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At least 73 records · Page 4Linked to original sources
PubMed2001

The effect of myocardial bridging of the coronary artery on vasoactive agents and atherosclerosis localization.

The relationship between alterations in the immunohistochemical expression of three vasoactive agents [endothelial nitric oxide synthase (eNOS), endothelin-1 (ET-1), and angiotensin-converting enzyme (ACE)] and the occurrence human atherosclerosis was investigated in relation to the myocardial bridge (MB) of the left anterior descending coronary artery (LAD), an anatomical site that experiences increased shear stress. Five millimetre cross-sections of LADs with MB from 22 autopsied cases were taken from the left coronary ostium to the cardiac apex and were immunohistochemically stained with antibodies against eNOS, ET-1, and ACE. The extent of atherosclerosis in each section was calculated using the atherosclerosis ratio (intimal cross-sectional area/medial cross-sectional area) determined by histomorphometry. The results were analysed according to their anatomical location relative to the MB, either proximal, beneath, or distal. The extent of atherosclerosis was significantly lower beneath the MB, compared with proximal and distal segments. The expression of eNOS, ET-1, and ACE was also significantly lower beneath the MB. The expression of these agents correlated significantly with the extent of atherosclerosis. Because nitric oxide, after its production by eNOS, is believed to be degraded by superoxide radicals, the effect of eNOS expression on atherosclerosis remains controversial. However, the present findings clearly indicate that the expression of ET-1 and ACE is directly related to the development of human coronary atherosclerosis in vivo through shear stress.

Adult↗
PubMed1990

Comparison of the effects of intra-arterial and locally applied vasoactive agents on pulpal blood flow in dog canine teeth determined by laser Doppler velocimetry.

The vasoactive agents norepinephrine, 5-hydroxytryptamine, isoproterenol and bradykinin, at concentrations which changed local arterial pressure without changing systemic arterial pressure significantly, were injected intra-arterially (i.a.) into the maxillary artery or applied directly in a deep dentinal cavity on the buccal surface of canine teeth. The probe of a laser Doppler velocimeter was placed in the cavity to monitor pulpal blood flow. Bolus i.a. injections of the vasoconstrictors norepinephrine and 5-hydroxytryptamine produced a statistically significant (p less than 0.05) reduction in pulpal blood flow, 21.1 +/- 3.7 and 30.7 +/- 15.2%, and the local arterial pressure from the lateral nasal artery increased with norepinephrine but decreased with 5-hydroxytryptamine. The i.a. injections of the vasodilators isoproterenol and bradykinin were found to decrease both local arterial pressure and pulpal blood flow, 17.7 +/- 6.0 and 22.7 +/- 4.2%, respectively (p less than 0.05). However, local application of isoproterenol and bradykinin caused a biphasic response: an increase in pulpal blood flow, 8.6 +/- 1.6 and 9.4 +/- 1.1% (p less than 0.05), followed by a decrease, 19.1 +/- 11.9 and 5.3 +/- 2.1% (p greater than 0.005). Local application of norepinephrine and 5-hydroxytryptamine caused a decrease in pulpal blood flow, 23.7 +/- 5.2% (p less than 0.05) and 9.3 +/- 5.2% (p less than 0.05), respectively. These findings were in accordance with those from other reliable methods, such as injections of radioisotope-labelled 15 microns microspheres and the 133Xe washout technique, making laser Doppler flowmetry a reliable alternative. In addition, the biphasic response to the locally applied vasodilators and the reduction of pulpal blood flow after i.a. injection of vasodilators suggest that regulation of pulpal blood flow is determined by the combined effects of the low compliance environment and the stealing of perfusion to the pulp by the neighbouring tissues.

Administration, Topical↗
PubMed1987

The effect of vasoactive agents on the contractions of the initial lymphatics of the bat's wing.

The effect of vasoactive agents on the spontaneous contractions of the initial lymphatics of the bat's wing was investigated. Initial lymphatic contractile frequency and pulsatile pressure were measured with the servo-null micropressure system. Norepinephrine, phenylepinephrine, isoproterenol, acetylcholine, histamine, serotonin, bradykinin, prostaglandin F2a, prostaglandin E2, indomethacin and ibuprofen were delivered to the immediate vicinity of the initial lymphatic by microinjection or iontophoresis. Only bradykinin produced changes in initial lymphatic contractions which were significantly different from control. The response to bradykinin was characterized by an increase in the frequency, strength or duration of the contraction.

Animals↗
PubMed1984

Effects of neutrophil elastase and other proteases on porcine aortic endothelial prostaglandin I2 production, adenine nucleotide release, and responses to vasoactive agents.

The effects of neutrophil elastase on endothelial prostacyclin (PGI2) production, nucleotide release, and responsiveness to vasoactive agents were compared with the effects of cathepsin G (the other major neutral protease of neutrophils), pancreatic elastase, trypsin, chymotrypsin, and thrombin. PGI2 production by pig aortic endothelial cells cultured on microcarrier beads and perfused in columns was stimulated in a dose-dependent manner by trypsin, chymotrypsin, and cathepsin G (1-100 micrograms/ml for 3 min). Thrombin, while active at low concentrations (0.1-10 National Institutes of Health U/ml), induced smaller responses. Neutrophil and pancreatic elastase had little or no effect on PGI2 production. Dose-dependent, selective release of adenine nucleotides was induced by neutrophil elastase (3-30 micrograms/ml). The other proteases were much less active; for example, trypsin (100 micrograms/ml) induced a response only approximately 5% as great as did 30 micrograms/ml neutrophil elastase. After exposure to 30 micrograms/ml neutrophil elastase, cells did not exhibit the characteristic burst of PGI2 production in response to extracellular ATP; responsiveness gradually returned after 40-120 min. This effect was not seen with the other proteases. Elastase partly inhibited responses to bradykinin and had no effect on PGI2 production that was stimulated by ionophore A23187. There was no evidence of cytotoxicity, as measured by release of lactate dehydrogenase. Neutrophil degranulation can generate concentrations of elastase and cathepsin G comparable with those tested in the present study, and the effects of these enzymes on endothelial function lead us to suggest that they may play a role in vasoregulation and vascular pathology.

Adenine Nucleotides↗
PubMed1985

Tissue plasminogen activator release in vivo in response to vasoactive agents.

Release of tissue plasminogen activator into the circulation of rats in response to intravascular injections of vasoactive agents is studied by using a sensitive and specific clot lysis assay. Intra-arterial bradykinin elicits a rapid and transient rise in circulating plasminogen activator, which is maximum within one minute and is cleared within four to eight minutes. The plasminogen activator is fibrin dependent and is neutralized by an antiserum to human tissue-type plasminogen activator. Bradykinin is 1,000-fold more potent than the other agonists tested, which include histamine, norepinephrine, epinephrine, eledoisin-related peptide, arginine-vasopressin, lysine-vasopressin, desmopressin acetate, carbachol, and acetylcholine. Potency of bradykinin is related to its amino acid sequence. Sequential infusions of bradykinin produce a tachyphylactoid response that could be overcome by increasing the dose of the sequential bradykinin challenge. It is concluded that the characteristics of the responses to bradykinin and other agents in vivo differ significantly from those observed in isolated tissue preparations.

Animals↗
PubMed1993

[The effects of angiotensin II and other vasoactive agents on the blood flow in Yoshida ascites hepatoma].

The effects of angiotensin II and other six vasoactive agents on tissue blood flow of Yoshida rat ascites hepatoma AH109A and normal liver were measured by the hydrogen clearance method. The mean blood flow in the tumor peripheral part under normotensin was 11.9 +/- 8.2 ml/min/100 g tissue and was not influenced by tumor size. Tumor blood flow was more significantly increased in infusion angiotensin II than 0.5 mg/ml methoxamine; however, normal liver blood flow of tumor-bearing rats was unchanged in contrast to an increase seen in the tumor. A Pronounced reduction of tumor blood flow was found after administration of epinephrine, norepinephrine and ethylphenylephrine. In addition, metaraminol, phenylephrine as well as 1.0 and 2.5 mg/ml methoxamine were not found to significantly change the blood flow of the tumor.

Angiotensin II↗
PubMed1990

Differences in vascular responses to vasoactive agents of basilar artery and aorta from rabbits with alloxan-induced diabetes.

Responses of the basilar artery and aorta to vasoactive agents in alloxan-induced diabetic and age-matched control rabbits were examined. There were no significant differences in the reactivity of the basilar artery to norepinephrine (NE), 5-hydroxytryptamine (5-HT), and K+ between age-matched control and diabetic rabbits. The maximal contraction of the aorta with endothelium in response to NE was significantly enhanced in the case of the aorta from diabetic rabbits. Pretreatment with 10(-6) M methylene blue or removal of the endothelium enhanced the contractile response of aorta to NE from control rabbits and, after such treatment, the concentration-response curve to NE was almost identical to that of aorta from diabetic rabbits. Basal levels of cyclic GMP but not cyclic AMP in the diabetic aorta with endothelium were significantly lower than those in the control aorta with endothelium. These results demonstrate that the cerebral artery is resistant to diabetes mellitus within 10 weeks as compared with the peripheral artery. The enhancement in the contractile response of aorta to NE in diabetic rabbits is due to the attenuation of the spontaneous release of endothelium-derived relaxing factor, through an impairment of the function of endothelial cells.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1988

The effects of vasoactive agents on the proliferation of vascular smooth muscle cells grown in vitro.

The present study was designed to investigate the effect of vasoactive agents on cellular proliferation in serially passed cultured vascular smooth muscle cells (VSMC). A substantial reduction in the number of vascular smooth muscle cells was observed with the addition of nifedipine, nicorandil, bunazocine and labetalol compared with that in a control sample. Furthermore, noradrenaline significantly increased the number of vascular smooth muscle cells. In contrast, neither propranolol nor captopril had any effect on number of vascular smooth muscle cells. The cell size, measured as water volume of vascular smooth muscle cells based on the equilibrium distribution of 3-O-(14C-methyl)-D-glucose, did not differ between treatments with the above-mentioned agents. It is suggested that in addition to a known calcium-mediated mechanism, an alpha-receptor-mediated property could be involved in the proliferation of vascular smooth muscle cells and that clinical use of a calcium antagonist or an alpha-blocker might be useful to prevent the hyperproliferation of vascular smooth muscle cells commonly seen in the vascular walls of patients with hypertension.

Amiloride↗
PubMed1980

Reactivity and contractility of rat main pulmonary artery to vasoactive agents.

In vitro studies were undertaken to determine the reactivity and contractility of the rat main pulmonary artery (RPA) to some selected vasoactive agents. Oxytocin was found to be inactive RPA exhibited a poor responsiveness to vasopressin, acetylcholine, histamine, and bradykinin. Prostaglandins B2 and E2, K+, angiotensin, sympathomimetic agents (epinephrine and isoproterenol), 5-hydroxytryptamine (5-HT), and [Ca2+]0 were found to produce, consistently, potent and concentration-related contractions of the RPA. Pulmonary arterial strips that were precontracted with 5-HT responded with relaxations to isoproterenol in low concentrations and with contractions in high concentrations. Blockade of isoproterenol-induced relaxation by propranolol provides evidence for the existence of specific beta-adrenoceptors in RPA. The selective antagonism of contractile responses induced by epinephrine, 5-HT, acetylcholine, and histamine by phentolamine, methysergide, atropine, and pyrilamine, respectively, provides evidence for the occurrence of specific alpha-adrenergic, "D"-serotonin as well as some cholinergic (muscarinic) and H1-histamine receptors in the RPA.

Animals↗
PubMed1991

Effects of CD-349, a dihydropyridine derivative, on contraction induced by vasoactive agents in canine basilar artery after subarachnoid hemorrhage.

We investigated the effects of CD-349, a dihydropyridine derivative, on contraction induced by vasoactive agents in canine basilar artery after subarachnoid hemorrhage (SAH). Ca(2+)-induced contraction of basilar arterial strips preincubated with serotonin (5-HT, 3x10(-6)M) was potentiated in strips from SAH. However, Ca(2+)-induced contraction of arterial strips which were depolarized with isotonic K+ (64mM) was attenuated in strips from SAH. These Ca(2+)-induced contractions of the basilar arteries preincubated with 5-HT and K+ from both control and SAH dogs were significantly inhibited by CD-349 and nicardipine, both dihydropyridine derivatives. 5-HT contracted the basilar arterial strips in a concentration-dependent manner; however, the maximal contraction of the basilar arterial strips to 5-HT was enhanced in SAH. Endothelium-dependent relaxation in response to substance-P was attenuated in SAH when compared to that in control dogs. Early treatment with CD-349 (1 or 2mg/kg/day, i.m.) for 1 week reversed not only the enhanced contraction of the basilar artery in response to 5-HT but also the impairment of endothelium-dependent relaxation in response to substance-P in SAH. It is expected that CD-349 may be a useful agent for the treatment of cerebrovascular diseases such as SAH.

Animals↗
PubMed1982

Effect of superior cervical ganglionectomy on the sensitivity of rabbit ear artery and cerebral arteries of rabbit and cat to vasoactive agents.

The effect of sympathetic denervation on the sensitivity of the rabbit ear and basilar arteries and the cat middle cerebral artery to vasoactive agents was examined in relation to the functional significance of the innervation. Fourteen days after superior cervical ganglionectomy, the catecholamine fluorescence disappeared and the norepinephrine content drastically decreased and transmural nerve stimulation ceased to elicit any response in all these arteries. In the rabbit ear artery, denervation resulted in a significant leftward shift of dose-response curves for norepinephrine (8.2-fold), serotonin (7.7-fold), histamine (2.9-fold) and potassium (1.2-fold). In contrast, there was no significant shift of dose-response curves to these drugs in the rabbit basilar and cat middle cerebral arteries. These results indicate that after chronic superior cervical ganglionectomy, postjunctional supersensitivity developed in the rabbit ear artery, but no pre- or postjunctional supersensitivity occurred in the rabbit basilar and cat middle cerebral arteries. The difference may be in part attributable to the reported closer synaptic cleft distance of the sympathetic nerve terminals in the ear than in the cerebral arteries examined. These results further suggest that the sympathetic adrenergic nerve exerts a tonic influence over the rabbit ear artery, but little or none in normal cerebral blood vessels.

Animals↗
PubMed1990

Effects of vasoactive agents on uptake of immunoglobulin G complexes by mesangial cells.

Mesangial handling of immune complexes may be important in immune injury. We examined whether vasoactive agents, independent of hemodynamic effects, could directly influence uptake of immunoglobulin G (IgG) complexes by mesangial cells (MC). Under basal conditions, MC took up more gold particles coated with IgG2b (P less than 0.05) than coated with IgG2a. Preincubation of MC with angiotensin II (ANG II) (5 x 10(-7) M) resulted in enhancement of uptake (P less than 0.05) of IgG2b-gold [7,578 +/- 968 counts per minute (cpm) per well], IgG2a-gold (4,566 +/- 295 cpm/well; P less than 0.01), and bovine serum albumin (BSA)-gold (2,532 +/- 66; P less than 0.05) when compared with respective controls (IgG2b-gold, 5,513 +/- 762 cpm/well; IgG2a-gold, 3,282 +/- 439; BSA-gold, 2,279 +/- 97). Cytochalasin B produced a significant reduction of uptake of IgG2b-gold (2,224 +/- 88 cpm/well) when compared with the uptake by control cells (3,711 +/- 287 cpm/well) (P less than 0.05). Pretreatment of MC with atrial natriuretic peptide (ANP, 10(-9) M) slightly decreased uptake of IgG-gold under basal conditions (P less than 0.05) and decreased the response to ANG II (P less than 0.05). Similarly, dopamine (DA, 10(-6) M) attenuated uptake of IgG2b-gold under basal (P less than 0.01) as well as ANG II-stimulated (P less than 0.01) states. ANP increased mesangial guanosine 3',5'-cyclic monophosphate (cGMP), DA, adenosine 3',5'-cyclic monophosphate (cAMP) content.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1987

Use of vasoactive agents to increase tumor perfusion and the antitumor efficacy of drug-monoclonal antibody conjugates.

The effects of both alpha 1- and beta-adrenergic blocking agents on the vascular perfusion of tumors were studied with the ultimate goal of improving diagnosis and therapy of solid tumors with the use of monoclonal antibody (MAb) conjugates. With the use of a subcutaneously growing murine thymoma, it was demonstrated that nonselective and cardioselective beta-adrenergic blocking agents were capable of increasing threefold tumor-to-blood and tumor-to-liver perfusion of 125I-labeled MAbs. Subsequently, these beta-adrenergic blocking agents were found to increase the antitumor efficacy of idarubicin (Ida)-MAb conjugates. Conjugate-treated mice that also received beta-adrenergic blocking agents had a smaller mean tumor size and a greater number of regressions than mice receiving Ida-MAb conjugate alone. By contrast, prazosin HCl, an alpha 1-adrenergic blocking agent, and Cyclospasmol, a peripheral vasodilator, did not enhance the tumor perfusion and antitumor efficacy of 125I- or Ida-conjugated MAbs, and no vasoactive agent enhanced the antitumor effect of Ida when used alone. By their selective action on normal blood vessels, vasoactive drugs can change the tumor-to-normal tissue perfusion ratio, thereby enhancing the access of drug-MAb conjugates to tumors and increasing the effectiveness of tumor therapy with the use of drug-MAb conjugates.

Adrenergic beta-Antagonists↗
PubMed1992

The role of intracavernosal vasoactive agents to overcome impotence due to spinal cord injury.

Twenty-two spinal cord injured men (mean age 35.2 years) referred because of impotence were treated with intracavernosal vasoactive agents. Papaverine 2-20 mg, papaverine 40 mg plus phentolamine 0.5 mg or prostaglandin E1 (1-20 micrograms) were used. Nineteen responded and were taught to self administer the medication with varying degrees of assistance from their partners. Fourteen men participated in a postal survey; 12 (86%) continued to use the drugs every 1 to 4 weeks and reported satisfaction with the method. Partner responses were positive in half of the group and when not so it influenced the patients to abandon or reduce the frequency of treatment. Counselling was essential to allay anxiety. Clinical management was not compromised and side effects were minimal. Overall we found this treatment effective, safe and worthwhile.

Adult↗
PubMed1976

Cerebral arterial spasm. Part 5: in vitro contractile activity of vasoactive agents including human CSF on human basilar and anterior cerebral arteries.

In vitro experiments were performed with a small volume chamber to determine the contractile activity of various vasoactive agents on human basilar and anterior cerebral arteries. Cumulative log-dose response curves were obtained for most of the agents tested including serotonin and three different prostaglandins; many of these curves were found to be similar to curves previously obtained with canine cerebral arteries. It was concluded from these similarities that canine cerebral arteries are a good in vitro model for studying human cerebral arterial spasm. It was also demonstrated that human cerebrospinal fluid, collected up to 17 days after a subarachnoid hemorrhage from patients with clinical and angiographic evidence of cerebral arterial spasm, would cause large, dose-dependent contractions in human anterior cerebral arteries.

Adolescent↗
PubMed1989

[The hepatic hemodynamic response to intra-arterial infusion of vasoactive agents--Part 1. Blood flow measurements in dogs].

The common hepatic arterial (CHA), portal venous (PV) and liver tissue (LT) blood flows were measured during continuous infusion of vasoactive agents to the celiac axis under the observation of systemic circulation. The infusions of Angiotensin II (AT) (0.05 microgram/kg/min) and Prostaglandin F2 alpha (PGF) (0.025-0.05 microgram/kg/min) reduced CHA and LT blood flow, but caused no remarkable change of PV blood flow. The infusions of AT (0.5 microgram/kg/min) and PGF (0.5 microgram/kg/min) caused a biphasic response in CHA blood flow: an initial decrease in CHA blood flow was followed by a marked increase in this parameter (p less than 0.05), while PV blood flow decreased, but LT blood flow remained unchanged. The infusion of PGF (1.0 microgram/kg/min) reduced all parameters of CHA, PV and LT blood flows. The infusion of Dibutyryl cyclic AMP (DBcAMP) (2.0 mg/kg/hr) increased all parameters of CHA, PV and LT blood flows. Preinfusion of DBcAMP weakened the primary effects of PGF (1.0 microgram/kg/min) infusion.

Angiotensin II↗
PubMed1976

Bioassay in vivo for circulating vasoactive agents after renal artery constriction in dogs.

We used the gracilis muscle vascular bed to bioassay blood from the two renal veins, vena cava, and aorta continuously for the presence of vasoactive agents before and for 45 minutes after partial occlusion of the left renal artery in dogs. Compared to comparable blood samples from control dogs, left renal venous, vena caval, and aortic blood, but not right renal venous blood, from dogs with renal artery constriction developed vasoconstrictor activity. This was associated with increased renin concentration in plasma from the left renal vein and the vena cava and an increase in systemic arterial pressure. In dogs pretreated with indomethacin, blood from the right renal vein also showed vasoconstrictor activity. Pretreatment with antirenin serum abolished all of the differences between control and experimental dogs. These findings suggest that during acute unilateral renal artery constriction the constricted kidney releases renin and the contralateral kidney releases prostaglandins in sufficient quantity to produce systemic vascular effects.

Animals↗