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)

We examined the combined effects of the calcium channel blockers 1,4-dihydropyridine (benidipine) and benzothiazepine (diltiazem) on vasopressin-induced myocardial ischemia in anesthetized rats, an experimental model of angina. Benidipine (3, 10 microg/kg, i.v.) and diltiazem (300, 1000 microg/kg, i.v.) caused dose-related inhibition of vasopressin-induced S-wave depression, an index of myocardial ischemia. Co-administration of low doses of benidipine (3 microg/kg) and diltiazem (300 microg/kg) almost completely inhibited the S-wave depression, where the efficacy was similar to that obtained with the use of high doses of benidipine (10 microg/kg) or diltiazem (1000 microg/kg). These results suggest that the administration strategy employed may be useful in the treatment of angina pectoris.
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PMID:Combined effects of benidipine and diltiazem in a rat model of experimental angina. 1527 17

Seventy-three patients with ischemic heart disease (IHD), who underwent coronary artery bypass grafting with artificial circulation (AC), were examined within a prospective randomized study. The patients were randomized between three groups. The group-1 patients were administered trasilol (T) according to the below scheme: 1 mln KIU from patient's admission to the surgery room to the time the skin incision is made plus 2 mln KIU from the moment the surgical approach is preformed to the beginning of AC. KIU was added to the artificial circulation apparatus (ACA) when it was initially filled (total T dose of 6 min KIU). T was administered in the group-2 patients similarly to the scheme used in group 1; however, it was not added to the ACA (total T dose of 3 mln KIU). And T was not used at all in the group-3 patients. The dose of mezatone administered at the AC stage was reliably higher in groups 3 and 4 versus group 1 (p < 0.05 and p < 0.1, respectively). Doses of mezatone that were used for the vasopressin management did not differ significantly between the groups after surgery. A statistically more significant increase of stroke index (deltaSI) and a decrease of general peripheral vascular resistance (GPVR--deltaGPVR) were registered in 12 hours after surgery in group 3 versus group 1, p < 0.05 and p < 0.01, respectively. The negative deltaGPRV was also more pronounced versus the parameters observed in group 1 and 2 (p < 0.01 and p < 0.02, respectively). Therefore, T, when used at 6 mln KIU in AC, provides for a smaller-scope vasopressin management in AC. And, when it is used before AC at 3 mln KIU, T dose not diminish the dose of vasopressin management in AC. The intraoperative use of T (6 or 3 mln KIU) arrests a pronounced decreased postoperative deltaGPRVR and an increased postoperative CI irrespective of a dose.
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PMID:[Aprotinin in the correction of the hemodynamic syndrome of systemic inflammatory response in surgeries with extracorporeal circulation]. 1546 47

To compare the antianginal effects of 1,4-dihydropyridine-type calcium-channel blockers, we evaluated the effects of benidipine, amlodipine, nifedipine, and efonidipine on vasopressin-induced myocardial ischemia in rats, an experimental model of angina. Intravenous administration of benidipine (3 microg/kg), amlodipine (1000 microg/kg), and nifedipine (100 microg/kg) suppressed the vasopressin-induced S-wave depression, an index of myocardial ischemia. Efonidipine (100 microg/kg, i.v.) tended to inhibit the S-wave depression. At the antianginal dose of each drug, amlodipine, nifedipine, and efonidipine decreased blood pressure significantly, whereas benidipine had little effect on blood pressure at a dose of 3 microg/kg. These results indicate that benidipine, unlike the other 1,4-dihydropyridine-type calcium-channel blockers examined in this study, inhibits vasopressin-induced coronary vasospasm with fewer undesirable effects such as hypotension in rats, suggesting that benidipine may be useful in the treatment of angina pectoris.
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PMID:Effects of benidipine in a rat model for experimental angina. 1713 63

Exercise is the most important physiological stimulus for increased myocardial oxygen demand. The requirement of exercising muscle for increased blood flow necessitates an increase in cardiac output that results in increases in the three main determinants of myocardial oxygen demand: heart rate, myocardial contractility, and ventricular work. The approximately sixfold increase in oxygen demands of the left ventricle during heavy exercise is met principally by augmenting coronary blood flow (~5-fold), as hemoglobin concentration and oxygen extraction (which is already 70-80% at rest) increase only modestly in most species. In contrast, in the right ventricle, oxygen extraction is lower at rest and increases substantially during exercise, similar to skeletal muscle, suggesting fundamental differences in blood flow regulation between these two cardiac chambers. The increase in heart rate also increases the relative time spent in systole, thereby increasing the net extravascular compressive forces acting on the microvasculature within the wall of the left ventricle, in particular in its subendocardial layers. Hence, appropriate adjustment of coronary vascular resistance is critical for the cardiac response to exercise. Coronary resistance vessel tone results from the culmination of myriad vasodilator and vasoconstrictors influences, including neurohormones and endothelial and myocardial factors. Unraveling of the integrative mechanisms controlling coronary vasodilation in response to exercise has been difficult, in part due to the redundancies in coronary vasomotor control and differences between animal species. Exercise training is associated with adaptations in the coronary microvasculature including increased arteriolar densities and/or diameters, which provide a morphometric basis for the observed increase in peak coronary blood flow rates in exercise-trained animals. In larger animals trained by treadmill exercise, the formation of new capillaries maintains capillary density at a level commensurate with the degree of exercise-induced physiological myocardial hypertrophy. Nevertheless, training alters the distribution of coronary vascular resistance so that more capillaries are recruited, resulting in an increase in the permeability-surface area product without a change in capillary numerical density. Maintenance of alpha- and ss-adrenergic tone in the presence of lower circulating catecholamine levels appears to be due to increased receptor responsiveness to adrenergic stimulation. Exercise training also alters local control of coronary resistance vessels. Thus arterioles exhibit increased myogenic tone, likely due to a calcium-dependent protein kinase C signaling-mediated alteration in voltage-gated calcium channel activity in response to stretch. Conversely, training augments endothelium-dependent vasodilation throughout the coronary microcirculation. This enhanced responsiveness appears to result principally from an increased expression of nitric oxide (NO) synthase. Finally, physical conditioning decreases extravascular compressive forces at rest and at comparable levels of exercise, mainly because of a decrease in heart rate. Impedance to coronary inflow due to an epicardial coronary artery stenosis results in marked redistribution of myocardial blood flow during exercise away from the subendocardium towards the subepicardium. However, in contrast to the traditional view that myocardial ischemia causes maximal microvascular dilation, more recent studies have shown that the coronary microvessels retain some degree of vasodilator reserve during exercise-induced ischemia and remain responsive to vasoconstrictor stimuli. These observations have required reassessment of the principal sites of resistance to blood flow in the microcirculation. A significant fraction of resistance is located in small arteries that are outside the metabolic control of the myocardium but are sensitive to shear and nitrovasodilators. The coronary collateral system embodies a dynamic network of interarterial vessels that can undergo both long- and short-term adjustments that can modulate blood flow to the dependent myocardium. Long-term adjustments including recruitment and growth of collateral vessels in response to arterial occlusion are time dependent and determine the maximum blood flow rates available to the collateral-dependent vascular bed during exercise. Rapid short-term adjustments result from active vasomotor activity of the collateral vessels. Mature coronary collateral vessels are responsive to vasodilators such as nitroglycerin and atrial natriuretic peptide, and to vasoconstrictors such as vasopressin, angiotensin II, and the platelet products serotonin and thromboxane A(2). During exercise, ss-adrenergic activity and endothelium-derived NO and prostanoids exert vasodilator influences on coronary collateral vessels. Importantly, alterations in collateral vasomotor tone, e.g., by exogenous vasopressin, inhibition of endogenous NO or prostanoid production, or increasing local adenosine production can modify collateral conductance, thereby influencing the blood supply to the dependent myocardium. In addition, vasomotor activity in the resistance vessels of the collateral perfused vascular bed can influence the volume and distribution of blood flow within the collateral zone. Finally, there is evidence that vasomotor control of resistance vessels in the normally perfused regions of collateralized hearts is altered, indicating that the vascular adaptations in hearts with a flow-limiting coronary obstruction occur at a global as well as a regional level. Exercise training does not stimulate growth of coronary collateral vessels in the normal heart. However, if exercise produces ischemia, which would be absent or minimal under resting conditions, there is evidence that collateral growth can be enhanced. In addition to ischemia, the pressure gradient between vascular beds, which is a determinant of the flow rate and therefore the shear stress on the collateral vessel endothelium, may also be important in stimulating growth of collateral vessels.
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PMID:Regulation of coronary blood flow during exercise. 1862 66

The present study sought to identify confounding factors for the interpretation of copeptin levels in healthy individuals. The natriuretic peptides are recognized as diagnostic and prognostic tools in HF (heart failure). Interpretation of BNP (brain natriuretic peptide) and NTproBNP (N-terminal pro-BNP) levels is multifaceted as their secretion is influenced by many variables. A newly identified glycopeptide called copeptin is comparable with the natriuretic peptides in the diagnosis and prognosis of HF and as a prognostic biomarker after AMI (acute myocardial infarction). Copeptin, derived from the C-terminal portion of the precursor to AVP (arginine vasopressin), is secreted stoichiometrically with vasopressin, hence it can be used as a surrogate marker of the AVP system. In the present study, 706 healthy volunteers were recruited from a local HF screening study. Participants with a history of cardiovascular disease and those with echocardiographic abnormalities were excluded from the study. Copeptin and NTproBNP levels were assayed using in-house immunoluminometric assays. Median copeptin levels were significantly higher in the male volunteers compared with the females [median (range): 4.3 (0.4-44.3) compared with 3.2 (1.0-14.8) pmol/l; P<0.001]. In males, copeptin was correlated with eGFR (estimated glomerular filtration rate; r(s)=-0.186, P<0.001). In females, the correlation of copeptin with eGFR was weak (r(s)=-0.097, P=0.095). DT (deceleration time) and left atrial size correlated with higher copeptin levels (r(s)=0.085, P=0.029 and r(s)=0.206, P<0.001 respectively). Only gender (P<0.001), eGFR (P<0.001), left atrial size (P=0.04) and DT (P=0.02) remained independently predictive of plasma copeptin. The present study suggests that gender and renal function specific partition values should be used to interpret copeptin values in future studies of this biomarker in HF or ischaemic heart disease.
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PMID:Gender and renal function influence plasma levels of copeptin in healthy individuals. 1864 34

Estrogens are known to contribute to endothelial function and sympathetic activity, both of which are strongly associated with the pathogenesis of ischemic heart disease. In addition, estrogens improve impaired lipid profile, a risk factor of endothelial dysfunction. In this study, we investigated the effects of OS-0544, a structurally new selective estrogen receptor modulator (SERM), on endothelial function, sympathetic activity, and plasma cholesterol level in ovariectomized (OVX) rats. Female Sprague-Dawley rats were ovariectomized and orally treated with OS-0544 (or OS-0689, the (R)-enantiomer of OS-0544), or 17beta-estradiol (E2) for 4 weeks, starting the next days after ovariectomy or for 1 week, starting 6 weeks after ovariectomy. Ovariectomy significantly increased vasopressin-induced mean blood pressure (AVP-MBP) (57+/-3.3 mm Hg vs. 46+/-3.5 mm Hg, P<0.05) and decreased acetylcholine (Ach)-induced maximum vasorelaxation response (69+/-5.6% vs. 81+/-4.0%, P<0.05). OS-0544 significantly inhibited AVP-MBP elevation (46+/-3.5 mm Hg vs. 57+/-3.3 mm Hg, P<0.05) and decreased Ach-induced maximum vasorelaxation response (90+/-3.3% vs. 69+/-5.6%, P<0.05) in OVX rats. In addition, OS-0689 as well as E2 significantly reduced (up to 67%) the increase in sympathetic activity in OVX rats. Moreover, like E2, OS-0544 significantly decreased plasma cholesterol level in OVX rats. These results demonstrate that OS-0544 has vascular protective effect on vascular function after ovariectomy. It is therefore believed that OS-0544 has vascular protective effect in postmenopausal woman.
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PMID:Effect of OS-0544, a selective estrogen receptor modulator, on endothelial function and increased sympathetic activity in ovariectomized rats. 1885 27

Echinocystic acid (EA), a pentacyclic triterpene, was isolated and identified from the fruits of Gleditsia sinensis Lam. The protective effects of EA were evaluated in rat models with acute myocardial ischemia induced by isoproterenol and vasopressin. In the electrocardiogram of anesthetized rats, EA prevented the ST-segment depression induced by isoproterenol or vasopressin in a dose-dependently manner. Furthermore, the mRNA expression of Bcl-2 was analyzed by RT-PCR. EA shows an elevation of Bcl-2 mRNA level in infarcted tissue induced by isoproterenol in rats. These results demonstrated for the first time EA has a cardioprotective effect and may be a natural drug.
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PMID:Protective effects of echinocystic acid isolated from Gleditsia sinensis Lam. against acute myocardial ischemia. 1957 79

A patient with a giant ovarian tumor weighing about 7 kg was successfully removed by operation. However, her ECG demonstrated ischemic changes after the operation. We report a case of ischemic heart disease due to persistent diuresis after giant ovarian tumor resection. A 75-year-old, 56.5 kg, 143.5 cm woman was admitted to our hospital for ovarian tumor resection. The preoperative ECG showed normal sinus rhythm and no ischemic changes. Both general anesthesia and epidural anesthesia were planed. An epidural catheter was inserted at T12-L1. Anesthesia was induced with propofol 100 mg, fentanyl 100 microg and vecuronium 8 mg under 100% oxygen inhalation. General anesthesia was maintained with sevoflurane while epidural anesthesia was achieved using 0.375% ropivacaine 6 ml. During the operation, blood pressure was 90-110/70-80 mmHg, with SaO2, 100% and heart rate, 70-80 beats x min(-1). The content of tumor was suctioned for 30 minutes. Surgery was successfully finished without any other incidence. After extubation, her ECG changed to atrial fibrillation from normal sinus rhythm and showed ST-T depression. And then her systolic blood pressure became 80 mmHg or below, but we found continued diuresis at about 10 ml x kg(-1) x hr(-1) for over 2 hr. The total of 7 unit vasopressin was intermittently given for vasoconstriction and antidiuresis. Her hemodynamic was immediately restored, and ECG turned to normal ST-T. The patient had uneventful postoperative recovery.
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PMID:[Case of ischemic heart disease resulting from persistent diuresis after giant ovarian tumor resection]. 2016 66

Apelin is a recently discovered biologically active peptide present in several isoforms that are agonists for orphan receptor APJ. Apelin and APJ receptor were found in the central nervous system and in different peripheral tissues. In the cardiovascular system the peptide is present both in the heart and in the endothelium and smooth muscles cells of the vascular wall. Acting on cardiomyocytes apelin exerts positive inotropic effect, in the endothelium it releases nitric oxide, which mediates its vasodilatory action, while acting directly on smooth muscles cells it causes vasoconstriction. Apelin interacts with other compounds regulating blood pressure; for instance with angiotensin II, vasopressin, and with the sympathetic nervous system. Special attention is focused on the possibility of positive role of apelin in hypertension, initial stages of heart failure and ischaemic heart disease. Synthesis of apelin in adipocytes permits to include this peptide among adipokines. In the adipose tissue its production is increased in obesity and by insulin. It appears that apelin may play essential role in pathogenesis of insulin-resistant obesity. In patients with type 2 diabetes apelin improves glucose tolerance in initial stages of the illness. However, further experimental and clinical studies are required for full evaluation of significance of positive and negative aspects of the role of apelin in the cardiovascular and metabolic diseases.
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PMID:[The role of apelin in pathogenesis of cardiovascular diseases and metabolic disorders]. 2212 10

One of the rationales for the use of vasopressin in septic shock has been its potential cardioprotective mechanisms. Lower heart rates, higher arterial pressures, and fewer norepinephrine doses during vasopressin therapy were hypothesized to protect the heart from myocardial ischemia. In a prospective sub-study of the VASST (Vasopressin in Septic Shock Trial) project, Mehta and colleagues specifically evaluated this hypothesis but failed to find lower cardiac biomarkers or fewer ischemic electrocardiogram changes in patients receiving vasopressin compared with subjects receiving norepinephrine alone. After recent evidence of a lacking survival benefit, the present study results further challenge the future role of vasopressin as a vasopressor in septic shock.
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PMID:On sepsis, troponin and vasopressin: the bitter truth. 2378 55


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