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)

The effects of the digitalis glycosides on systemic vascular resistance (SVR) in patients with congestive heart failure (CHF) are controversial. Most investigators report a reduction in total SVR, an action that has been attributed primarily to withdrawal of elevated sympathetic tone. Direct proof of this hypothesis is lacking, however, and the roles played by the renin-angiotensin-aldosterone and vasopressin systems have not been fully explored. Moreover, in several studies of patients with CHF, SVR did not decrease after the administration of digitalis. To clarify these issues, the hemodynamic and hormonal effects of digoxin were correlated in 11 normotensive men in sinus rhythm with CHF due to dilated cardiomyopathy. Patients were evaluated at rest and during submaximal exercise before and 6 hours after the intravenous infusion of 1.0 mg of digoxin (mean serum concentration 1.7 ng/ml). With digoxin therapy, heart rate, pulmonary wedge pressure and right atrial pressure declined and cardiac output increased. Although vasopressin was unchanged, both plasma norepinephrine concentrations and plasma renin activity decreased, the reduction in norepinephrine correlating with the increase in cardiac output. Despite these hemodynamic and hormonal effects, there was no change in total SVR at rest or during exercise. It is concluded that the improvement in cardiac function with digoxin in this patient group was a result of the inotropic properties of the drug, without an associated reduction in impedance. The failure of total SVR to decrease despite decreases in plasma norepinephrine levels and plasma renin activity might be explained by concomitant digitalis-induced vasoconstriction, impaired ability of arterioles to dilate in CHF, or offsetting alterations in other vasoactive hormone systems.
Am J Cardiol 1985 Nov 15
PMID:Acute effects of digoxin on total systemic vascular resistance in congestive heart failure due to dilated cardiomyopathy: a hemodynamic-hormonal study. 390 88

As a model to study effects of chronic, excessive salt loading on circulation, Pekin ducks were adapted to 2% saline solution as their sole water supply, while fresh-water-adapted animals were used as controls. Due to the development of salt-eliminating glands, salt-adapted ducks are able to cope indefinitely with this salt stress which means a daily ingestion of 5-6 g NaCl per kg body weight per day, associated with a chronic elevation of plasma osmolality and plasma sodium by 5-8% above normal and an up to 3-fold increase of antidiuretic hormone concentration in comparison to animals maintained on fresh water. Salt loading for up to 14 months did neither increase arterial mean, nor diastolic, nor pulse pressure. On the contrary, arterial mean and diastolic pressure were slightly lower in the salt-adapted than in the fresh-water-adapted animals, while pulse pressure and heart rate did not differ. Circulatory adaptation to removal and reinfusion of 10% of the estimated blood volume was identical in salt-water and fresh-water-adapted ducks. It is concluded that even excessive chronic salt loading resulting in chronic hyperosmolality with high plasma levels of sodium and antidiuretic hormone does not alter hemodynamic adaptation, provided that efficient compensating mechanisms are at the animal's disposal.
Basic Res Cardiol
PMID:Blood pressure and arginine vasotocin in normonatremic and hypernatremic ducks. 400 22

The effects of vasopressin on the coronary circulation have been studied with regard to its general hemodynamic effects. Aortic blood pressure (BP), left ventricular pressure (LVP), aortic blood flow (AoBF), and circumflex blood flow (CBF), were measured in 12 open-chest dogs, under control conditions and during vasopressin infusion (25 mU/kg/min). During vasopressin infusion, the mean aortic blood pressure (MBP) was increased from 104 +/- 23 mm Hg to 161 +/- 23 mm diastolic blood pressure (DBP) was more increased (+55%) than the systolic blood pressure (SBP) (+40%). AoBF was decreased from 2.169 +/- 0.408 l/min to 1.118 +/- 0.303 l/min; and the heart rate was decreased by 18%. The total combined left ventricular power did not change significantly. The increase in total peripheral resistance (TPR) (+200%) was the main change in impedance spectrum. The mean circumflex coronary blood flow (MCBF) was decreased from 48 +/- 8.6 ml/min to 33.4 +/- 9.7 ml/min. This decrease was more important in the diastolic circumflex blood flow (DCBF) (-33%) than in the systolic one (-0.8%). The diastolic pressure time index (DPTI) was more increased than the systolic pressure time index (SPTI). The DPTI/SPTI ratio was increased from 0.91 to 1.3. Long diastoles, induced by vagus nerve stimulation, have permitted to characterise the relationship between pressure and coronary blood flow during diastole. This relationship was linear under basal condition, and during vasopressin perfusion. This made it possible to determine the critical closing pressure (Pf0), and the coronary conductance (the slope of the regression curve). Vasopressin induced an increase in Pf0, from 33.7 +/- 95 to 77.4 +/- 16.07 mm Hg (p less than 0.001), and a decrease in coronary conductance, from 0.8 +/- 0.32 to 0.5 +/- 0.1 ml/min/mm Hg. The effect of an acute change in perfusion pressure on the coronary flow, under control conditions and during vasopressin infusion was studied by opening a large arteriovenous fistula. Unclamping of the fistula, under control conditions, allowed to realize an acute fall in DBP from 82.5 +/- 6.36 to 35.5 +/- 9.19 mm Hg, and in DCBF, from 58.5 +/- 9.2 to 20 +/- 9.8 ml/min. During vasopressin infusion, a similar fall in perfusion pressure lead to a zero diastolic circumflex blood flow, for a diastolic aortic blood pressure of 56 +/- 12 mm Hg. However, vasopressin did not affect the delayed active coronary vasodilatation.
Basic Res Cardiol
PMID:Effect of vasopressin on phasic coronary blood flow. 402 82

The effect of i.v. ergonovine tartrate infusions (0.05-20 micrograms/kg/min, 12 minutes duration) on coronary arteries was studied in 14 conscious dogs instrumented to continuously measure vascular diameter by an ultrasonic dimension gauge using 10-MHz piezoelectric crystals. Ergonovine induced a biphasic coronary response: small, transient dilation during the first minutes of infusion, followed by slowly developing constriction reaching its maximum 5 to 15 minutes after the end of the infusion and persisting at this level for at least 10 minutes. The threshold dosage for significant constriction was 0.05 microgram/kg/min. A dosage of 5 micrograms/kg/min (cumulative 60 micrograms/kg, corresponding to 35 micrograms/kg ergonovine maleate) caused a decline in mean left circumflex artery diameter by 137 +/- 15 micrometers (= 4.6%) without significantly altering heart rate, plasma catecholamines or plasma renin activity. Coronary venous O2 saturation did not decline, indicating the absence of coronary resistance vessel constriction. The epicardial artery constriction was not attenuated by a vasopressin antagonist. Under adrenergic blockade (2 mg/kg phentolamine and 2 mg/kg nadolol) or under ganglionic blockade (5 mg/kg pentolinium tartrate), ergonovine (5 micrograms/kg /min) caused substantial elevation in mean arterial pressure, while the decline in coronary artery diameter was attenuated. When this increase in arterial pressure was prevented by appropriate bleeding, the ergonovine-induced coronary constriction was not diminished by adrenergic or ganglionic blockade. The serotonin antagonist methysergide (0.5 mg/kg) completely abolished the ergonovine-induced coronary artery vasomotion. It is concluded that ergonovine in dogs causes an epicardial coronary artery constriction comparable to the diffuse coronary artery narrowing in men not suffering from variant angina pectoris. These constrictions are not mediated by an adrenergic mechanism.
Basic Res Cardiol
PMID:Ergonovine-induced constrictions of epicardial coronary arteries in conscious dogs: alpha-adrenoceptors are not involved. 612 80

Hormonal factors may be important in the regulation of peripheral vascular resistance (PVR) in congestive heart failure (CHF). The role of the renin-angiotensin system in the development of CHF was studied in 16 unanesthetized dogs. CHF was induced by rapid right ventricular pacing, with and without chronic converting-enzyme inhibition (CEI) by captopril. The hemodynamic changes and the activity of renin, aldosterone, norepinephrine and vasopressin were studied. The control dogs showed a greater decrease in cardiac output and a greater increase of mean pulmonary artery pressure than the captopril-treated group. In the group with CEI, only a small, transient increase in PVR was observed during the development of CHF; in the control group, there was an increase of 94% of basal values. The control group showed a continual increase of renin, aldosterone and norepinephrine. Four control dogs showed an inappropriately high secretion of arginine vasopressin. The increase of sympathetic nervous activity was only insignificantly attenuated by angiotensin II inhibition and was without a considerable influence on PVR except for an early transient increase in vascular tone. In our animal model, the renin-angiotensin system plays an important role in the regulation of PVR in CHF. In this kind of CHF the sympathetic nervous system appears to be of minor importance for the long-term regulation of PVR. Plasma arginine vasopressin levels were increased in control dogs; this increase may contribute to the increased vascular tone.
Am J Cardiol 1984 Feb 01
PMID:Role of the renin-angiotensin system in the development of congestive heart failure in the dog as assessed by chronic converting-enzyme blockade. 632 Jun 25

The effects of age and chronic caffeine use (approximately 300 mg/day) on the cardiovascular and humoral responses to 250 mg of oral caffeine (the equivalent of 2 to 3 cups of coffee) were examined. Older subjects had greater increases in blood pressure than younger subjects (p less than 0.03), and caffeine nonusers had greater blood pressure increases than caffeine users, regardless of age (p less than 0.05). Caffeine increased the product of systolic blood pressure and heart rate (an estimate of myocardial oxygen demand) in older caffeine nonusers, but this effect was absent in older caffeine users (p less than 0.01). Cardiovascular effects of caffeine could not be related temporally to changes in plasma epinephrine, which were greater in caffeine nonusers and younger subjects, or to plasma norepinephrine, renin activity or vasopressin, which did not change. Thus, age accentuates and moderate prior caffeine use attenuates the cardiovascular effects of oral caffeine; these effects are not mediated solely through the sympathoadrenal system.
Am J Cardiol 1983 Oct 01
PMID:Age and prior caffeine use alter the cardiovascular and adrenomedullary responses to oral caffeine. 635 97

Arginine vasopressin, a potent vasoconstrictor and regulator of body water, is frequently increased in the plasma of patients with congestive heart failure. Other neurohumoral control networks, such as the sympathetic nervous system and the renin-angiotensin system, also demonstrate increased activity in congestive heart failure, but fail to respond normally to physiologic stress, such as orthostatic tilt. To assess the response of plasma vasopressin to orthostasis in heart failure, vasopressin was measured before and at 10 and 45 minutes during passive upright tilt in 15 patients with congestive heart failure and their response was compared with that in 9 normal control subjects. Arginine vasopressin was measured by radioimmunoassay. In the normal subjects, plasma arginine vasopressin was 5.3 +/- 2.3 pg/ml at control, was unchanged at 10 minutes, but significantly increased to 7.0 +/- 2.5 pg/ml at 45 minutes (p less than 0.05). In contrast, patients with congestive heart failure showed no significant changes in arginine vasopressin levels from the control levels of 11.6 +/- 5.5 pg/ml. Both plasma norepinephrine and renin activity increased in the normal subjects, but failed to increase from higher baselines in patients with congestive heart failure. Thus, plasma arginine vasopressin, like plasma norepinephrine and renin activity, does not increase in response to upright tilt in patients with congestive heart failure. The explanation is not evident but could involve either abnormalities in reflex control of plasma vasopressin in congestive heart failure or in clearance of the hormone during orthostasis.
J Am Coll Cardiol 1983 Dec
PMID:Impaired response of plasma vasopressin to orthostatic stress in patients with congestive heart failure. 635 40

Three cases of transient central diabetes insipidus after cardiopulmonary bypass are presented. All 3 patients responded promptly to administration of vasopressin, and were completely recovered from polyuria 10 days after cardiac surgery. It is postulated that transient diabetes insipidus after cardiac operation occurred in some patients who had preexisting selective osmoreceptor dysfunction when cardiac standstill during extracorporeal circulation alters the left atrial nonosmotic receptor function, resulting in suppression of antidiuretic hormone release.
Am J Cardiol 1983 Dec 01
PMID:Transient central diabetes insipidus after aortocoronary bypass operations. 660 51

The mechanism of ergonovine-provoked coronary vasospasm is poorly understood. We tested the effect of ergonovine in perfused hearts from normal and cholesterol-fed (18 weeks, 2% cholesterol diet) rabbits in a constant-flow Langendorff perfusion. Aortic perfusion pressure was monitored to measure coronary vascular resistance, and left ventricular pressure was measured with an isovolumetric balloon in the left ventricle. Control coronary vascular resistance was 1.12 +/- 0.11 mm Hg/ml/min in hearts from normal rabbits and 1.53 +/- 0.16 mm Hg/ml/min in hearts from cholesterol-fed rabbits (n = 9 each, mean +/- SEM, p less than 0.05). The cholesterol content of aortae from cholesterol-fed rabbits was markedly increased (432 +/- 85 mg/g protein vs. 14.9 +/- 8.2 in controls, p less than 0.001; for coronaries: 396 +/- 136 mg/g protein vs. 125 +/- 25, p less than 0.05). In both groups, increases in coronary vascular resistance were observed with vasopressin (40 IU/l) and phenylephrine (30 microM) and decreases with adenosine (10 microM), isoprenaline (0.1 microM) and 30 sec stop-flow (all p less than 0.05). Ergonovine maleate (10 microM) and serotonin (10 microM) did not increase coronary vascular resistance. Although in whole heart perfusion small changes in the caliber of epicardial vessels may not be detectable, changes severe enough to produce measurable changes in total coronary resistance were not found. Therefore the absence in our model of an increase in coronary vascular resistance after ergonovine is not compatible with a local direct mechanism in epicardial arterial wall, even when sensitized by a high cholesterol diet.
Basic Res Cardiol
PMID:Effects of vasoactive stimuli on coronary vascular resistance in isolated perfused rabbit hearts: no vasospastic response to ergonovine with or without atherogenic diet. 662 20

The content of vasopressin (AVP) and oxytocin (OXT) in the septum, hippocampus, hypothalamus and cortex was determined at 5 min and 24 hr after peripheral (intraperitoneal) administration of histamine (20.0 mg/kg) and pentylenetetrazol (45.0 mg/kg) and in the cerebrospinal fluid at 24 hr after pentylenetetrazol treatment. At 5 min after administration of histamine the AVP content in the septum was increased whereas the OXT level in the various areas was not changed. At 24 hr, neurohypophyseal peptide contents were unaffected in the brain regions analyzed. Pentylenetetrazol did not alter AVP content at 5 min after its administration, however, the OXT level in the septum and the cortex was diminished. At 24 hr after administration of pentylenetetrazol a decreased AVP content in the hippocampus and in the cortex was observed. In contrast, OXT content in the cortex was increased at this time. AVP and OXT levels in CSF were not changed at 24 hr following pentylenetetrazol treatment. The present results suggest that the levels of neurohypophyseal hormones can be differentially altered in particular brain regions at short- (5 min) and long- (24 hr) term intervals after treatment with histamine or pentylenetetrazol. Long-term changes in AVP and OXT levels after pentylenetetrazol may be implicated in the amnesic properties of this convulsive drug. Furthermore, the present findings point to a possible relationship with previously reported pentylenetetrazol-induced changes in peptide levels in the CSF.
 ...
PMID:Vasopressin and oxytocin content in cerebrospinal fluid and in various brain areas after administration of histamine and pentylenetetrazol. 664 96


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