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PubMed1991

Lack of neural control and reactivity to vasoactive agents in malignant glioma arteries.

Vessels in malignant brain tumors have a defective blood-brain barrier. It is important to know if tumor vessels respond to vasoactive agents, since systemic administration of vasodilatory agents together with chemotherapy could increase the access of these drugs to the tumor. It was found that arteries in human malignant gliomas have no neural control and are totally nonreactive to various vasoactive agents. The vessels lose their reactivity within 1 to 2 mm outside the visible tumor front.

Brain Neoplasms↗
PubMed1993

Lack of cross-tolerance between nitroglycerin and endothelium-derived relaxing factor-mediated vasoactive agents in spontaneously hypertensive rats.

The purpose of this study was to determine whether cross-tolerance develops between nitroglycerin and endothelium-derived relaxing factor (EDRF)-mediated vasoactive agents in vivo. Spontaneously hypertensive rats (SHR) were made tolerant by pretreatment with high doses of nitroglycerin (100 mg/kg s.c., 3 times/day, for 3 consecutive days). The hypotensive effect of challenge doses of nitroglycerin (1, 10, 300, 100 micrograms/kg i.v.) was completely abolished in nitroglycerin-pretreated SHR. To evaluate cross-tolerance, the effects of the following EDRF-dependent vasoactive agents on blood pressure were determined in groups of nitroglycerin-pretreated and vehicle-pretreated SHR: acetylcholine, bradykinin and L-arginine. In addition, the hypotensive effects of zaprinast (M & B 22,928), a cyclic guanosine monophosphate (cGMP) phosphodiesterase inhibitor, and the hypertensive effects of the nitric oxide-synthase inhibitor N omega-nitro-L-arginine were also evaluated. In all cases, there was no difference in the effects of these agents on blood pressure when compared in nitroglycerin-pretreated (tolerant) and vehicle-pretreated (non-tolerant) SHR. The use of a variety of agents which modulate EDRF release or its effects by several different mechanisms suggests that cross-tolerance does not occur between nitroglycerin and EDRF in vivo.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed1977

The poor reactivity of retinal vessels to systemic administration of vasoactive agents in pentobarbital anesthetized rats.

The responsiveness of retinal vasculature to i.v. administration of several potent vasoactive agents was studied in pentobarbital anesthetized rats by taking fundus photographs. Since cerebral vasculature had been claimed to react in a similar manner but less liably than retinal vessels to some vasoactive substances, the findings were applied to the problem of reactivity of brain vessels. Sublethal doses of noradrenaline, adrenaline, 5-hydroxytryptamine, angiotensin amide and arginine orlysine vasopressin caused no marked acute ( less than or equal to 2 min) vasoconstriction in retinal vessels. Nor did any of these agents or bradykinin elicit vasodilatation. The late vasoconstriction (greater than 2 min) found in succumbing animals was most likely unspecific, since it did not occur until severe toxic symptoms appeared. The findings support the concept that intracerebral vessels are quite resistant to the direct action of many vasoactive agents given i.v.

Animals↗
PubMed1990

Effects of vasoactive agents on isolated human umbilical veins in preeclamptic women.

Increased peripheral vascular reactivity has been noted in preeclampsia. However, in a recent study we found decreased reactivity to vasoactive agents in umbilical arteries of preeclamptic patients. A similar preliminary study, therefore, was carried out on umbilical veins to determine whether preeclampsia affected umbilical venous reactivity. Helical strips of human umbilical veins from 7 preeclamptic and 8 control patients were set up isometrically in physiological salt solution. The resting tensions did not differ between the groups, but spontaneous rhythmic contractions began much earlier in the preeclamptic group than in the controls (8.29 +/- 4.14 vs. 49.22 +/- 9.71 min). There were no differences in the mean amplitudes of the contractions at their time of onset, but in 5 patients of each group the mean amplitudes progressively rose to a maximum at approximately 90 min after incubation, and this maximum was significantly lower in the preeclamptic group (234.43 +/- 72.95 vs. 751.64 +/- 186.13 mg). The frequencies of the contractions did not vary with time or between groups. Log-dose response curves were made for serotonin and KCl, and there were no differences in threshold doses, ED50, maximal tensions or relaxation times between groups. These results are similar to those reported in human umbilical arteries from preeclamptic patients in that no increase in reactivity to vasoactive agents was noted. In conclusion, the differences in the spontaneous rhythmic contractions between preeclamptic patients and controls may be new evidence of pathological changes in the umbilical venous system in preeclampsia.

Adult↗
PubMed1991

Cytokeratin filament modulation in pulmonary microvessel endothelial cells by vasoactive agents and culture confluency.

Recently, bovine pulmonary microvascular endothelial cells (PMV) were shown to contain cytokeratin 8 and 19 intermediate filaments (Patton et al., 1990). In this study, we examine the effect of culture contiguity and vasoactive agents on the content and assembly of cytokeratins in PMV. Immunofluorescent staining of PMV cultures show a progressive increase in cytokeratin filament assembly. In freshly plated PMV, keratin appears as hazy staining (less than 4 hr) and later organizes into keratin 'plaques' (4 days) associated with cell-cell contacts; post confluent (greater than 7 days) PMV cultures contain fully assembled cytokeratin filaments which extend to the cell periphery and approach filaments in apposed cells. Vimentin filaments are also present in freshly plated PMV cultures but unlike cytokeratins, become less filamentous at confluency. This cell density-dependent modulation of cytokeratins is also demonstrated by densitometric analysis of autoradiographs of 35S-methionine labeled keratins in which PMV keratin content is elevated at high cell densities, while vimentin content remains constant. Desmoplakins I and II, components of desmosomes, could not be demonstrated in PMV by immunoblotting. PMV treated with permeability modulating agents (4 x 10(-3) M EGTA, 1 microM cytochalasin B, 1 microM bradykinin, 1 microM A23187, and 1 microM PMA) exhibit border retraction and altered keratin filament staining. From these studies we conclude: 1) cytokeratin 8 and 19 containing intermediate filaments are present in confluent PMV cultures with vimentin but without desmosomes, 2) the state of assembly of PMV cytokeratin and vimentin filaments appears to be oppositely affected by culture contiguity, and 3) treatment of monolayers with vasoactive agents alters the state of assembly of cytokeratin filaments. We speculate that modulation of cytokeratin assembly in PMV may be involved in regulation of pulmonary microvascular structure and function.

Animals↗
PubMed2006

Influence of tangential stress on mechanical responses to vasoactive agents in human saphenous vein with and without perivascular adipose tissue.

AIM: Improvement in short-term patency of vein grafts harvested with the surrounding tissue and no distention has been noted. The influence of transient tangential stress on mechanical function to vasoactive agents in isolated human saphenous veins stripped or with attached perivascular adipose tissue was assessed. METHODS: Concentration-response curves to noradrenaline, 5-hydroxytryptamine, methylcholine, sodium nitroprusside and nicardipine were constructed for veins exposed to no, low (approximately 120 mmHg) or high (approximately 240 mmHg) tangential stress. RESULTS: Tangential stress did not affect contractile effects of noradrenaline or relaxant effects of methylcholine and sodium nitroprusside. Regression analysis of the concentration-response curve to 5-hydroxytryptamine revealed a significant (P=0.042) increase in sensitivity in saphenous veins without perivascular adipose tissue exposed to no tangential stress, compared with veins with attached adipose tissue. Exposure to high stress significantly (P=0.024) increased the potency of 5-hydroxytryptamine in blood vessels without perivascular adipose tissue, as opposed to veins with adipose tissue. Relaxant responses to nicardipine in veins with perivascular adipose tissue were significantly (P=0.001) affected by exposure to low tangential stress compared with no or high tangential stress. A parallel comparison revealed that intact veins compared with those without perivascular adipose tissue exposed to low stress were significantly (P=0.020) more resistant to the relaxant effects of nicardipine. CONCLUSION: The findings of the present report support the view that tangential stress has an impact on the actions of vasoactive agents, but this influence is variable and factor(s) released from perivascular adipose tissue may have a bearing on the observed effect.

Adipose Tissue↗
PubMed1997

[What vasoactive agent should be chosen in rupture of esophageal varices in cirrhosis?].

Variceal esophageal bleeding is a frequent and severe complication of portal hypertension. Balloon compression was the standard therapy for many years. Currently, endoscopic hemostasis with sclerosis or ligation appears to be more effective but requires an experienced operator who is not always present at emergency situations. Parenteral administration of vasoactive agents is one therapeutic option offering new perspectives for the future. Data in the literature suggest that terlipressin or somatostatin would be the preferential choice because of the adverse effects of vasopressin. Data is insufficient concerning sandostatin. Currently, the trend is to administer vasoactive agents as soon as possible, prior to hospitalization and, perhaps, in association with endoscopic hemostasis. Treatment should be maintained for several days although the cost/benefit ratio remains a question of debate.

Esophageal and Gastric Varices↗
PubMed1975

Effect of vasoactive agents on the distribution of renal cortical blood flow in dogs.

The distribution of renal cortical blood flow was studied in 6 Nembutal anesthetized dogs during control periods and during infusions of adrenaline, noradrenaline, angiotensin and vasopressin. Local cortical blood flow was measured as H2 gas desaturation rate recorded polarographically by platinum electrodes in outer and inner cortex. The total renal blood flow (RBF) was measured by an electromagnetic flow meter. In the control period the outer cortical blood flow (OCF) and inner cortical blood flow (ICF) averaged 3.59 (+/- S.D. 0.85) ml/min - g and 3.23 (+/- S.D. 0.64) ml/min - g, respectively. Infusions of the various vasoactive agents caused essentially equal vascular responses. All agents caused increased local renal resistance and reduction of RBF whether given intravenously or intraarterially. The RBF could be lowered to 20-50% of initial control flow by increasing doses of vasoactive agents. OCF and ICF fell proportionately and almost to the same extent as RBF, or OCF fell slightly more than ICF. There was no evidence for patchy or zonal hypoperfusion in cortex caused by infusion of adrenaline, noradrenaline, angiotensin and vasopressin.

Angiotensin II↗
PubMed1987

The response of arterioles in skeletal muscle grafts to vasoactive agents.

Arteriolar responses to the vasodilator adenosine and to the vasoconstrictor norepinephrine (NE) were examined in small bundles of extensor digitorum longus muscle grafted onto the cheek pouches of hamsters. Responses of arterioles to topically applied adenosine or NE were measured from 30 to 180 days after grafting and compared with the response of arterioles in control cheek pouches. Verapamil and potassium chloride (KCl) were applied to 120- and 180-day grafts to determine the response of arterioles to vasoactive agents not mediated by receptors. Arterioles in grafted muscle did not respond to adenosine until 60 days. The response increased with time but was significantly less than the control value even after 180 days. Arterioles in grafts did not respond to NE until 90 days. At both 90 and 120 days the degree of constriction in response to NE was not uniform along the length of a given arteriole (punctate response). By 180 days, the response of a given arteriole to NE was uniform but significantly less than the control value. In 120- and 180-day grafts the responses of arterioles to verapamil and KCl were similar to the responses of arterioles to adenosine and NE, respectively. We conclude that the diminished response of arterioles in small EDL muscle grafts to vasoactive agents may be caused by either a structural or a functional impairment in the smooth muscle layer of arterioles.

Adenosine Diphosphate↗
PubMed1984

Responses of sheep and kitten isolated coronary arteries to some vasoactive agents.

In the present study, the effects of a range of vasoactive agents were assessed in sheep isolated coronary artery strips and in kitten isolated perfused coronary arteries. Both preparations contained muscarinic cholinoceptors. However, these receptors mediated contraction of sheep coronaries while dilatation was seen in the kitten. In sheep arteries, 5-hydroxytryptamine caused increases in resting tone and relaxation of acetylcholine-induced tone, while vasoconstriction was the predominant response in the kitten. Angiotensin increased tone in both preparations, although tachyphylaxis was evident. Conversely, adenosine and ATP caused reductions in tone in both preparations. Alpha-adrenoceptor agonists caused vasodilatation in kitten coronaries and decreased acetylcholine-induced tone in sheep arteries. However, weak contractions were observed in sheep coronaries in the absence of induced tone. Results also indicate that sympatomimetic amines mediate relaxation of sheep coronary arteries via beta 1-adrenoceptors. Sheep coronaries are readily and inexpensively obtained and provide a useful tool for the further study of coronary vascular smooth muscle.

Acetylcholine↗
PubMed1987

Inhibition of vasoactive agents by perfluorochemical emulsion.

Perfluorochemicals are widely used in clinical and experimental studies as volume expanders with high oxygen carrying capacity. We noticed that contractions of rabbit aortic strips, induced by norepinephrine, were inhibited in FC-43 emulsion as compared to Krebs-Henseleit solution (KH). To study this inhibition, a comparative evaluation was made of the contractile responses of norepinephrine, serotonin and histamine in FC-43 emulsion and KH. The effect of these agents was significantly diminished in FC-43 emulsion; concentration-response curves were shifted to the right and the maximum response was diminished. A search was made for the individual constituents of FC-43 responsible for diminution of contraction of vascular smooth muscle. After centrifugation of FC-43 emulsion, the supernatant caused a reduction of contractility and reduced EC50-values of norepinephrine to the same degree as the fully constituted emulsion. This excluded perfluorotributylamine, the oxygen carrying particles, as being responsible for this inhibition. When the detergent Pluronic F-68 was added to KH in concentrations equal to that in FC-43 emulsion, inhibition of contraction occurred and EC50-values increased. Contractions induced by norepinephrine were equally inhibited by the addition to KH of a volume expander, hydroxyethylstarch, in a concentration equal to that in FC-43 emulsion. It is concluded that FC-43 emulsion inhibits vasoactive agents and attenuates its pharmacologic effects on vascular smooth muscle. The fractions of FC-43 emulsion responsible for inhibiting the effect of vasoactive agents are Pluronic F-68 and hydroxyethylstarch.

Animals↗
PubMed1994

Glucocorticoid inhibits cAMP production induced by vasoactive agents in aortic smooth muscle cells.

It is well-known that atherosclerotic change and hypertension are common manifestations in patients with glucocorticoid excess. We previously reported that pituitary adenylate cyclase activating polypeptide (PACAP), prostaglandin E2 (PGE2) and carbacyclin, a stable analog of prostacyclin, have suppressive effects on vasopressin-induced DNA synthesis of rat aortic smooth muscle cells through cAMP production (Murase et al., J. Hypertens., 10 (1992) 1505; Oiso et al., Biochem. Cell. Biol., 71 (1993) 156). In the present study, we investigated the effect of glucocorticoid on cAMP production induced by PACAP, PGE2 and carbacyclin in aortic smooth muscle cells. The pretreatment with dexamethasone significantly inhibited cAMP accumulation induced by these vasoactive agents in a dose dependent manner in the range between 10 pM and 10 nM. These inhibitory effects of dexamethasone were dependent on the time of pretreatment up to 8 h. Dexamethasone inhibited cAMP accumulation induced by NaF, a GTP-binding protein activator, and forskolin which directly activates adenylate cyclase. Moreover, forskolin-induced adenylate cyclase activity was significantly reduced in membranes prepared from the cells treated with dexamethasone. These results strongly suggest that glucocorticoid inhibits cAMP production induced by vasoactive agents in primary cultured rat aortic smooth muscle cells and the inhibitory effect is exerted at the level of adenylate cyclase.

Animals↗
PubMedDate not supplied

The influence of vasoactive agents on metabolic activity of the liver in cirrhosis: a study of the effects of posterior pituitary extract, vasopressin, and somatostatin.

We studied the influence of posterior pituitary extract, vasopressin, and somatostatin on hepatic elimination function. Hepatic clearance and its two biological determinants, hepatic blood flow and metabolic activity (clearance Vmax/Km), were determined from hepatic indocyanine green elimination at steady-state in cirrhotic patients. Intravenous infusion of posterior pituitary extract (oxytocin, 59%; vasopressin, 41%) at the constant rate of 0.3 unit per kg per hr decreased hepatic clearance (p less than 0.05) and Vmax/Km (p less than 0.05) but did not change hepatic blood flow. Intravenous infusion of vasopressin (0.3 unit per kg per hr) decreased hepatic clearance (p less than 0.05), Vmax/Km (p less than 0.05) and hepatic blood flow (p less than 0.05). Intravenous infusion of somatostatin (250 micrograms per hr following a bolus i.v. injection of 250 micrograms) decreased hepatic clearance (p less than 0.05), Vmax/Km (p less than 0.05), and hepatic blood flow (p less than 0.05). This study shows that the vasoactive agents used in the management of upper digestive bleeding in cirrhotic patients may have deleterious effects on the metabolic activity of the liver in addition to their effects on hemodynamics. The results suggest that the vasoactive substances either increased the fraction of total hepatic blood which bypassed intact hepatocytes or directly impaired metabolic activity of hepatocytes. Reduction in the metabolic activity of the liver produced by vasoactive agents may have important implications in therapy of portal hypertension.

Female↗
PubMed1989

[Responsiveness of peripheral blood vessels to physiologically vasoactive agents in myocardial infarct].

Changes in skin vascular responsiveness (VR) to six vasoactive agents were examined in 25 patients with myocardial infarction during its acute period. In small myocardial infarction, there was a synchronous increase in all VR types on days 1-7 followed by its normalization on day 14. VR synchronization was also observed in transmural myocardial infarction, yet increased VR to vasoconstrictive agents such as noradrenaline, adrenaline, and angiotensin II remained until the end of the fourth week without showing a tendency to normalization. Abnormal VR was seen in the most severe fatal cases. The synchronous and cyclic VR changes observed in myocardial infarction were absent in patients with unstable angina that did not result in myocardial infarction.

Adult↗
PubMed1981

Stimulation of cyclic AMP production by vasoactive agents in cultured bovine aortic and pulmonary artery endothelial cells.

The ability of selected vasoactive agents to influence cyclic AMP levels of confluent, early-passaged bovine calf aortic and pulmonary artery endothelial cells was investigated. Among the agents tested, only the catecholamines (isoproterenol, epinephrine, norepinephrine) and prostaglandins (PGE1, PGE2, PGF2 alpha) resulted consistently in increased cyclic AMP production in both cell populations. The degree of cyclic AMP stimulation obtained with other vasoactive compounds (angiotensins I and II, bradykinin, and serotonin) tended to be either very small or difficult to reproduce. Isoproterenol stimulation was blocked completely by propanolol, a beta-blocking agent, but not by phentolamine, and alpha-blocking agent. These results reveal that bovine calf aortic and pulmonary artery endothelial cells are responsive to catecholamines and prostaglandins, and therefore presumably possess both sensitive adenylate cyclases and plasma membrane receptors for these compounds.

Angiotensins↗
PubMed1983

A possible mechanism of vasoactive agents on plasminogen activator release in isolated perfused pig ears.

The mechanism of vasoactive agents on plasminogen activator (PA) release was studied in isolated perfused pig ears. In the perfusion with atropine (3 microM)-containing Tyrode's solution, the enhancement of PA release caused by acetylcholine (1.0 micrograms) was completely inhibited; however, increases caused by other potentiators, namely, bradykinin (1.0 micrograms), histamine (1.0 micrograms), dilazep (30 micrograms), and thrombin (6 U) were not affected. In the case of mepyramine (10 microM), the increase of PA release caused by histamine (1.0 micrograms) was completely inhibited; and that caused by dilazep (30 micrograms) was partially inhibited, however, increases caused by acetylcholine, bradykinin, and thrombin were not influenced. Papaverine (30 microM) which could completely abolish the hypertensive effect of norepinephrine (1.0 micrograms) exerted a partial inhibition of the enhancement of PA release caused by dilazep; however, it did not affect those caused by other agents. Quinacrine (50 microM) and indomethacin (100 microM) did not have any effects on the enhancements of PA release caused by the five potentiators.

Acetylcholine↗
PubMed1992

Blood pressure and heart rate response to vasoactive agents in conscious diabetic rats.

Blood pressure and heart rate responses to different vasoactive agents were observed in conscious streptozotocin-diabetic rats. An indwelling femoral artery catheter was used for direct measurement of arterial pressure and heart rate. The femoral vein was cannulated for drug administration. In a resting state diabetic rats showed lower heart rates and lower systolic blood pressure. The vasodepressor response to both acetylcholine and sodium nitroprusside was decreased, while the heart rate increase induced by the baroreceptor reflex was not altered. Both the increase in blood pressure and the reflex bradycardia to norepinephrine were decreased in the diabetic group. When the change in heart rate was plotted against blood pressure in response to norepinephrine, there was no difference in the two groups of animals. The vasodepressor response to isoproterenol, hydralazine, and verapamil in diabetic rats was unchanged. The results demonstrate a decreased vascular responsiveness in diabetic rats to norepinephrine, acetylcholine, and nitroprusside. The diabetes-induced vascular system changes require further study to understand the mechanisms involved.

Acetylcholine↗
PubMed1991

Role of endothelium in responses of isolated hepatic vessels to vasoactive agents.

The role of the endothelium as a participant in the responses to vasoactive agents was evaluated in isolated canine hepatic artery (HA) and portal vein (PV) rings. Endothelial and smooth muscle integrity was determined by pharmacologic responses as well as by histologic examination. Smooth muscle relaxation was expressed as the percent of decrease of norepinephrine-induced isometric contraction. Acetylcholine (ACh)-induced relaxation of the HA was abolished by removing the endothelium or by the addition of either hemoglobin, methylene blue (MB) or Ng-mono-methyl-L-arginine. In addition, relaxation induced by nitroglycerin, but not that induced by prostaglandin E1, was attenuated by MB. These data suggest endothelium-dependency of the relaxation to ACh and mediation of the response by endothelium-derived relaxing factor through activation of guanylate cyclase. In contrast, ACh produced contraction of the PV which was unaffected by removing the endothelium. The calcium ionophore, A23187, on the other hand, produced relaxation of the PV, which was significantly decreased by removing the endothelium. Relaxation of both HA and PV, produced by 2-chloroadenosine (2-C-Ado) was partially attenuated by removing the endothelium. With the endothelium intact, neither hemoglobin, MB, Ng-monomethyl-L-arginine nor indomethacin affected the responses to 2-C-Ado in the HA and PV, suggesting that the responses were not mediated by endothelium-derived relaxing factor or products of guanylate cyclase or cyclooxygenase activity. Nitroglycerin relaxed both vessels in the presence or absence of endothelium, indicating that removal of the endothelium had not affected smooth muscle function.(ABSTRACT TRUNCATED AT 250 WORDS)

2-Chloroadenosine↗