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PubMed1999

[Effects of temperature on the vasoconstrictive force of norepinephrine in rat aorta].

This study aimed at the influence of temperature on the vasoconstrictive effect of norepinephrine on rings of rat aorta and at the cause of the change observed. At the temperatures of 39.5 degrees C, 36.5 degrees C and 33.0 degrees C respectively, the vasoconstrictive force-time curve induced by norepinephrine and the equation of function were fitted. Statistical evaluation of the data was performed by F test. The difference was statistically significant (P < 0.01) among the three groups for relation constant X1 of function equation, but no significant difference (P > 0.05) was noted among the three groups for relation constant X2. Our experiments demonstrated that norepinephrine-induced vasoconstrictive force, in rat aorta, was obviously modulated by temperature. As the temperature of rat aorta was raised, the vasoconstrictive force and vasoconstrictive speed increased, and the effects of norepinephrine on vasculature were raised. The results suggest that the constant X1 for vasoconstrictive force is a factor sensitive to temperature.

Animals↗
PubMed1991

The role of intrarenal prostaglandins and angiotensin II in acute cyclosporine-induced vasoconstriction.

Cyclosporine causes intrarenal vasoconstriction, which may account for its nephrotoxic effects. In this study we investigated the role of endogenous prostaglandins and angiotensin II in cyclosporine-induced intrarenal vasoconstriction. Split hydronephrotic kidneys in decerebrate rats (n = 16) were suspended in an environmentally controlled tissue bath. Interlobular, afferent, and efferent arteriolar diameters and red blood cell velocity were measured by in vivo video-microscopy and Doppler velocimetry. After topical application of cyclosporine to the kidney in the tissue bath, a 12% +/- 2% constriction of the interlobular and a 28% +/- 5% reduction in interlobular blood flow occurred. The afferent and efferent arterioles also constricted by 13% +/- 2% and 10% +/- 3%, respectively. Prostaglandin inhibition with mefenemate augmented this vasoconstriction (16% +/- 2% at interlobular and 21% +/- 4% at afferent arterioles) and reduction in interlobular blood flow (38% +/- 8%) below baseline values. Mefenemate alone resulted in a 35% +/- 5% reduction in interlobular blood flow, which was not further augmented by cyclosporine. In contrast, local competitive angiotensin II-receptor inhibition with saralasin maintained blood flow after cyclosporine and prevented intrarenal vasoconstriction by cyclosporine. This suggests that prostaglandins protect against intrarenal vasoconstriction and that acute cyclosporine-induced vasoconstriction is mediated through angiotensin II receptors.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1991

Abnormal sodium metabolism and plasma renin activity (renal renin secretion) and the vasoconstriction volume hypothesis: implications for pathogenesis and treatment of hypertension and its vascular consequences (heart attack, stroke).

Arterial hypertension is sustained by either of two long-term mechanisms of arteriolar vasoconstriction or by an inappropriate reaction between them. One mechanism is renin-mediated, the other is related to antecedent renal sodium retention. The plasma renin value directly reflects the presence and degree of renin-mediated vasoconstriction, and, inversely, defines the predominance of sodium-related vasoconstriction. A hypotensive response, or lack of it, to angiotensin-converting enzyme inhibitor is similarly informative. Because the normal kidney exposed to high arterial pressure and normal salt intake will reduce its renin secretion to near zero, any renin secretion in a hypertensive setting can be considered abnormal. Typically, high-renin hypertensive patients are more vasoconstricted than low-renin patients with similar blood pressures. The intense vasoconstriction leads to relative hypovolemia, hemoconcentration, hyperviscosity, postural hypotension, and in severe forms even to acrocyanosis, all of which are dramatically reversed with anti-renin therapy. Conversely, low-renin equally hypertensive patients have relatively more sodium volume and are less vasoconstricted; they are generally responsive to natriuretic drugs (e.g., diuretics or calcium antagonists) and appear relatively protected from vascular sequelae such as stroke and heart attack. These observations provide a new means for evaluating prognosis and a basis for mechanistically differentiating and treating hypertensive patients, allowing increasingly simpler and more-specific long-term therapies.

Animals↗
PubMed1986

[Inhibition of hypoxic pulmonary vasoconstriction by leukotriene blockade].

The mechanism of hypoxic pulmonary vasoconstriction is still unclear. Since leukotrienes are pulmonary vasoconstrictors and lung cells are able to produce leukotrienes, it has been proposed that leukotrienes are mediators of hypoxic pulmonary vasoconstriction and then inhibition of their synthesis should block hypoxic pressure responses. In order to test this hypothesis we investigated whether diethylcarbamazine (DEC), a known leukotriene synthesis blocker, blocks hypoxic pulmonary vasoconstriction in isolated rat lungs. DEC blocked ongoing and subsequent hypoxic pressure responses in a relatively specific and dose-dependent fashion. We therefore extended our observations to awake rats and found that DEC reversibly inhibited acute hypoxic pulmonary vasoconstriction. Furthermore, pulmonary hypertension and right ventricular hypertrophy in rats exposed to chronic hypobaric hypoxia could be prevented by DEC treatment. From these data we conclude that DEC inhibits both acute and chronic hypoxic pulmonary vasoconstriction. Thus, leukotrienes could be important mediators of hypoxic pulmonary vasoconstriction.

Angiotensin II↗
PubMed1983

Renal vasoconstrictive response to contrast medium. The role of sodium balance and the renin-angiotensin system.

The injection of contrast medium into the renal artery causes a biphasic change in renal blood flow, a transient vasodilation followed by a more prolonged vasoconstrictive phase. The role of sodium balance in the vasoconstrictive response to contrast medium was evaluated in sodium-deplete dogs (n = 5) and sodium-replete dogs (n = 5). Contrast medium, 2 ml of diatrizoate solution per 4 sec, was injected into the renal artery in anesthetized dogs. Renal blood flow was 117 +/- 25 ml/min and 173 +/- 12 in the sodium-deplete and sodium-replete dogs, respectively. After the injection of contrast medium and following the transient vasodilation phase, renal blood flow significantly decreased from baseline by 42.2% +/- 4.2 and 12.2% +/- 1.1 in sodium-deplete and sodium-replete dogs, respectively. The duration of the vasoconstriction phase was significantly prolonged in the sodium-deplete dogs, 343 +/- 27 sec vs. 147 +/- 48 in sodium-replete dogs. Blockade of the intrarenal renin-angiotensin system with the renal artery infusion of Sar1-Ala8-All (50 micrograms/kg/min) did not significantly alter the magnitude of vasoconstrictive response to contrast medium in sodium-deplete animals; however, the duration of the vasoconstrictive phase was decreased from 277 +/- 59 sec to 86 +/- 13. We conclude that (1) sodium depletion accentuates both the magnitude and duration of the vasoconstrictive phase of the renal blood flow response to injection of contrast medium and (2) blockade of the intrarenal renin-angiotensin system shortens the duration of this response.

Animals↗
PubMed1994

Effect of Intralipid on hypoxic and angiotensin-II induced pulmonary vasoconstriction in the isolated rat lung.

OBJECTIVE: Lipid infusions are reported to cause hypoxemia by increasing intrapulmonary shunt fraction. However, the mechanism by which they worsen gas exchange is unknown. We hypothesized that a reduction in hypoxic pulmonary vasoconstriction, caused by lipid infusion, could be the cause of increased shunt. DESIGN: A prospective, controlled laboratory study. SETTING: A postgraduate teaching hospital laboratory. SUBJECTS: Male Wistar rats weighing 250 to 300 g. INTERVENTIONS: Four separate series of experiments were performed: a) The pulmonary vasopressor response to angiotensin-II was compared before and after adding either 0.9% sodium chloride (control n = 5) or 20 microL of Intralipid (n = 8). b) The pulmonary vasopressor response to hypoxia (FIO2 of 0.3) was compared before and after either 0.9% sodium chloride (control n = 5) or 20 microL of Intralipid (n = 8). c) 1 microM of indomethacin was added before either 0.9% sodium chloride (control n = 5) or Intralipid (n = 5) and the hypoxic pulmonary vasoconstriction response was compared. d) 10(-3) M L-monomethyl-n-arginine was added before 20 microL of Intralipid and the hypoxic pulmonary vasoconstriction response was compared (n = 5). MEASUREMENTS AND MAIN RESULTS: Changes in pulmonary arterial pressure were measured before and after interventions. Intralipid reduced the angiotensin-II pressor response by 36 +/- 3% (p = .005) and the hypoxic pulmonary vasoconstriction response by 50 +/- 2% (p = .0003). This action was not blocked by pretreatment with either indomethacin or L-monomethyl-n-arginine. CONCLUSIONS: Intralipid reduces the hypoxic pulmonary vasoconstriction response in the isolated, blood perfused rat lung. This action is nonspecific, as shown by a similar reduction in the pulmonary pressor response to angiotensin-II. Pharmacologic blockade of prostaglandin release, by indomethacin, and nitric oxide release, by L-monomethyl-n-arginine did not prevent the reduction in hypoxic pulmonary vasoconstriction, thereby suggesting that neither agent mediates the lipid-induced change in pulmonary vasoreactivity.

Analysis of Variance↗
PubMed1993

Vasoconstriction in response to activated leukocytes: implications for vasospasm.

Three sets of experiments are presented demonstrating that activated leukocytes produce significant vasoconstriction. (1) Responses to human mononuclear leukocytes were studied in intact femoral arteries in vitro. Vasoconstriction of about 35-40% of the maximal effect obtained with KCl was found with mononuclear cells activated by thrombin or complement component C5a, but not with unactivated mononuclear cells. This vasoconstriction was endothelium-independent, and could not be inhibited by radical scavengers or by pre-treatment of the cells with inhibitors of the cyclooxygenase or lipoxygenase pathway. Additional experiments suggest that this contractile effect is partially mediated by the release of a stable factor. (2) Vascular responses to intra-arterial complement C5a (10 and 100 micrograms) were studied in the blood-perfused hind limb of normal and atherosclerotic monkeys in vivo. C5a injection produced pronounced constriction of the hind limb large arteries in atherosclerotic, but not in normal animals. Perfusion of the hind limb with a cell-free blood substitute almost abolished C5a-induced vasoconstriction. These findings suggest that C5a induces vasoconstriction by activation of blood cells, probably leukocytes. (3) Vascular responses to the chemotactic peptide, N-formyl-methionyl-leucyl-phenylalanine (fMLP), were studied in the human coronary circulation. Intracoronary fMLP (1 x 10(-8) moles) produced a transient increase in blood flow velocity and a significant decrease of the diameter of the epicardial arteries. This effect was accompanied by a decrease in leukocyte count in the coronary sinus blood. These studies suggest that activated leukocytes produce vasoconstriction by the release of vasoactive factor(s), and thus may contribute to the pathogenesis of cardiovascular complications in patients with atherosclerosis.

Animals↗
PubMed1995

Forearm vasoconstriction to endothelin-1 is mediated by ETA and ETB receptors in vivo in humans.

The role of endothelin (ET)-B (ETB) receptors in mediating vasoconstriction in humans is unclear. As yet, in vitro data have been contradictory, and there have been no in vivo studies in resistance vessels. We investigated the function of ETB receptors in vivo in human forearm resistance vessels using ET-1 as a nonselective agonist at ETA and ETB receptors and ET-3 and sarafotoxin S6c as ETB receptor agonists. Brachial artery infusion of ET-1 and ET-3 caused slow-onset, dose-dependent forearm vasoconstriction. Although ET-3 caused significantly less forearm vasoconstriction than ET-1 at low doses, vasoconstriction to the two isopeptides was similar at the highest dose (60 pmol/min). ET-3 caused initial transient forearm vasodilatation at this dose, whereas ET-1 showed only a nonsignificant trend toward causing early vasodilatation. Intra-arterial sarafotoxin S6c caused a progressive reduction in forearm blood flow, although less than that to ET-1. Therefore, ETB receptor agonists contract human resistance vessels in vivo. The effects of ET-3 and sarafotoxin S6c, compared with ET-1, suggest that both ETA and ETB receptors mediate vasoconstriction. Antagonists at both ETA and ETB receptors, or inhibitors of the generation of ET-1, may be necessary to completely prevent vasoconstriction to endogenously generated ET-1.

Adult↗
PubMed1996

Nitric oxide mediates the inhibitory action of platelet-activating factor on angiotensin II-induced renal vasoconstriction, in vivo.

The objective of our study was to determine the mechanism(s) involved in the inhibitory effect of platelet-activating factor on renal vascular reactivity, in vivo. Bolus injections of vasoconstrictor agonists were administered into the renal circulation of pentobarbital anesthetized male Wistar rats at a dose to cause a transient 45 to 50% decrease in renal blood flow. Intrarenal infusion of platelet-activating factor (PAF) at 2.5 ng/min/kg attenuated the vasoconstrictor response to angiotensin II by 66%, a significantly smaller reduction of 35% for norepinephrine-mediated vasoconstriction, 22% for vasopressin-mediated vasoconstriction and no alteration of KCl-mediated vasoconstriction. The preferential inhibitory effect of platelet-activating factor on angiotensin II-mediated renal vasoconstriction was mimicked by the intrarenal infusion of either 0.2 to 5 micrograms/min/kg methacholine (endothelium-dependent vasodilator) or 2 micrograms/min/kg sodium nitroprusside (nitric oxide donor). After inhibition of nitric oxide synthesis with NG-monomethyl-L-arginine, intrarenal infusion of PAF or methacholine reduced angiotensin II-mediated renal vasoconstriction significantly less than that observed in the absence of NG-monomethyl-L-arginine. Therefore, this study provides evidence that the shared ability of platelet-activating factor and methacholine to selectively reduce angiotensin II-mediated renal vasoconstriction involves endothelium-derived nitric oxide.

Angiotensin II↗
PubMedDate not supplied

beta-Carotene attenuates peroxide-induced vasoconstriction in the human placenta.

OBJECTIVE: Placental lipid peroxides and thromboxane are abnormally increased in preeclampsia. Peroxides stimulate thromboxane to increase placental vasoconstriction. Antioxidants, such as beta-carotene, control lipid peroxidation. Reduced levels of beta-carotene (0.25 mumol/L) have been found in preeclamptic women. We hypothesized that normal (0.5 mumol/L) or elevated (1.0 mumol/L) levels of beta-carotene would attenuate peroxide-induced vasoconstriction in the human placenta, whereas low levels would not. METHODS: Isolated human placental cotyledons (n = 8) were sequentially perfused with control Krebs-Ringer-bicarbonate buffer, 200 mumol/L t-butyl hydroperoxide, and then with progressively increasing concentrations of beta-carotene (0.25, 0.5, and 1 mumol/L) plus t-butyl hydroperoxide. Fetal perfusion pressure was monitored continuously, and maternal and fetal effluent samples were collected for each treatment. Samples were analyzed for lipid peroxides and for thromboxane and prostacyclin by their stable metabolites thromboxane B2 (TXB2) and 6-keto-prostaglandin (PG)F1 alpha. RESULTS: Compared with control, t-butyl hydroperoxide significantly increased perfusion pressure, vascular resistance, and the secretion rates of lipid peroxides, TXB2 and 6-keto-PGF1 alpha. Perfusion with normal (0.5 mumol/L) or increased (1 mumol/L) levels of beta-carotene significantly or completely inhibited t-butyl hydroperoxide-induced vasoconstriction and the increases in lipid peroxide and TXB2 secretion, but did not inhibit peroxide-induced increases in 6-keto-PGF1 alpha secretion. Reduced levels of beta-carotene (0.25 mumol/L) did not inhibit t-butyl hydroperoxide-induced vasoconstriction or the increases in lipid peroxide secretion. CONCLUSIONS: beta-carotene at levels found in normal pregnant women (0.5 mumol/L) or at levels achieved with beta-carotene supplementation (1 mumol/L) inhibited peroxide-induced vasoconstriction and lipid peroxide and thromboxane secretion. Levels of beta-carotene found in preeclamptic women (0.25 mumol/L) did not inhibit peroxide-induced vasoconstriction or lipid peroxide secretion.

6-Ketoprostaglandin F1 alpha↗
PubMed1997

Contribution of endothelin-1 to renal vasoconstriction in unilateral ureteral obstruction: reversal by verapamil.

PURPOSE: In unilateral ureteral obstruction (UUO) vasoconstriction occurs both during and after release of UUO. ET-1, an endogenous peptide, causes marked vasoconstriction mediated by an increase in cytosolic calcium. We measured renal output of endothelin-1 (ET-1) in dogs with UUO and examined if the renal vasoconstriction that persisted after release of UUO could be reversed by a calcium antagonist, verapamil. MATERIALS AND METHODS: Hemodynamic and clearance experiments were performed in anesthetized mongrel dogs in three groups. Group I consisted of 9 dogs with sham-operation. Group 2 consisted of 7 dogs in whom ureteral obstruction was released 1.9 hours after UUO. Group 3 consisted of 5 dogs in whom verapamil was infused into the renal artery at two doses (5 and 10 microg./min., respectively) after release of UUO of 19-hour duration. ET-1 concentrations (measured by radioimmunoassay) were determined for renal venous and arterial plasma. RESULTS: In Group 1 renal venous plasma ET-1 level was 16.7 +/- 2.2, significantly lowered than 22.8 +/- 3.2 pg./ml. in arterial plasma, indicating a net clearance of ET-1. In Group 2 and 3, renal venous plasma ET-1 levels (28.2 +/- 5.2 and 27.2 +/- 2.4 pg./ml., respectively) were significantly greater than those in arterial plasma (24.2 +/- 5.7 and 17.4 +/- 0.8 pg./ml., respectively), indicating a net output of ET-1 in the kidney, In addition, renal vasoconstriction occurred in Groups 2 and 3 as indicated by significantly lower renal blood flow and GFR than those in Group 1. In Group 3, intrarenal infusion of verapamil at two doses did not change arterial pressure but caused an ipsilateral, significant increase in RBF (from 132 +/- 4 17 to 1.84 +/- 19 and 180 +/- 16 ml./min., respectively) and dose-dependent increases in GFR (from 12 +/- 2 to 25 +/- 3 and 38 +/- 7 ml./min., respectively), associated with a profound dose-dependent ipsilateral diuresis and natriuresis. CONCLUSION: Profound renal vasoconstriction in UUO was associated with an increase in renal production of ET-1, possibly contributing to renal vasoconstriction, and was reversed by intrarenal infusion of verapamil.

Animals↗
PubMed1999

Role of shear stress in nitric oxide-dependent modulation of renal angiotensin II vasoconstriction.

1. Renal vasoconstriction in response to angiotensin II (ANGII) is known to be modulated by nitric oxide (NO). Since shear stress stimulates the release of a variety of vasoactive compounds from endothelial cells, we studied the impact of shear stress on the haemodynamic effect of ANGII in isolated perfused kidneys of rats under control conditions and during NO synthase inhibition with L-NAME (100 microM). 2. Kidneys were perfused in the presence of cyclo-oxygenase inhibitor (10 microM indomethacin) with Tyrode's solution of relative viscosity zeta=1 (low viscosity perfusate, LVP) or, in order to augment shear stress, with Tyrode's solution containing 7% Ficoll 70 of relative viscosity zeta=2 (high viscosity perfusate, HVP). 3. Vascular conductance was 3.5+/-0.4 fold larger in HVP as compared with LVP kidneys, associated with an augmentation of overall wall shear stress by 37+/-5%. During NO inhibition, vascular conductance was only 2.5+/-0.2 fold elevated in HVP vs LVP kidneys, demonstrating shear stress-induced vasodilatation by NO and non-NO/non-prostanoid compound(s). 4. ANGII (10 - 100 pM) constricted the vasculature in LVP kidneys, but was without effect in HVP kidneys. During NO inhibition, in contrast, ANGII vasoconstriction was potentiated in HVP as compared with LVP kidneys. 5. The potentiation of ANGII vasoconstriction during NO inhibition has been shown to be mediated by endothelium-derived P450 metabolites and to be sensitive to AT2 receptor blockade in our earlier studies. Accordingly, in HVP kidneys, increasing concentrations of the AT2 receptor antagonist PD123319 (5 and 500 nM) gradually abolished the potentiation of ANGII vasoconstriction during NO inhibition, but did not affect vasoconstriction in response to ANGII in LVP kidneys. 6. Our results demonstrate, that augmentation of shear stress by increasing perfusate viscosity induces vasodilatation in the rat kidney, which is partially mediated by NO. Elevated levels of shear stress attenuate renal ANGII vasoconstriction through enhanced NO production and are required for AT2 sensitive potentiation during NO inhibition.

Angiotensin II↗
PubMed1987

Thromboxane A2 analogue induced coronary artery vasoconstriction in the rabbit.

Diffuse coronary artery vasoconstriction was provoked in the rabbit by a stable thromboxane A2 analogue, STA2 (9,11-epithio-11,12-methano thromboxane A2). Injection of 25 micrograms.kg-1 STA2 into the left main trunk caused complete occlusion of the left anterior descending artery and narrowing of the left circumflex artery. Two minutes after injection, however, the diameter of the coronary artery returned to the control value (n = 10). The right coronary artery was also temporarily occluded by an injection of 25 micrograms.kg-1 STA2. Left ventricular end diastolic pressure increased significantly, and ST segment elevation of the electrocardiogram occurred during vasoconstriction. The angiographic findings showed that the vasoconstriction in the coronary artery induced by STA2 was similar to the diffuse vasoconstriction seen clinically. Induction of the vasoconstriction by STA2 was prevented by the preadministration of 25 micrograms.kg-1 of either a calcium antagonist, diltiazem, or a thromboxane A2 receptor antagonist, ONO 3708 (n = 10). The relation of the calcium movement to this vasoconstriction was studied in vitro using the isolated left circumflex artery in the rabbit. STA2 (50 micrograms.litre-1 to 0.5 mg.litre-1) produced a concentration dependent contraction of helical strips of left circumflex artery. Diltiazem (50-100 g.litre-1) suppressed this contraction dose dependently. ONO 3708 (10 micrograms.litre-1 to 1 mg.litre-1) caused a significant rightward and downward shift of the dose-response curve.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1973

Further observations on mesenteric vasoconstriction, survival and the clotting defect after endotoxin administration.

1. The initial response after endotoxin administration (3 mg/kg) in cats involved pulmonary vasoconstriction. This was not seen when endotoxin was given by slow infusion and it could be prevented after a bolus injection of endotoxin by pretreatment of the cats with aspirin (10 mg/kg). Intense mesenteric vasoconstriction occurred in all the cats.2. The mesenteric vasoconstriction was a specific response of the mesenteric blood vessels. At the time the mesenteric bed constricted, the renal bed dilated, the hepatic arterial bed remained unchanged and the smooth muscle of the intestinal wall relaxed.3. Arterial blood from cats with a fully developed mesenteric vasoconstriction after endotoxin administration was perfused through a normal intestine. No immediate vasoconstriction developed but the perfused intestine constricted slowly over 60 minutes. This suggests that mesenteric constriction was not due to circulating vasoconstrictor factors or the intestinal innervation, but involved a slow local mechanism within the intestine. It could not be prevented or reversed by a variety of pharmacological agents.4. These observations suggest that endotoxin caused a unique type of mesenteric vasoconstriction in cats by a local mechanism which took up to 60 min to develop, was sufficiently potent to reduce mesenteric flow to <30% control, and was maintained until death of the cats. Blood from these animals did not clot when placed in a glass tube.5. The mesenteric constriction and the clotting defect could be prevented by repeated administration of aminophylline and dextran solution before and after a bolus intravenous injection of endotoxin. Arterial pressure and mesenteric flow were maintained for at least 10 h in these experiments. Inadequate treatment intensified rather than reduced the intestinal mucosal damage.6. Cats were treated with aspirin, endotoxin and the optimal regimen for prevention of the mesenteric constriction and allowed to recover from the anaesthetic agent. In this series, 63% survived indefinitely compared to 25% after aspirin and endotoxin treatment and 0% after endotoxin alone.7. The possible mechanisms of action of aspirin and aminophylline-dextran solution are discussed. Our failure to obtain 100% survival is probably due to pulmonary damage which develops 10-24 h after endotoxin administration. This delayed pulmonary action of endotoxin is not prevented by aspirin treatment and it seems unlikely that aspirin will be of any value in the treatment of the pulmonary lesion in man.

Aminophylline↗
PubMed2004

Cerebral vasoconstriction syndromes.

Stroke from reversible cerebral arterial vasoconstriction has been described in a variety of conditions, including migraine, pregnancy, puerperium (postpartum angiopathy), use of vasoconstrictive drugs, Call-Fleming syndrome, and benign angiopathy of the central nervous system. Although vasoconstriction is an important cause of ischemic and hemorrhagic stroke in young individuals, vasoconstriction syndromes have not been well characterized and remain under-recognized. Misdiagnosis is common because the clinical and radiological features can overlap with conditions such as primary cerebral vasculitis. With the advent of newer, noninvasive angiography techniques and the escalating use of vasoactive drugs, it is likely that clinicians will encounter more patients with vasoconstriction-induced stroke. This article reviews the history, clinical and radiological characteristics, differential diagnosis, and management of cerebral vasoconstriction syndromes.

Cerebral Arteries↗
PubMedDate not supplied

[Reversible segmental cerebral vasoconstriction: the value of duplex transcranial Doppler in its diagnosis and follow up].

INTRODUCTION: Reversible segmental cerebral vasoconstriction, also known as Call Fleming syndrome, is a clinical entity that consists of segmental vasoconstriction of the arteries in the brain, which can course with focal neurological deficits and which is characteristically reversible. Diagnosis and follow up of reversible segmental cerebral vasoconstriction is performed using cerebral arteriography, but no previous evaluation has been conducted of the role that duplex transcranial Doppler can play in this syndrome. CASE REPORT: Here we describe the case of a 57 year old female patient who began suffering from sudden bouts of headaches with no other accompanying clinical features. After ruling out the possibility of a subarachnoid haemorrhage by means of a spinal tap, a suspicion diagnosis of reversible segmental cerebral vasoconstriction was made through duplex transcranial Doppler and this was later confirmed by arteriography, which revealed a segmental stenosis in the upper branch of the left middle cerebral artery. Following treatment with nimodipine, the patient presented a clear clinical improvement and the reversibility of the cerebral vasoconstriction was confirmed by duplex transcranial Doppler. CONCLUSION: Contrast enhanced duplex transcranial Doppler would enable us to obtain an early diagnostic approximation in patients in whom segmental vasoconstriction is suspected; it could also constitute the choice non invasive follow up method in these patients.

Cerebral Angiography↗
PubMed2001

Melatonin counteracts potentiation by homocysteine of KCL-induced vasoconstriction in human umbilical artery: relation to calcium influx.

Homocysteinemia is a major and independent risk factor for vascular disease. Oxidative stress is a possible mechanism for homocysteine (HCY)-induced vascular disease. Herein, we evaluated the antioxidant property of melatonin (MLT) in relation to the vasoconstrictive effect of HCY on the human umbilical artery. Helical umbilical arterial strips without endothelium were obtained at elective Cesarean delivery near term. Changes in potassium chloride (KCl)-induced vasoconstriction were measured. Arterial strips were treated with HCY (10 or 100 microM) plus FeSO(4) (10 microM) alone or pretreated with a hydroxyl radical ((*)OH) scavenger, mannitol (20 mM), or MLT (1 or 10 microM). The effect of HCY on the response of arterial strips to external calcium (Ca(2+)) in the presence of KCl (20 mM) was determined. HCY plus FeSO(4) potentiated KCl-induced vasoconstriction in a concentration-dependent manner; pretreatment with mannitol significantly reduced this vasospastic effect. HCY (100 microM) significantly augmented the contractile response to external Ca(2+). MLT (10 microM) significantly suppressed the contractile response to external Ca(2+). These results suggest that HCY potentiates KCl-induced umbilical artery vasoconstriction, in part by increasing Ca(2+) influx in vascular smooth muscle cells via activation of Ca(2+) channels. MLT significantly suppressed the vasoconstrictive effect of HCY, probably by scavenging (*)OH arising from HCY autooxidation.

Antioxidants↗
PubMed1994

Mechanisms of renal vasoconstriction following furosemide in conscious rats.

Regional hemodynamics following intravenous injection of furosemide were studied in conscious rats instrumented with Doppler flowprobes. Furosemide caused a dose-dependent acute (within 3 min) transient increase in renal resistance (RR) followed by a later generalized vasoconstriction in the renal, mesenteric and hindquarter (HQR) vascular bed. With in vitro experiments a possible direct effect of furosemide on renal artery segments was excluded. The acute rise in RR was partly (approximately 40%) attenuated by pretreatment with phentolamine or prazosin, but not prevented by renal denervation, volume repletion or pretreatment with captopril, losartan, indomethacin, aminophylline, nifedipine, or a vasopressin V1A-receptor-antagonist. However, the acute renal vasoconstriction was absent in water diuretic rats. The later vasoconstriction was blunted by captopril (RR+HQR), losartan (RR) and phentolamine (HQR) pretreatment. We conclude that the later generalized vasoconstriction following furosemide involves regional specific stimulation of angiotensin II and alpha-adrenoceptors. The mechanism of the acute renal vasoconstriction could not be fully determined. Because of its absence in water diuretic rats, its rapid onset, transient nature and relative insensitivity for pharmacological tools in euvolemic rats, the acute increase in RR following furosemide may be caused by cell swelling as a result from dissipation of the renal medullary gradient.

Animals↗