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)

When adult male rats with lesions of the cerebellar fastigial nucleus were subjected to sinoaortic denervation and instrumented for aortic pressure recording, their elevated mean arterial pressure was found to rise no higher than that of rats with sinoaortic denervation alone; however all of the doubly operated rats died or became moribund within 4 days. Pulmonary edema and gastric ulcers were frequently seen. When the order of operations was reversed, all animals survived. The possible mechanism and involvement of other brain nuclei, catecholamines and vasopressin in these pathological changes is discussed.
 ...
PMID:Pulmonary edema and death induced by sinoaortic denervation in fastigial nucleus-lesioned rats. 404 58

1. Study of the delayed responses to lethal doses of endotoxin in cats is complicated by acute pulmonary vasoconstriction which results in hypotension, cardiac failure and pulmonary oedema. This acute response is abolished if the animal is pretreated with aspirin (10-100 mg/kg). In these cats, pretreated with aspirin, arterial pressure and right atrial pressure remain unchanged in the first 2 h after administration of endotoxin. Later, arterial pressure falls and the animals die but no haemorrhagic lung lesions are visible.2. These results confirm our previous conclusion that the delayed lethal response to endotoxin is an independent action and not a secondary consequence of the acute response. The mechanism of the action of aspirin is discussed and it is suggested that it prevents the release by endotoxin of vasoactive substances, possibly from platelets.3. In cats pretreated with aspirin, administration of endotoxin results in a marked mesenteric vasoconstriction. Although arterial pressure does not decrease significantly, superior mesenteric arterial flow decreases to 20% of control in the first hour after endotoxin and remains at this low level until the animal dies. Mesenteric ischaemia may contribute to the cat's death.4. The mesenteric vasoconstriction is not reduced by prior administration of phenoxybenzamine and is only slightly reduced after phenoxybenzamine, hypophysectomy and nephrectomy. It is concluded that catecholamines, vasopressin and angiotensin play at most a minor role in the mechanism of this vasoconstriction and that other unknown factors are predominant.
 ...
PMID:Mesenteric vasoconstriction after endotoxin administration in cats pretreated with aspirin. 433 2

The effects of beta-adrenergic-receptor stimulation with ritodrine on systemic and pulmonary hemodynamics and on renal handling of water and electrolytes were studied in unanesthetized, chronically instrumented pregnant sheep. Each animal was studied during control, ritodrine, and recovery periods, each lasting 60 minutes, with the use of three different modes of hydration. beta-receptor stimulation produced a significant increase in heart rate and cardiac output and a decrease in systemic vascular resistance. Pulmonary arterial and wedge pressures tended to increase. These circulatory effects were similar for the three types of hydration and they persisted after cessation of infusion. In terms of its renal effects, beta-receptor stimulation elicited a profound decrease in urine flow and in the excretions of sodium and potassium, irrespective of the mode of hydration. The antidiuresis and antinatriuresis were accompanied by no changes in plasma osmolality and sodium concentration, whereas plasma potassium levels decreased. All of these effects persisted for 60 minutes after the cessation of infusion. In the water-loaded experiments, the antidiuresis seemed to be related to increased antidiuretic hormone secretion; in the saline-loaded experiments, however, both the antidiuresis and antinatriuresis appeared to be related to increased renal reabsorption. The changes in renal hemodynamics seemed to have an insignificant role. The amount of fluid retained in the body was greater when ritodrine was infused with saline solution than with dextrose solution. These cardiovascular and renal studies suggest that a circulatory overload may be the major factor in the pathogenesis of pulmonary edema observed during beta-adrenergic-receptor stimulation.
 ...
PMID:Circulatory and renal effects of beta-adrenergic-receptor stimulation in pregnant sheep. 608 66

The effects of long-term infusion of fenoterol (a beta 2-sympathomimetic drug) in combination with the calcium antagonist verapamil on water balance, the renin-angiotensin-aldosterone system and antidiuretic hormone during pregnancy were studied. Within two hours of the start of infusion, plasma renin and antidiuretic hormone levels were significantly increased, but plasma aldosterone was strongly decreased. There was a concomitant marked reduction of urinary, sodium, and potassium excretion and a decreased creatinine clearance. The long-lasting reduction of urinary excretion which resulted in an elevated water retention is apparently due to other unknown factors. Results are discussed with special regard to the relationship between water balance disturbances and pulmonary edema.
 ...
PMID:The renin-angiotensin-aldosterone system, antidiuretic hormone levels and water balance under tocolytic therapy with Fenoterol and Verapamil. 610 79

Bilateral injection of the inhibitor of histamine-N-methyltransferase, SKF 91488, which is also known as homodimaprit (5 micrograms), into the preoptic area of the rat produced delayed hypertension, tachycardia and hyperthermia. Some animals exhibited pulmonary edema. These effects were only noted 18-24 hr after an injection and were not an artifact of the injection, since the administration of artificial cerebrospinal fluid produced none of these effects. At the time noted, lesions of the rostral hypothalamus, including the preoptic area, were evident. Injection of a vasopressin antagonist, intravenously, did not lower the blood pressure of the hypertensive animals nor did previous bilateral adrenal demullation prevent or delay the hypertension or tachycardia. Therefore, it does not appear that hypersecretion of either vasopressin or adrenal catecholamines contributed to the cardiovascular effects. Peripheral pretreatment with the sympathetic neurotoxin 6-hydroxydopamine however, did prevent the delayed rise in blood pressure following an injection of homodimaprit. From these studies, it is concluded that the injection of homodimaprit produces lesions in the preoptic area, resulting in hypertension that is maintained by excessive activation of the sympathetic nervous system.
 ...
PMID:The effect of intrahypothalamic injection of homodimaprit on blood pressure. 623 59

Experiments in the anesthetized rabbit have demonstrated that the caudal ventrolateral medulla oblongata contains tonically active vasodepressor neurons which are themselves inhibited by GABAergic and glycine-like inputs. Alteration of neuronal function in this region also elevates plasma vasopressin levels, contributing to, but not completely accounting for, the hypertension and pulmonary edema observed after destruction of neurons in the region.
 ...
PMID:Arterial pressure and plasma vasopressin: regulation by neurons in the caudal ventrolateral medulla of the rabbit. 636 66

Two children with inappropriate antidiuretic hormone secretion associated with meningococcal septicaemia are described. The syndrome was diagnosed despite the patients' serum sodium concentrations being within the normal range when, with normal fluid intake and in the absence of hypovolaemia, they developed oliguria and concentrated urine. Early diagnosis prevents cerebral water intoxication and pulmonary oedema that may occur if hyponatraemia is allowed to develop.
 ...
PMID:Early clinical diagnosis of the syndrome of inappropriate secretion of antidiuretic hormone. Case reports. 683 32

In 58 patients with progressive neurological deterioration from angiographically confirmed cerebral vasospasm after spontaneous subarachnoid hemorrhage, arterial hypertension was induced in an attempt to improve their deficits. The most effective regimen consisted of intravascular volume expansion, blockade of the vagal depressor response, and the administration of antidiuretics and vasopressor agents. With this protocol, arterial blood pressure could be sustained at high levels for prolonged periods. Neurological deterioration was reversed in 47 patients, transiently in 4; permanent improvement occurred in 43. Complications experienced during therapy included pulmonary edema, dilutional hyponatremia, aneurysmal rebleeding, coagulopathy, hemothorax, and myocardial infarction. Elevating systemic arterial pressure in states of cerebrovascular insufficiency resulting from vasospasm is safe if meticulous attention is paid to physiological, biochemical, and hematological parameters, with the exception that it may be hazardous in the presence of an untreated ruptured or intact aneurysm. Intravascular volume expansion and induced hypertension are effective in reversing ischemic deficits from vasospasm provided that treatment commences before cerebral infarction and that adequate pressures are maintained for a sufficient period. The production of a hypervolemic state by the use of colloid and crystalloid infusion accompanied by atropine blockade of the vagal depressor response and blunting of the diuresis with vasopressin enables arterial pressure to be elevated for longer than 1 week.
 ...
PMID:Treatment of ischemic deficits from vasospasm with intravascular volume expansion and induced arterial hypertension. 713 49

The pathogenesis of high-altitude pulmonary edema (HAPE) is not well understood. Ventilation and fluid-handling abnormalities at high altitude (HA) may play a role in HAPE. Because ventilatory and cardiopulmonary responses to chronic HA exposure in the Hilltop (H) strain of Sprague-Dawley rat are different from those in the Madison (M) strain, it was hypothesized that these strains would have different susceptibilities to developing HAPE. M and H rats were studied at sea level (SL) and in a hypobaric chamber after 9 and 12 h at a simulated altitude of 24,000 ft (barometric pressure = 295 mmHg) and 1, 12, and 24 h at a simulated altitude of 18,000 ft (barometric pressure = 380 mmHg). Both strains developed HAPE, but the M rat was more susceptible to HAPE, as demonstrated by a higher mortality rate from hemorrhagic pulmonary edema after 9 h at 24,000 ft and an earlier increase in lung water after exposure to 18,000 ft. Minute ventilation was similar in both strains at HA, but arterial PO2 was significantly higher in the M rat. Both strains had a significant decrease in fluid intake and negative sensible water balance at HA. No changes in plasma renin activity, aldosterone concentrations, antidiuretic hormone levels, and atrial natriuretic peptide levels were found at HA. The increased susceptibility of the M rat to HAPE is therefore not explained by ventilation or fluid-handling abnormalities.
 ...
PMID:Susceptibility to high-altitude pulmonary edema in Madison and Hilltop rats. I. Ventilation and fluid balance. 766 30

Acute altitude illnesses include acute mountain sickness (AMS), a benign condition involving headache, nausea, vomiting, irritability, insomnia, dizziness, lethargy, and peripheral edema, and potentially lethal high-altitude cerebral edema and pulmonary edema (HAPE). Recent evidence is summarized that AMS is related to cerebral edema secondary at least in part to hypoxic cerebral vasodilation and elevated cerebral capillary hydrostatic pressure. This results in reduced brain compliance with compression of intracranial structures in the absence of altered global brain metabolism. It is postulated that these primary intracranial events elevate peripheral sympathetic activity that acts neurogenically in the lung possibly in concert with pulmonary capillary stress failure to cause HAPE and in the kidney to promote salt and water retention. The adrenergic responses are likely modulated by striking increases of aldosterone, vasopressin and atrial natriuretic peptide. The effects of exercise on altitude-induced illness and various therapeutic regimens (acetazolamide, CO2 breathing, dexamethasone, and alpha adrenergic inhibitors) are discussed in light of this hypothesis.
 ...
PMID:A neurogenic basis for acute altitude illness. 816 37


<< Previous 1 2 3 4 Next >>