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)

An endogenous ouabain-like sodium pump inhibitor was demonstrated originally in serum or plasma of acutely extracellular fluid volume (ECFV) expanded animals and humans. Since then numerous studies have confirmed the presence of ouabain-like factor(s) (OLF) in blood, urine, cerebrospinal fluid, and various tissues including the heart and hypothalamus. Some of these OLFs represent well-known endogenous compounds, eg, free unsaturated fatty acids, which in vitro exhibit inhibition of transepithelial sodium transport, direct inhibition of the Na-K-ATPase enzyme, displacement of 3H-ouabain from its membrane receptor, and crossreaction with a digoxin antibody. Small molecular weight (MW) OLFs of yet unknown peptidic or nonpeptidic nature, which may be of hypothalamic origin, were also detected in various animal models of hypertension and in hypertensive patients. They may play a pathophysiological role especially in salt- and volume-dependent forms of hypertension. Our results show that OLFs increase basal and vasopressin-stimulated intracellular Ca2+ release in rat vascular smooth muscle cells in culture and in human platelets similar to the newly discovered endothelin. In addition, a natriuretic factor (natriuretic hormone) was detected by bioassay in plasma and urine, whose activity changes in parallel with sodium intake. We found that this natriuretic factor is associated with small peptides with a MW of less than 1,000. It is, however, unlikely that the two biological properties, ie, the ouabain-like and natriuretic activities, reside in a single compound. A number of circulating OLFs is certainly not identical with a humoral natriuretic factor. Nevertheless, there is increasing evidence for multiple interactions between OLF and the atrial natriuretic peptide (ANP).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endogenous natriuretic and ouabain-like factors. Their roles in body fluid volume and blood pressure regulation. 184 64

We have followed the hormonal response to exercise in twelve normal males cycling at a constant moderate load for ten minutes. Plasma concentrations of a variety of hormones were measured at set times before and during exercise and for twenty minutes afterward. The plasma concentration of norepinephrine and epinephrine and plasma activity of renin rose to a maximum at the end of exercise and then declined. The plasma concentrations of neurotensin and atrial natriuretic peptide followed a similar course. Plasma vasopressin rose to a peak at the end of exercise and then fell transiently below the initial value ten minutes after exercise. The plasma concentrations of aldosterone, prolactin and adrenocorticotropin increased during exercise but continued to do so, reaching a peak at ten minutes after exercise. Plasma growth hormone increased during exercise and continued to increase throughout the period of twenty minutes' recovery. Cortisol did not change during exercise but rose progressively during the recovery period. Plasma concentrations of glucagon did not change while that of insulin decreased during exercise. The plasma concentration of bombesin slowly increased during exercise and declined during recovery, reaching a basal value 10 minutes later.
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PMID:Temporal relations of the endocrine response to exercise. 187 87

Hormonal response to Finnish sauna bath was investigated in 20 prepubertal children (age 5-10 years). Blood leukocyte count, plasma potassium, serum aldosterone, growth hormone and prolactin concentrations increased; plasma volume, plasma sodium, catecholamines, serum antidiuretic hormone, atrial natriuretic peptide (ANP), cortisol, and thyrotropin concentrations remained unchanged during sauna bath. One hour after sauna, serum thyrotropin, atrial natriuretic peptide and blood glucose concentrations decreased, whereas the rest of the hormones remained unchanged. Our results implicate that maintenance of homeothermia resulted in moderate hormonal changes in children during Finnish sauna bath which indicate similar adequate hormonal thermoregulatory adjustment as previously documented in adults.
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PMID:Children in sauna: hormonal adjustments to intensive short thermal stress. 192 56

Male Sprague-Dawley rats were uninephrectomized and given either deoxycorticosterone (DOC) pivalate (12.5 mg three times weekly) and 1% NaCl/0.2% KCl to drink for 4 weeks (DOC-treated), after which DOC was stopped and tap water substituted (post-DOC), or tap water to drink throughout (controls), DOC treatment increased blood pressure, serum sodium, plasma atrial natriuretic peptide (P-ANP) and plasma deoxycorticosterone (P-DOC) (P less than 0.05), while serum potassium, plasma renin and plasma angiotensin II were lower (P less than 0.05) than in control animals. Plasma vasopressin (P-AVP) was also raised but not significantly. These changes persisted for up to 4 weeks post-DOC and, in the case of plasma renin, plasma angiotensin II, P-AVP and P-ANP, for up to 12 weeks. Total body sodium was also increased at 2 weeks post-DOC (P less than 0.05). Rats which were adrenalectomized after 4 weeks of DOC treatment in which DOC injections were stopped, then drank either NaCl/KCl or tap water; blood pressure and P-DOC remained elevated while plasma renin remained suppressed. There were more deaths in rats given NaCl/KCl (five of six) than in the group given water (one of six). Rats treated with a subcutaneous DOC silastic implant had a comparable rise in blood pressure to rats given DOC injections. However, after removal of the implant, while blood pressure remained elevated, P-DOC levels were not raised and plasma renin rose to control levels after 4 weeks. These findings indicate that, in rats given DOC injections, post-DOC hypertension results from sodium and fluid retention as a consequence of chronic hangover of exogenously administered DOC.
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PMID:Hormone and electrolyte changes in post-deoxycorticosterone salt hypertension in rats. 196 84

The effect of 50 and 150 mg cicletanine, a new vasodilator antihypertensive, on plasma atrial natriuretic peptide (ANP), cyclic GMP and antidiuretic hormone has been investigated at rest and during standardized exercise, in a double blind cross over study in healthy subjects. Exercise significantly increased in plasma ANP, cyclic GMP and antidiuretic hormone concentrations, and cicletanine did not affect any of them either at rest or during exercise. Since the alpha-1 adrenoceptor blocker prazosine decreases, beta-adrenoceptor blockers increase and the vasodilator cicletanine does not alter the plasma ANP response to exercise, it is suggested that adrenergic receptors may be directly involved in the regulation of ANP secretion.
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PMID:Cicletanine does not affect plasma atrial natriuretic peptide concentration in healthy subjects. 196 45

The effect of a non selective and a cardio-selective beta-blocker on basal and exercise-stimulated plasma atrial natriuretic peptide concentrations in healthy volunteers has been studied. Nine healthy volunteers received single oral doses of 5 mg tertatolol, 100 mg atenolol or placebo, at one week intervals, in a double blind cross over trial. At rest plasma atrial natriuretic peptide, aldosterone, antidiuretic hormone and cyclic GMP concentrations and plasma renin activity were not modified by the treatments. During exercise plasma atrial natriuretic peptide concentrations were significantly increased by each treatment, the increment being significantly greater on beta-blockers than on placebo. The rise in atrial natriuretic peptide was 72% after placebo (from 24 to 42 pg/ml), 184% after atenolol (from 30 to 86 pg/ml), and 183% after tertatolol (from 34 to 95 pg/ml), respectively. Thus, the study has shown that in healthy subjects the plasma natriuretic peptide concentration is increased by exercise and that the increase is considerably and equally potentiated by selective and non selective beta-adrenoceptor blockade. The effect may be mainly due to a reduction in ventricular contractility with an increase in atrial pressure. The beta-blockers did not influence the resting plasma atrial natriuretic peptide levels, which suggests that in healthy subjects basal atrial natriuretic peptide secretion is not controlled via beta-receptors.
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PMID:Beta-adrenoceptor blockade potentiates exercise-induced release of atrial natriuretic peptide. 197 99

Circulatory autonomic functions and resting and exercise hemodynamics were studied before and six months after daily administration of 5 mg of carteolol in seven elderly patients with mild hypertension. Blood pressure was reduced in all but one patient. In maximal exercise tests, blood pressure and heart rate responses were significantly attenuated after carteolol treatment, without reduction in exercise capacity. Cardiac index at rest was not affected. Cardiac parasympathetic activity, baroreflex function, and plasma catecholamine, renin, aldosterone, atrial natriuretic peptide, and vasopressin levels did not change during treatment. The results suggest that long-term use of low doses of carteolol may reduce blood pressure without affecting circulatory regulatory functions, even in elderly patients with mild hypertension.
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PMID:Effects of long-term treatment with low doses of carteolol on cardiovascular regulatory functions in elderly patients with mild hypertension. 197 51

Cardiovascular and endocrine responses were evaluated in 12 adult patients over a 5-day period following 30% to 66% burn injury. Heart rate, mean arterial pressure, central venous pressure, pulmonary capillary wedge pressure, cardiac output, systemic vascular resistance, and stroke volume were measured. Plasma concentrations of angiotensin II, atrial natriuretic peptide, vasopressin, neuropeptide Y, norepinephrine, and epinephrine were measured. On the day of burn injury, systemic vascular resistance was markedly elevated, and stroke volume and cardiac output were low, but all normalized by day 3, and cardiac output and stroke volume increased by day 5 without significant changes of central venous pressure or pulmonary capillary wedge pressure. Mean arterial pressure and heart rate did not change significantly over the 5-day period. Vasopressin, angiotensin II, neuropeptide Y, norepinephrine, and epinephrine concentrations in plasma were elevated on admission. Vasopressin concentrations were elevated 50 times normal on admission and returned to normal levels by days 4 to 5. Plasma atrial natriuretic peptide concentrations were normal on admission and increased significantly on days 3 to 5. The reciprocal relationship between systemic vascular resistance and cardiac output and between vasopressin and atrial natriuretic peptide correlate with each other and the observed physiologic events that occurred following burn injury and resuscitation. All of these changes in cardiac performance occurred without significant alterations in preload or afterload as measured by central venous pressure, pulmonary capillary wedge pressure, and mean arterial pressure. Increases in plasma levels of atrial natriuretic peptide correlated with the increased stroke volume and cardiac output observed in these patients. The results of this study are consistent with the conclusion that the extreme elevations of plasma vasopressin levels contribute to the vascular complications of increased systemic vascular resistance and decreased cardiac output and contractility seen following burn injury.
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PMID:Cardiovascular and neurohumoral responses following burn injury. 197 29

1. Effects of atrial natriuretic peptide (ANP) on tension development, particulate guanylate cyclase activity and guanosine 3':5'-cyclic monophosphate (cyclic GMP) concentrations of uteri from oestrogen-treated, progesterone-treated, ovariectomized and pregnant rats were determined in vitro. 2. ANP inhibited the tension development by myometrial tissues from oestrogen-treated virgin rats and the sterile horn of 10 to 14 day pregnant rats but not of the uterus from pregnant and progesterone-treated rats. 3. Inhibition of cyclo-oxygenase and lipoxygenase activities did not restore the tocolytic activity of ANP on gravid uterus. ANP exerted a tocolytic effect on nongravid uterus submaximally stimulated by prostaglandin F2 alpha (PGF2 alpha), oxytocin, vasopressin, angiotensin II or 5-hydroxytryptamine (5-HT). 4. Ovariectomy decreased the tocolytic effects of ANP, which could be restored by oestrogen treatment. 5. The refractoriness to the tocolytic effect of ANP in pregnant rats was not accompanied by a decrease in its relaxant effects on isolated aortic strips. 6. Tocolytic effects of isoprenaline, isobutylmethyl xanthine and hydroxylamine were not influenced by pregnancy or progesterone treatment. Up to a concentration of 3 mM, sodium nitroprusside did not affect myometrial tension development. 7. Pregnancy and progesterone treatment markedly inhibited ANP-induced increases in myometrial particulate guanylate cyclase activity and cyclic GMP concentrations but did not influence the effects of ANP on aortic cyclic GMP concentrations. 8. It is concluded that exposure of the myometrium to circulating and placentally-produced progesterone is responsible for the pregnancy-induced decrease in the effects of ANP on myometrial particulate guanylate cyclase activity and cyclic GMP concentrations and in turn on myometrial tension development.
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PMID:Refractoriness of the gravid rat uterus to tocolytic and biochemical effects of atrial natriuretic peptide. 197 61

This article reviews the evidence that congestive heart failure is accompanied by an increased plasma norepinephrine concentration and that this is due not only to a reduced tissue clearance of the substance but also to a marked increase in sympathetic nerve activity. It also reports data that indicate that the sympathetic activation is associated with an activation of the renin-angiotensin system and an increased plasma level of vasopressin. At which degree of congestive heart failure these phenomena become manifest is not clear, but some studies suggest that the sympathetic and renin-angiotensin systems may be normal in asymptomatic congestive heart failure but already somewhat activated when this condition reaches New York Heart Association class II. There is also evidence that this activation, though initially compensatory, is eventually responsible for a number of adverse cardiovascular effects that account for the negative relationship between this event and survival. Finally, the article discusses the inability of the increased plasma level of atrial natriuretic peptide that characterizes congestive heart failure to offset the adverse effects of the neurohumoral activation and the variable influence of drug treatment on this phenomenon. This is not impossible to achieve, however, because heart transplantation appears to rapidly normalize a major factor in the increased sympathetic activity observed before surgical intervention, that is, impairment of the arterial baroreflex.
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PMID:Neurohumoral activation in congestive heart failure. 197 80


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