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PubMed1992

Effects of hypoxia and other vasoactive agents on pulmonary and cerebral artery smooth muscle cells.

Smooth muscle cells (SMC) were isolated from cat cerebral arteries and three sizes of pulmonary artery (less than 200-, 200- to 600-, and greater than 800-microns diameter) and used within 72-96 h. Change in cell length in response to hypoxia and other vasoactive agents was measured in a specially constructed cell chamber on an inverted microscope. Pulmonary artery SMC responded to hypoxia differently according to artery size. SMC from less than 200- and 200- to 600-microns-diameter pulmonary arteries shortened 18.6 +/- 4.85 and 24.2 +/- 2.70%, respectively. However, SMC from greater than 800-microns-diameter pulmonary arteries shortened 0.81 +/- 0.44%. Cerebral artery SMC plated on a flexible polydimethyl siloxane membrane showed loss of tension during exposure to hypoxia. The shortening of SMC from the 200- to 600-microns pulmonary arteries was accompanied by myosin phosphorylation. SMC from greater than 800-microns-diameter pulmonary arteries and cerebral arteries contained myosin that did not phosphorylate during hypoxia. The SMC from both artery types responded to norepinephrine, serotonin, prostaglandin F2 alpha and indomethacin and exhibited alpha-adrenergic receptor population patterns similar to those of intact arteries. The pattern of hypoxic responses exhibited by these nondedifferentiated pulmonary and cerebral artery SMC supports the idea that, at least in the cat, the hypoxic sensor is located within the SMC.

Animals↗
PubMed1990

The use of vasoactive agents in the treatment of refractory hypotension seen in tricyclic antidepressant overdose.

In this review, the physiologic and pharmacologic effects of tricyclic antidepressants are discussed as they apply to an overdose situation. Systemic arterial hypotension is a frequent occurrence in major overdoses. Occasionally conventional resuscitative measures such as crystalloid or colloid infusion are inadequate and vasoactive agents must be employed in an attempt to normalize blood pressure. The use of these agents is discussed in terms of their physiologic and pharmacologic actions in the management of refractory hypotension induced by tricyclics.

Antidepressive Agents, Tricyclic↗
PubMed1992

Effect of vasoactive agents on induction of Egr-1 in rat mesangial cells: correlation with mitogenicity.

The early growth response gene 1 (Egr-1) is a member of the family of immediate early response genes. Egr-1 encodes a nuclear phosphoprotein that binds a specific nonameric DNA sequence through three zinc-finger domains and functions as a transcriptional activator. We tested whether the vasoactive agents platelet-derived growth factor (PDGF), arginine vasopressin (AVP), serotonin (5-HT), and angiotensin II (ANG II) induced Egr-1 mRNA in cultured rat mesangial cells (MCs) and investigated the role of protein kinase C (PKC) in mediating the induction process. PDGF, AVP, and 5-HT induced Egr-1 mRNA within 15 min, reaching peak levels at 45-60 min. After PDGF and 5-HT stimulation, Egr-1 mRNA levels returned to baseline within 4 h, whereas AVP induced a sustained increase for up to 8 h. There was a very close correlation between doses required for Egr-1 induction and induction of MC proliferation. ANG II was a very weak MC mitogen and induced only a small increase in Egr-1 mRNA. Comparison of control cells with cells depleted of PKC by 48 h of PMA treatment revealed that induction of Egr-1 by PDGF and 5-HT is independent of PKC. In contrast, however, the Egr-1 response to AVP was diminished in PKC-depleted cells. AVP induced Egr-1 mRNA 10.9-fold in control cells, compared with 7.8-fold in PKC-depleted cells. Egr-1 mRNA after AVP stimulation remained elevated in control cells for up to 8 h but returned to baseline after 120 min in PKC-depleted cells. Similar results were obtained using the PKC-inhibitor H-7. Using immunocytochemistry, PDGF and AVP were found to induce Egr-1 protein within 30 min localized to the nucleus. We conclude that there is a strong correlation between induction of Egr-1 after stimulation with PDGF, AVP, 5-HT, and ANG II and the proliferative response elicited by these agents in MCs. AVP induces Egr-1 by both PKC-dependent and PKC-independent pathways, whereas the effects of PDGF and 5-HT are independent of PKC.

Angiotensin II↗
PubMed1981

Influence of various hexoses and vasoactive agents on osmotically induced oncolysis.

Local destruction of malignant growths was achieved rapidly by creating around their cells a strongly hypertonic environment. Various hexoses, injected in and around tumors at 37 degrees, were utilized to produce the osmotic disturbance. Homeostatic correction of the osmotic disturbance was prevented by local ischemia, induced by vasoconstriction, and maintained soon afterwards by thrombosis. Of the few vasoactive agents tested for this purpose, serotonin was the safest and most effective. It worked better when mixed with the hexose than when injected separately s.c. at a distance. The best response to treatment was obtained from tumors which were unattached to deep structures, poorly vascularized, and resistant to an increase of internal pressure, whereas special precautions had to be taken with friable neoplasms to avoid dissemination of metastases. Under certain conditions, by causing acute tumor necrosis, a single treatment achieved a high ratio of cure; in which a favorable immune response to dramatic reduction of tumor burden and to resorbed lysed material perhaps played a part.

Animals↗
PubMed2005

Effects of vasoactive agents on intracellular calcium and force in myometrial and subcutaneous resistance arteries isolated from preeclamptic, pregnant, and nonpregnant woman.

OBJECTIVE: Preeclampsia is a common and serious complication of pregnancy, characterized by maternal hypertension and proteinuria, placental insufficiency, and fetal growth restriction. The purpose of this study was to investigate whether intracellular Ca 2+ ([Ca 2+ ] i ) and contractile responses of vascular smooth muscle to vasoactive agents are altered in preeclampsia compared with normal pregnancy and the nonpregnant state. STUDY DESIGN: Subcutaneous and myometrial resistance arteries from women who had preeclampsia, normal pregnancy, and nonpregnant women were obtained at the time of cesarean section or hysterectomy. Arteries were mounted on an isometric myograph and loaded with the Ca 2+ indicator, fura-2AM, to permit simultaneous measurement of force and [Ca 2+ ] i . Reponses to endothelium-dependent relaxants (acetylcholine and substance P) and vasoconstrictors (depolarizing potassium solution, phenylephrine, and angiotensin II) were examined. RESULTS: The fall in [Ca 2+ ] i and relaxation in response to acetylcholine was significantly inhibited in both myometrial and subcutaneous arteries from preeclamptic women compared with arteries from nonpregnant or normal pregnant women. However, responses to substance P did not differ between the 3 groups. There were no significant differences in [Ca 2+ ] i or force responses to high potassium, phenylephrine, or angiotensin II in myometrial and subcutaneous resistance vessels in women with preeclampsia compared with normal pregnant women. However, force, but not [Ca 2+ ] i responses to angiotensin II, in subcutaneous vessels from normal pregnant and preeclamptic women were reduced compared with subcutaneous arteries from nonpregnant women, indicating that pregnancy is associated with a reduction in Ca 2+ sensitization in this tissue. A similar effect was not seen in myometrial arteries. CONCLUSION: Endothelial function is altered in preeclampsia, with loss of effect of acetylcholine, but not substance P. Vasoconstrictor reactivity is not increased in preeclampsia compared with uncomplicated normal pregnancy, and this is unlikely to be an explanation for the increased peripheral vascular resistance seen in preeclampsia.

Adult↗
PubMed1986

Effect of preload on rat aortic smooth muscle sensitivity to vasoactive agents.

Concentration-response curves to potassium chloride, phenylephrine, serotonin and calcium chloride were obtained from rat aortic strips subjected to preloads of 0.75, 1.5 or 3.0 g. The sensitivity of the aortic smooth muscle to potassium chloride, phenylephrine and serotonin increased with increasing preload; whereas the calcium chloride concentration-response curves of K+-depolarized strips were unaffected by preload. These results demonstrate that the sensitivity of rat aortic smooth muscle to many vasoactive agents is a function of preload and also indicate that an alteration in the influx of external Ca2+ is not sufficient to explain the effect of preload on sensitivity.

Animals↗
PubMed1975

Effects of ethanol and its interaction with vasoactive agents in bovine vascular smooth muscle.

The vascular effects of ethanol were evaluated using isolated arteries from bovine brain, eye, and kidney. Ethanol induced contraction in all vessels, but only at concentrations in excess of lethal blood levels in man. At a concentration approximating that found in the blood during intoxication (43 mM), ethanol had no effect on renal vascular responses to norepinephrine, serotonin, or histamine. The response of ocular vessels to norepinephrine and histamine was significantly diminished by 43 mM ethanol, suggesting a possible mechanism underlying the "bloodshot" eyes found in acute intoxication. Cerebral vascular responses to vasoactive agents were generally unaffected by 43 mM ethanol, indicating that regional differences in brain perfusion are probably not a cause of the behavioral changes found during intoxication.

Animals↗
PubMed1990

Possible involvement of endothelium in the responses of various vasoactive agents in rabbit isolated perfused kidney.

1. Perfusion of the kidney with methylene blue, a soluble guanylate cyclase inhibitor, significantly enhanced the vasoconstrictor effects of angiotensin II, noradrenaline and phenylephrine but significantly reduced the vasodilator effect of acetylcholine without altering that of iloprost. 2. In the kidneys, which were perfused with Triton X-100 to remove endothelium, acetylcholine-induced vasodilation was completely abolished and angiotensin II-, noradrenaline- and phenylephrine-induced vasoconstriction was greatly reduced. 3. The vasodilator effect of iloprost was unchanged after perfusion of kidney with Triton X-100. 4. Neither methylene blue nor Triton X-100 significantly altered urine volume form normal and angiotensin II induced increase of urine volume. 5. These results were taken as evidence for the involvement of renal vascular endothelium originated EDRF in the responses of various vasoactive agents in the rabbit isolated perfused kidney.

Acetylcholine↗
PubMed1983

Effect of vasoactive agents and applied stress on the albumin space of excised rabbit carotid arteries.

Experiments were undertaken on excised rabbit common carotid arteries to assess whether the distribution volume for radioactively labelled albumin is influenced by smooth muscle tone or externally applied stress. In arteries at relaxed length and zero transmural pressure, the distribution volume in the media was reduced by noradrenaline at concentrations exceeding 10(-9) M and increased by both sodium nitrite and isosorbide dinitrate at concentrations exceeding 10(-4) M. The distribution volume was lower in both the media and adventitia of segments at in vivo length pressurized with air to prevent convection through the wall, than in segments at relaxed length and zero transmural pressure. Noradrenaline decreased and sodium nitrite increased the medial distribution volume of the tracer in these air-pressurized segments. The vasoactive agents did not change the [51Cr]EDTA space in vessels at relaxed length and zero transmural pressure, although there were small alterations of medial water content. Transient conditions raise interpretative difficulties because of uncertainty about endothelial permeability and time-dependent changes of wall properties. The changes of the distribution volume for labelled albumin are thought to reflect changes in the properties of the interstitium.

Albumins↗
PubMed1996

Validation of a flow-differential technique for the recording of splenic blood-volume changes to vasoactive agents.

Splenic blood-volume changes to norepinephrine were determined in the anesthetized cat by recording the integral of the difference between splenic arterial flow and splenic venous flow (flow-differential technique) with ultrasonic transit-time flowmeters, and the changes recorded with this technique were compared with those recorded with an independent technique, the gravimetric method. Norepinephrine (0.003-0.3 microgram/min/kg of body weight) induced dose-related decreases in splenic volume, and the values recorded by the flow-differential technique were not significantly different from those recorded with the gravimetric technique. The values recorded by the two methods were highly correlated (r = 0.86). The slope of the line plotting the relation between the two methods was close to unity (0.97 +/- 0.12), and the intercept of the line was close to zero (-0.46 +/- 1.6 ml). The results suggest that the recording of the flow differential between splenic arterial flow and splenic venous flow with ultrasonic transit time flowmeters is a valid method for the recording of splenic blood-volume changes to vasoactive agents.

Animals↗
PubMed1997

The influence of total porto-systemic shunting on the noradrenaline response and on the contractile effects of various vasoactive agents in small rat portal veins and hepatic arteries.

Contractile responses were studied in isolated tubal segments of branches of the rat portal vein (diameter 300 microns) and hepatic artery (diameter 200 microns) 1, 3 and 6 weeks after total porto-systemic shunt operation (PCS). 5-Hydroxytryptamine contracted hepatic arteries concentration-dependently, whereas it produced only weak and inconsistent contractions in portal veins. Vasopressin effectively contracted hepatic arteries, but had no effect on portal veins. Both vessel types responded to prostaglandin F2 alpha with contractions, although the drug potency was relatively low. The responses to these agents were not changed significantly in hepatic arteries or portal veins of PCS rats compared with controls at any of the postoperative time intervals. In both portal veins and hepatic arteries noradrenaline produced contraction-dependent contractions, portal veins being 3 times more sensitive to noradrenaline than hepatic arteries. PCS did not change the nor-adrenaline sensitivity in hepatic arteries, whereas it increased the noradrenaline sensitivity in portal veins after 1, but not after 3 or 6 weeks. This effect was enhanced by cocaine, suggesting a partial sympathetic denervation of branches of the portal vein as well as a complete reinnervation within 3 weeks. Furthermore, the results of this study indicate no influence in any vessel type on the response to several vasoactive agents after depriving the liver of splanchnic venous blood.

Adrenergic alpha-Agonists↗
PubMed1981

Effect of vasoactive agents on polymorphonuclear leukocyte emigration in vivo.

During many acute inflammatory reactions, neutrophil infiltration, probably initiated by locally generated chemotactic stimuli, is often accompanied by simultaneous increases in vascular permeability and blood flow. Although mediators such as bradykinin, histamine, and prostaglandins increase permeability and/or blood flow, usually they do not induce neutrophil infiltration. This study investigated the possibility that such mediators may, however, modulate neutrophil infiltration initiated by chemotactic stimuli in vivo. Neutrophil infiltration, vascular permeability, and blood flow in skin sites in rabbits were quantitated simultaneously with 51Cr-labeled rabbit blood leukocytes, 125I-albumin, and 86RbCl, respectively. The intradermal injection of prostaglandins E1 (0.25 microgram), E2 (0.5 microgram), or F2 alpha (1 microgram) into sites which had previously been injected with chemotactic stimuli, such as zymosan-activated plasma, zymosan, or N-formyl-methionyl-leucyl-phenylalanine, markedly enhanced the rate of neutrophil influx induced by the latter stimuli. The injection of histamine (0.25 microgram), bradykinin (0.02 microgram), or compound 48/80 (100 microgram) similarly enhanced the neutrophil infiltration induced by zymosan-activated plasma. None of the vasoactive agents, when injected into a normal skin, caused neutrophil infiltration. Simultaneous permeability and blood flow measurements suggested that an increase either in vascular permeability or in local blood flow may enhance the degree of neutrophil infiltration of the tissues during chemotactic stimulus-mediated inflammation.

Animals↗
PubMed1985

Evidence for constriction of canine prenodal lymphatic vessels by vasoactive agents and carotid occlusion.

We measured pressure in a prenodal lymphatic in the canine forelimb during constant flow pump-perfusion of the brachial artery. We made bolus i.a. injections of 1.0 micrograms angiotensin II, norepinephrine, bombesin, or bradykinin, 20 micrograms 5-hydroxytryptamine (5HT), or occluded the carotid arteries. Norepinephrine, 5HT, or carotid occlusion produced regular rises in forelimb perfusion pressure and in lymphatic pressure. Angiotensin II increased forelimb arterial pressures but increased lymphatic pressure in only four experiments. Bombesin increased artery pressures but did not affect lymphatic pressure. Small vein pressure was increased by carotid occlusion, 5HT and norepinephrine. Increases in lymphatic pressure were coincident with increases in vein pressure but no related in magnitude. Bradykinin decreased forelimb arterial and venous pressures but did not affect lymphatic pressure. Either active constriction of lymphatic vessels or passive compression by movements of adjacent blood vessels could increase lymphatic pressure. These data do not preclude a passive component of pressure rise in the lymphatics nor do they support the concept. We conclude that active constriction of prenodal lymphatic vessels in the dog forelimb can occur in response to circulating vasoactive agents and bilateral carotid occlusion.

Angiotensin II↗
PubMed1987

Quantitative method for the study of the morphological changes induced by vasoactive agents in single aortic myocytes grown in primary cultures.

Morphological changes of aortic myocytes grown in primary cultures on collagen gels, were induced by two adrenergic agonists, in the absence or presence of specific antagonists. Their effects were quantified by means of the measurement of the surface areas of the images of the cells. The alpha-adrenoreceptor agonist phenylephrine induced a concentration-dependent decrease of the surface areas of the images of the cells, which was competitively antagonized by phentolamine, and was reduced in the presence of CdCl2 (an inhibitor of calcium entry). The beta-adrenoreceptor agonist isoproterenol induced an increase in the surface areas of the images of prostaglandin F2-alpha pretreated cells and this effect was antagonized by propranolol. It is concluded that the morphological changes of myocytes in primary culture, induced by phenylephrine or isoproterenol can be quantified by the measurement of the surface areas of their images. These changes were in good agreement with the response of isolated thoracic aorta rings or strips to the same agonists with regard to their sensitivity, specificity, and kinetic features. Thus the measurement of the changes of the surface area of the images of myocytes induced by vasoactive agents constitutes a noninvasive, nondestructive method for the quantification of their responses to these agents at the single cell level.

Animals↗
PubMed1987

Penile function following intracavernosal injection of vasoactive agents or saline.

Few studies on the pharmacological assessment or treatment of impotence have included controls. In a double-blind crossover study, 18 impotent men received either a 2 ml injection of a solution containing 30 mg papaverine and 1 mg phentolamine or a similar volume of normal saline into the corpus cavernosum. The immediate and delayed effects (4 weeks later) were assessed independently and the alternative injection then given. All injections with papaverine and phentolamine were followed by an immediate increase in penile length and rigidity, and 70% of these patients were able to have sexual intercourse for periods of 1 to 4 weeks. No change in penile length or rigidity occurred following the saline injection and only one patient showed some improvement in erection over the next 4 weeks. In the crossover study, no patient developed any increase in length or rigidity of the penis following injection of saline, and improvement in spontaneous erection occurred in only two cases. In contrast, all patients who received papaverine and phentolamine had an increase in penile length and rigidity, and 50% were able to have normal sexual intercourse over the next 4 weeks. This study confirms the value of a combination of vasoactive agents in the management of impotence, irrespective of its aetiology, and suggests that any placebo effect is minimal in this group of patients with considerable psychological overlay.

Adult↗
PubMed1998

Assessment of vasoactive agents and vascular aging by the second derivative of photoplethysmogram waveform.

To evaluate the clinical application of the second derivative of the fingertip photoplethysmogram waveform, we performed drug administration studies (study 1) and epidemiological studies (study 2). In study 1, ascending aortic pressure was recorded simultaneously with the fingertip photoplethysmogram and its second derivative in 39 patients with a mean+/-SD age of 54+/-11 years. The augmentation index was defined as the ratio of the height of the late systolic peak to that of the early systolic peak in the pulse. The second derivative consists of an a, b, c, and d wave in systole and an e wave in diastole. Ascending aortic pressure increased after injection of 2.5 microg angiotensin from 126/74 to 160/91 mm Hg and decreased after 0.3 mg sublingual nitroglycerin to 111/73 mm Hg. The d/a, the ratio of the height of the d wave to that of the a wave, decreased after angiotensin from -0.40+/-0.13 to -0.62+/-0.19 and increased after nitroglycerin to -0.25+/-0.12 (P<0.001 and P<0.001, respectively). The negative d/a increased with increases in plethysmographic and ascending aortic augmentation indices (r=0.79, P<0.001, and r=0.80, P<0.001, respectively). The negative d/a reflects the late systolic pressure augmentation in the ascending aorta and may be useful for noninvasive evaluation of the effects of vasoactive agents. In study 2, the second derivative of the plethysmogram waveform was measured in a total of 600 subjects (50 men and 50 women in each decade from the 3rd to the 8th) in our health assessment center. The b/a ratio increased with age, and c/a, d/a, and e/a ratios decreased with age. Thus, the second derivative aging index was defined as b-c-d-e/a. The second derivative wave aging index (y) increased with age (x) (r=0.80, P<0.001, y=0.023x-1.515). The second derivative aging index was higher in 126 subjects with any history of diabetes mellitus, hypertension, hypercholesterolemia, and ischemic heart disease than in age-matched subjects without such a history (-0.06+/-0.36 versus -0.22+/-0.41, P<0.01). Women had a higher aging index than men (P<0.01). The b-c-d-e/a ratio may be useful for evaluation of vascular aging and for screening of arteriosclerotic disease.

Aged↗
PubMed1987

Vasoactive agents and production of thrombosis during intravascular coagulation. 3. Comparative effects of catecholamines.

Epinephrine (E), isoproterenol (I), and dopamine (D) were compared with norepinephrine (N) for production of microthrombi during thrombin-induced disseminated intravascular coagulation (DIC) in rabbits. Only catecholamines acting on alpha-adrenoreceptors produced glomerular capillary thrombosis (GCT) typical of the generalized Shwartzman reaction (GSR). Epinephrine produced GCT three times (P less than 0.05) less severe than that produced by N, but beta-blockade with propranolol (P) rendered E equal to N in potency. I and D reduced fibrinogen consumption produced by thrombin. I (0.5-0.66 microgram/kg/min), as opposed to D, prevented the GSR produced by endotoxin in the pregnant rat and the cortisone-sensitized rabbit, and P increased the severity of the GSR in the pregnant rat. Alpha-adrenergic blockade with dibenzyline prevented the GSR produced by endotoxin in rats, whether pregnant, diabetic, or having a unilateral ureteral occlusion, and the classic reaction in rabbits, but not that produced in renal-hypertensive rats. Simultaneous alpha + beta stimulations by E triggered coronary and hepatic microthrombi, which were prevented by P. It is concluded that beta-adrenergic stimulation, as opposed to D-adrenergic stimulation, counterbalances alpha-adrenergic effects occurring in endotoxemia, which are required for production of the GSR in most models. These studies stress the risks and benefits of beta-blockade and provide additional evidence for the role of vasoactive agents and microcirculatory changes on selection of target organs for production of microthrombi during DIC.

Animals↗
PubMed1994

Subarachnoid hematoma attenuates vasodilation and potentiates vasoconstriction induced by vasoactive agents in newborn pigs.

The effects of perivascular blood on pial arteriolar vasoreactivity to selected vasodilators and vasoconstrictors were examined in vivo in a newborn pig model. alpha-Chloralose-anesthetized newborn pigs were fitted with closed cranial windows 4 d after cortical subarachnoid injections of autologous blood. The responsiveness of pial arterioles to topical application of dilator agents [iloprost, prostaglandin E2 (PGE2), histamine, and sodium nitroprusside (SNP)] and vasoconstrictor agents [leukotriene C4 and endothelin-1 (ET-1) in artificial cerebrospinal fluid was studied in control and blood-injected piglets. Pial arterioles dilated dose dependently in response to topical application of iloprost, PGE2, histamine, and SNP in the control group, with increases in diameter of 54, 44, 67, and 50% at 10(-8) M, 10(-5) M, 10(-5) M, and 10(-5) M, respectively. These dilations in response to iloprost, PGE2, and histamine in the blood-injected piglets were significantly attenuated to 23, 18, and 34%, respectively, whereas the dilation in response to SNP was not changed (64%). Constrictions in response to 10(-8) M leukotriene C4 and ET-1 were 16 and 26% and were potentiated by hematoma to 36 and 43%, respectively. The lowest dose of ET-1 (10(-12) M) significantly dilated pial arterioles in the control but not in the blood-treated group. We conclude that prolonged exposure of pial arterioles to perivascular blood attenuates cerebrovascular dilation in response to selected vasoactive agents (iloprost, PGE2, and histamine) but not to SNP, suggesting that blood-induced attenuation of vasodilation and the generalized vasoconstriction may involve inhibiting the prostanoid/cAMP signaling pathway.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗