisited: clinical implications of inhibitory reflexes originating in the heart. 682 48

Vasovagal syncope is associated with an abnormal reflex and the physiopathological mechanisms of the phenomenon overall are only partially known. Experimental and clinical studies suggest that the main factor which triggers the syncope is the brusque interruption of the alpha-adrenergic tone with marked, sudden peripheral vasodilation. Although documented, vagal hypertony, with consequent bradycardia and asystolia, is only occasional and is almost always a secondary phenomenon. The most commonly suggested cause of vasovagal syncope is a Bezold-Jarish reflex starting from the cardiac receptors in the walls of the ventricle, mediated by the paradoxical activation of afferent vagal fibres. However, recent studies are suggesting that there may be other pathogenetic mechanisms such as the paradoxical activation of the venous-atrial baroceptors and other "extracardiac" vascular receptors. The neuro-endocrine aspect of the vasovagal reaction is very complex and in spite of the many studies carried out on the catecholamine, renal-angiotensive system, arginine-vasopressin, and b-endorphine trends, there are still many points awaiting clarification. The response of the autonomous nervous system linked to age also require further research.
 ...
PMID:[Physiopathology of vasovagal syncope: review of the most endorsed theories and recent findings]. 755 40


1 2 3 Next >>