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)

Temporary small intestinal ischemia was induced by mesenteric arteriolar embolization of degradable starch microspheres in cats. During ischemia, the small intestine received a surface dose of 7 Gy 200 kV x-ray irradiation. One group of animals also had received 7 Gy to the intact abdomen 72 hr earlier. The risk of thrombosis in small intestinal vessels during or after starch microsphere-induced ischemia combined with irradiation was evaluated by monitoring superior mesenteric arterial blood flow, by determination of blood platelets, fibrinogen, and factor VIII consumed across the mesenteric vascular bed, and by histologic examination of small intestinal vessels. Vascular integrity was inferred from intact response to isoproterenol and vasopressin after the combined trauma of ischemia and irradiation. No signs of thrombosis were detected in small intestinal vessels after temporary ischemia and irradiation. Hypoxic radioprotection of the small intestine in the cat can thus be achieved by mesenteric arterial microembolization of degradable starch spheres without evidence of thrombotic complications of significant vascular damage.
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PMID:Hypoxic radioprotection by temporary intestinal ischemia: degradable starch microsphere embolization in the cat. 679 40

This patient demonstrates that peripheral vascular ischemia and gangrene may complicate the use of intraarterial vasopressin in the absence of catheter-related phenomena such as microemboli or catheter dislodgement. Discontinuation of vasopressin effectively reverses ischemic changes. Sympathetic blocking agents or direct-acting vasodilators may accelerate the reversal of the vasopressin induced ischemia. In the patient with a history of previous extremity cold injury, vasopressin may precipitate severe ischemia or gangrene by its direct effect at the arteriolar level in an extremity with already increased sympathetic vascular tone. Peripheral circulatory status must be assessed frequently during vasopressin infusion especially in patients with a history of frostbite.
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PMID:Upper extremity gangrene secondary to superior mesenteric artery infusion of vasopressin. 697 39

Certain key parameters of energy metabolism in a complex mechanism of energy transport in the myocardium cells were studied in experiments on dogs with dosed limitation of the coronary blood flow (by 90%) as well as in experiments on rabbits with the intravenous injection of vasopressin (0.2 units per 1 kg of mass). Animals of all groups under study revealed essential changes in the content of creatine phosphate and in the activity of creatine phosphokinase as compared with the control groups. A possible role of creatine phosphokinase is discussed in the processes of myocardium function energy supply under conditions of creatine phosphate deficiency during a slightly pronounced ischemia.
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PMID:[Components of the creatine kinase system in the myocardium with experimental disturbance of coronary blood flow]. 708 Feb 19

The mechanisms by which elevated levels of vasopressin (ADH) in man and animals cause serious myocardial dysfunction, evidenced by arrhythmias, reduction in cardiac output and coronary blood flow, are not settled. Experiments were conducted in 16 isolated working left ventricles to examine their metabolic and hemodynamic responses to the infusion of vasopressin and the combination of vasopressin and epinephrine. Contractile performance was evaluated by analysis of positive dP/dt, contractile element velocities, and ventricular work-curves using stroke work/end-diastolic pressure. Relaxation parameters, including negative dP/dt and the early diastolic relaxation time constant, were also studied. Coronary blood flow was reduced 22% or less by vasopressin while cardiac output was maintained at a constant level. Myocardial oxygen consumption, lactate and potassium balances were determined from arterial and coronary sinus concentrations. Vasopressin produced myocardial dysfunction indicated by decrements in contractile and relaxation indices, without evidence of global ischemia. Epinephrine restored the mechanical performance to normal without significant change in coronary blood flow, myocardial oxygen consumption, or lactate and potassium balance.
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PMID:Mechanisms of impaired cardiac function by vasopressin. 736 15

Renal artery occlusion has been extensively used in animal models to cause acute renal failure. The present isolated tubule microperfusion studies were designed to examine the transport characteristics of multiple nephron segments of the rabbit after 60 min of total renal ischemia. Preliminary studies showed that this maneuver produced significant and persistent elevations of serum creatinine. The tubules were perfused and bathed with artificial solutions simulating ultrafiltrate and studied at 37 degrees C. Four nephron segments were examined. Ischemia reduced proximal convoluted tubule fluid reabsorption 77% (0.72 +/- 0.11 vs. 0.14 +/- 0.06 nl . mm-1 . min-1, P less than 0.01) and cortical proximal straight tubule fluid reabsorption 88% (0.54 +/- 0.10 vs. 0.06 +/- 0.03 nl . mm-1 . min-1, P less than 0.005). Ischemia reduced the ability of the thick ascending limb of Henle's loop to lower perfusate chloride ion concentration 60% (-47 +/- 9 vs. -19 +/- 3 meq/liter, P less than 0.02) and its diluting ability 49% (-87 +/- 15 vs. -44 +/- 7 mosmol/kg H2O, P less than 0.01). Ischemia reduced the antidiuretic hormone-dependent osmotic water permeability of the cortical collecting tubule 59% (0.0203 +/- vs. 0.0083 +/- 0.0020 cm/s, P less than 0.01). Morphologic alterations were noted in the proximal segments but not in the distal segments of the nephron. The current studies demonstrate that 60 min of renal ischemia impairs the transport capability of all proximal and distal nephron segments studied.
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PMID:Isolated nephron segments in a rabbit model of ischemic acute renal failure. 739 91

Reactions from the rectal mucosa often give rise to troublesome side-effects during and after radiotherapy in the pelvic region. Local vasoconstriction in the rectal mucosa will cause an ischemia which will decrease the sensitivity of the mucosal cells to radiation and thereby these side-effects can be reduced. Triglycyl-lysine-vasopressin applied rectally in 1% Blanose solution gave in the present study significant radioprotection of the rectal mucosa in the doses of 0.8, 1.6, and 3.2 mg. These doses are, however, very high. Triglycyl-lysine-vasopressin in 1.2% Natrosol solution in a dose of 128 micrograms did not show any certain protective effects. However lysine-vasopressin in 1.2% Natrosol solution in a dose of 16 micrograms gave significant radioprotection of the rectal mucosa. This dose level has in a previous study not given any significant effects on the systemic circulation. Lysine-vasopressin in Natrosol solution seems to be a suitable combination for further studies.
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PMID:Radioprotective effect of local administration of lysine-vasopressin and triglycyl-lysine-vasopressin on the rectal mucosa in rats. 760 56

The effect of SR 49059, a new potent non-peptide vasopressin (AVP) V1a receptor antagonist, was investigated on AVP-induced electrocardiogram modifications. A high intravenous dose of AVP (0.5 IU or 1.23 micrograms/animal) produced an important transient t-wave elevation (from 4.7 +/- 0.2 to 8.9 +/- 0.7 mm) and heart rate decrease (from 199 +/- 5 to 99 +/- 6 bpm) in conscious rabbits. The t-wave increase was a significant index of coronary vasoconstriction-induced cardiac ischemia. SR 49059 had potent protective effects in this model both by intravenous (0.125 to 0.5 mg/kg) and oral (2.5 to 10 mg/kg) routes. After a 30-min pre-treatment, SR 49059 showed dose-dependent protection on t-wave elevation and heart rate decrease with ED50's of 95 (95% CL:168-22) and 30 (95% CL:54-6) micrograms/kg i.v., respectively. Complete blockade occurred with doses of 2 mg/kg i.v. and upwards. By the oral route, SR 49059 was rapidly absorbed and a dose of 10 mg/kg displayed a protective effect lasting more than 6 hours on both electrocardiogram parameters. Moreover, SR 49059 exerted a high stereospecific inhibitory effect since its enantiomer was totally inactive at 0.5 mg/kg i.v., suggesting that protection occurred by interaction with vascular AVP V1a receptors. Thus, SR 49059 is the first specific non-peptide V1a antagonist with long-lasting oral activity on AVP-induced coronary vasoconstriction and bradycardia. With this original profile, SR 49059 could be a promising therapeutical antivasospastic agent for preventing AVP-induced cardiac damage.
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PMID:Effects of SR 49059, a non-peptide antagonist of vasopressin V1a receptors, on vasopressin-induced coronary vasoconstriction in conscious rabbits. 776 83

New nitro ester 3-[(nitrooxy)alkyl]-2H-1,3-benzoxazin-4(3H)-ones show marked inhibitory activity against ischemia-induced electrocardiographic changes, with only limited systemic hemodynamic effects, and are reported in the present study. These new nitro vasodilators are potent inhibitors of the electrocardiographic T-wave and S-T segment elevation induced by intravenous or intracoronary administration of Arg-vasopressin or methacholine in the anesthetized rat. The most active compounds are up to 300- and 600-fold more potent than glyceryl trinitrate or Nicorandil, respectively. These nitro esters relax in a concentration-dependent manner the isolated rabbit aorta, at higher concentrations (2-40-fold) than glyceryl trinitrate, and reduce the mean arterial blood pressure at doses 7-300-fold higher than those required by glyceryl trinitrate to exert a similar hypotensive effect. Remarkably, these compounds retain their anti-ischemic and hemodynamic profile after oral (po) administration. These new nitro ester derivatives, endowed with a marked antianginal activity, which is not associated with concurrent and pronounced falls in systemic blood pressure, represent the leads of a new class of selective nitrovasodilators having a preferential action on large coronary vessels, which could be clinically relevant in the treatment of coronary artery diseases.
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PMID:New antianginal nitro esters with reduced hypotensive activity. Synthesis and pharmacological evaluation of 3-[(nitrooxy)alkyl]-2H-1,3-benzoxazin-4(3H)-ones. 783 24

Endothelin is a 21-amino-acid, vasoactive peptide. Sequence analysis of cloned cDNAs for porcine and human endothelin precursors showed that endothelin-1 (ET-1) is produced in the endothelial cells. The peptide, endothelin (ET), was first identified as a potent vasoconstrictor. It is one of the most potent endogenous vascular smooth-muscle constrictors, ten times more potent than angiotensin II, vasopressin, and neuropeptide Y. Shortly after the discovery of this vasoconstrictor peptide, it was revealed that endothelin also possesses vasodilator properties at doses lower than those necessary to produce vasoconstriction. However, controversy still exists over the mechanism(s) of action; prostacyclin and endothelium-derived relaxing factor (EDRF) have mainly been implicated as the source of the initial vasodepressor effect. ET also elicits markedly different regional hemodynamic response patterns. There is a heterogeneity in the observed vasodilation or vasoconstriction, depending on species and on vascular beds studied in the same species. Endothelin has been implicated in a number of pathologic situations, including tissue ischemia and vasospasm. ET seems to be produced more actively around the site of endothelial damage; the loss of balance between its vasodilator- and vasoconstrictor-induced responses could contribute to its patho-physiologic properties. Experimental results strongly support the concept that ET could be important in controlling vascular tonus, both in the healthy and the diseased vessel.
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PMID:Endothelin: an endothelium-derived vasoactive peptide. 788 38

The anatomy of the human uterine vascular tree changes repeatedly with the variations in hormonal state during each menstrual cycle, with progressive differentiation of arterioles up to the premenstrual state. Hormonal factors also influence the innervation of uterine arteries, both cholinergic, adrenergic and peptidergic, and regulate the spontaneous contractile activity of the smooth muscle of vessel walls as well as the motor responses of these tissues to different vasoactive substances. The smaller branches of uterine arteries, i.e., the resistance arteries appear to be of particular importance in the regulation of uterine blood flow, since they are most densely innervated. Furthermore, the most effective uterine vasoconstrictors in vitro, vasopressin, endothelin, oxytocin and noradrenaline have a more pronounced effect on these vessels than on the main branches of the uterine artery. Vascular compression may also result from changes in the myometrial activity. A hormonal disturbance may cause dysfunctional bleeding by changing vessel growth as well as the uterine smooth muscle activity of both vessels and myometrium. An example of the latter phenomenon is primary dysmenorrhoea, women with this condition having an increased secretion of vasopressin. By an action on type V1 vasopressin receptors of the uterus, this peptide causes myometrial hyperactivity and vasoconstriction, with resultant uterine ischemia and pain. Further support for a pathophysiological role of vasopressin and also of oxytocin in dysmenorrhoea is the therapeutic effect of a competitive type V1 vasopressin and oxytocin receptor antagonist in the condition.
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PMID:Vascularization of human endometrium. Uterine blood flow in healthy condition and in primary dysmenorrhoea. 797 51


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