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PubMed1998

Forearm vasoconstriction during dynamic leg exercise in patients with chronic heart failure.

Previous studies assessing vascular responses in nonexercising beds during exercise in patients with chronic heart failure (CHF) have yielded varying results. We proposed that the clinical and hemodynamic severity of heart failure may explain some of the variation. We reasoned that diastolic ventricular interaction (DVI), by limiting the ability of such patients to increase left ventricular (LV) volume and stroke volume during exercise, would attenuate baroreflex activation, resulting in increased sympathetic activation and hence exaggerated vasoconstriction. We hypothesized therefore that vasoconstriction in nonexercising beds would be exaggerated in patients with symptomatic and hemodynamically severe heart failure, particularly if associated with DVI. We measured forearm vascular resistance (FVR) during semierect cycle exercise in 22 CHF patients and 23 control subjects. DVI was assessed by measuring changes in ventricular volumes (radionuclide ventriculography) during volume unloading (-30 mm Hg lower-body negative pressure) in the heart failure patients and was inferred when LV end-diastolic volume paradoxically increased. Patients with symptoms of heart failure developed larger increases in FVR during exercise than did asymptomatic patients. There were significant correlations between the change in FVR during peak exercise and the resting mean pulmonary arterial pressure and pulmonary vascular resistance. CHF patients with DVI developed exaggerated increases in FVR (median [25th to 75th percentile]) compared with the remaining patients during low-workload exercise (138 [66 to 171] vs 6.4 [-4.3 to 28] units, P = 0.002) and during peak exercise (160 [90 to 384] vs 61 [-7.4 to 75] units, P < 0.02). Vasoconstriction in nonexercising beds is exaggerated in CHF patients with clinically and hemodynamically severe heart failure, particularly if associated with DVI. This may explain some of the reported variation in the degree of sympathetic activation that occurs during exercise in CHF patients.

Analysis of Variance↗
PubMed1997

The Y1 antagonist BIBP 3226 inhibits potentiation of methoxamine-induced vasoconstriction by neuropeptide Y.

We investigated the interaction of neuropeptide Y (NPY) with the alpha 1-adrenoceptor agonist, methoxamine, in control of mean arterial pressure, renovascular resistance and mesenteric vascular resistance in anaesthetized rats. Infusion of 3.0 but not 0.3 microgram/kg/min NPY enhanced the elevations of all three haemodynamic parameters caused by bolus injections of methoxamine (10-100 micrograms/kg). These enhancements largely involved a prolongation of the methoxamine effects. While infusion of the Y1 NPY receptor-selective antagonist, BIBP 3226 (10 micrograms/kg/min), alone did not alter methoxamine-induced vasoconstriction, it inhibited the potentiation by NPY. We conclude that NPY can potentiate methoxamine-induced vasoconstriction in vivo. This is mediated predominantly, if not exclusively, via the Y1 receptor. Endogenously released NPY does not appear to reach sufficient concentrations to cause tonic systemic vasoconstriction or potentiation thereof in the anaesthetized rat.

Animals↗
PubMed1998

Circadian changes in the sweating-to-vasoconstriction interthreshold range.

Thermoregulatory defenses are characterized by thresholds, the core temperatures triggering each response. Core body temperature is normally maintained within the interthreshold range, temperatures between the sweating and vasoconstriction thresholds that do not trigger autonomic defenses. This range usually spans only some 0.2 degrees C, but it remains unknown whether similar precision is maintained during the circadian core temperature cycle of about 0.8 degrees C. Accordingly, we evaluated the interthreshold range at four times of the day. We studied ten male volunteers, each at 3 a.m., 8 a.m., 3 p.m., and 8 p.m. At least 12 h elapsed between tests, and the order was randomly assigned. At each study time, volunteers were warmed peripherally until sweating was observed. Skin temperature was subsequently kept constant while core temperature was decreased by central-venous infusion of ice-cold fluid until peripheral vasoconstriction was detected. The volunteers were not permitted to sleep during threshold determinations, although sleep was not otherwise controlled. The core temperature triggering an evaporative water loss of 40 g.m-2.h-1 identified the sweating threshold. Similarly, the vasoconstriction threshold was defined by the core temperature triggering the initial decreases in plethysmographic finger tip blood flow. The interthreshold range at 3 a.m. was twice that observed at the other study times (P<0.05). Our data suggest that autonomic control of body temperature is reduced at 3 a.m., even when sleep is denied. This result contradicts the general perception that circadian variation alters the thermoregulatory target temperature, but not precision of body temperature control.

Adult↗
PubMed2006

Effect of peripheral vasoconstriction on pulse oximetry.

OBJECTIVE: We tested the hypothesis that peripheral vasodilation has an effect on arterial oxygen saturation measurements by pulse oximetry, independent of temperature. METHODS: Study 1 compared finger arterial oxygen saturation values (SpO(2)), before and after peripheral vasoconstriction while temperature was kept constant. This was achieved by administering dexmedetomidine (peripheral vasoconstrictor) to 16 volunteers given general anesthesia. Study 2 compared SpO(2) before and after peripheral vasodilation (brachial plexus block) in a neurally denervated left hand and a neurally innervated right hand in ten awake volunteers. In both studies measurements were also made of finger blood volume (an indicator of vasoconstriction) by photoplethysmographic determination of light transmission through a finger (LTF), finger temperature and of hemodynamic variables. RESULTS: In Study 1, systolic blood pressure, SpO(2) and LTF values increased (vasoconstriction) during dexmedetomidine infusion, (P<0.0001 for all) while there were no changes in finger temperature. In Study 2, in the left hand (axillary block), temperature increased by 1.9 +/- 1.6 degrees C (P=0.004), SpO(2) decreased by 2.5 +/- 1.0 % (P<0.0001) and LTF values decreased (vasodilation) by 42 +/- 8 % (P<0.0001) after axillary block. Simultaneously, the axillary block did not induce any changes in temperature, SpO(2) or LTF values in the neurally innervated right hand. CONCLUSIONS: Our results demonstrate that finger pulse oximeter SpO(2) measurements can be affected by peripheral vascular tone independent of temperature. The mechanism for this effect remains speculative and unproven.

Adult↗
PubMed1981

Synergistic relation between vasoconstriction and fixed epicardial vessel stenosis in coronary artery disease.

The clinically important hemodynamic consequences of epicardial coronary artery vasoconstriction were examined in the presence of stenosis of major vessels. For this purpose, a special isolated canine circumflex coronary artery preparation was used to provide elimination of reflex, humoral, and distal coronary vasculature resistance influences. Without stenosis, active vasoconstriction induced by either phenylephrine (10-3 M), angiotensin (10-5 M), or acetylcholine (10-5 M) had no effect on flow through the circumflex artery. Coronary arterial stenosis was created by intraluminal obstruction, which itself produced only insignificant effect on vessel flow. When the vasoconstrictor agent stimulation was superimposed on the fixed underlying vascular stenosis, there occurred dose-dependent marked flow decreases through the partially obstructed vessel accompanied by major trans-stenotic pressure gradient increases. Phenylephrine, angiotensin, and acetylcholine separately caused significant (54%, 59%, and 46%) flow decreases with 48, 54 and 50 mm Hg pressure gradient increases respectively. This study demonstrates that vasoconstriction and stenosis act synergistically to reduce flow through obstructed major vessels in coronary artery disease.

Acetylcholine↗
PubMed1994

Coronary artery vasoconstriction after successful single angioplasty of the left anterior descending artery.

Percutaneous transluminal coronary angioplasty is associated with spontaneous transient vasoconstriction. The mechanisms by which coronary vasoconstriction occurs distally to a successful dilated stenosis after coronary artery angioplasty are still unknown. The present study was planned to investigate the effect of successful coronary artery angioplasty on coronary vasomotion distal to a dilated stenosis and in the control vessel and the role of alpha-adrenergic receptors on coronary vasomotion after successful coronary artery angioplasty. We prospectively studied 32 consecutive patients scheduled for elective single coronary artery angioplasty of the left anterior descending coronary artery. Only aspirin, 325 mg, or nitroglycerin was allowed in the week before the study; no premedication with diazepam or other drugs was given. In group 1 (control patients, n = 20), quantitative coronary angiography was performed in the control state; 5 and 15 minutes after coronary artery angioplasty; and after intracoronary nitroglycerin infusion, 300 micrograms. In group 2 (n = 12), intracoronary phentolamine, 2 mg, was infused regionally through the balloon catheter before the coronary artery angioplasty, and coronary angiography was performed at baseline, 15 minutes after balloon deflation, and after nitroglycerin infusion. In group 1, constriction of the coronary segment distal to a dilated stenosis (2.4 +/- 0.8 to 2.1 +/- 0.6 mm, -14.6% vs baseline; p < 0.05) and of the circumflex coronary artery segment (2.8 +/- 0.7 to 2.5 +/- 0.6 mm, -10.7% vs baseline, p < 0.05) occurred 15 minutes after coronary artery angioplasty. The degree of vasoconstriction was not correlated with the lesion severity before coronary artery angioplasty.(ABSTRACT TRUNCATED AT 250 WORDS)

Angioplasty, Balloon, Coronary↗
PubMed1995

Attenuation of acetylcholine-induced vasoconstriction by L-arginine is related to the progression of atherosclerosis.

To determine if L-arginine, a precursor of the endothelium-derived relaxing factor, restores endothelium-dependent dilation in human coronary arteries, we studied 21 patients in whom the lumina of the coronary arteries were angiographically smooth or slightly irregular and in whom there was a constrictor response to acetylcholine (ACh) in the left anterior descending coronary artery or the circumflex coronary artery. We examined the response to intracoronary ACh before and after infusion of L-arginine by measuring coronary diameter with quantitative angiography. Intracoronary injection of ACh produced vasoconstriction in the majority of patients with coronary risk factors. The percentage diameter change in smooth segments in patients with entirely smooth coronary arteries (group 1, n = 44) from baseline was -20.7% +/- 17.4%. During systemic infusion of L-arginine, the constrictor response to ACh in these segments was significantly attenuated (-2.2% +/- 15.1% from baseline, p < 0.01, ACh alone vs ACh during L-arginine infusion). In smooth segments in patients with luminal irregularities in the other coronary arteries (group 2, n = 19), ACh produced a marked constriction (-32.5% +/- 22.5% from baseline, p < 0.05, group 1 vs group 2). Infusion of L-arginine also attenuated ACh-induced vasoconstriction in these segments (-9.7% +/- 14.1% from baseline, p < 0.01, ACh vs ACh during L-arginine infusion). In segments with irregular lumina (group 3, n = 26), ACh produced more prominent vasoconstriction. The percentage diameter change was -40.9% +/- 26.5% from baseline (p < 0.01 vs group 1).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1986

Inhibitory effect of calcium antagonist drugs on vasoconstriction induced by vascular alpha 2-adrenoceptor stimulation.

A survey is given of the mechanisms of the antihypertensive effect of calcium entry blockers. The main background of the antihypertensive/hypotensive action is dilatation of precapillary arterioles (resistance vessels that cause a reduction in total peripheral resistance and, hence, a decrease in blood pressure). The vascular relaxation is caused by an inhibition of the transmembranous calcium influx and, probably less so, by interference with calmoduline. Calcium entry blockers significantly reduce the vasoconstriction induced by the excitation of vascular postsynaptic alpha 2 adrenoceptors. The inhibitory effect of calcium entry blockers is reversed by the calcium entry promoter Bay k 8644. The vasoconstriction induced by alpha 1-adrenoceptor stimulation is less generally influenced by calcium entry blockers than the alpha 2 effects. The interference with alpha 2-adrenoceptor-induced vasoconstriction may contribute to the vasodilator action of the calcium entry blockers, especially in hypertensive patients who show a hyperreactivity to pressor responses toward catecholamines.

Adrenergic alpha-Agonists↗
PubMed1992

Reversal of endothelin-1-induced vasoconstriction by nifedipine in human resistance vessels in vivo in healthy subjects.

The influence of blockade of voltage-operated calcium channels by nifedipine on endothelin-1-induced vasoconstriction was investigated in 10 healthy volunteers. Brachial artery infusions of nifedipine (0.25, 0.5, 1 and 3 micrograms/min/100 ml forearm tissue) resulted in dose-dependent increases (mean +/- SD) in forearm blood flow (103 +/- 63% to 833 +/- 426%). Intraarterial infusions of endothelin-1 (50 ng/min/100 ml) resulted in transient increases in forearm blood flow (2.6 +/- 0.9 vs 3.9 +/- 2.0 ml/min/100 ml, p less than 0.01) in the first minute of infusion and subsequent decreases (to 1.0 +/- .5 ml/min/100 ml, p less than 0.01) in the third minute of infusion. Endothelin-1-induced vasoconstriction was reversed by the lowest dose of nifedipine, whereas the higher dosages of nifedipine further increased forearm blood flow to 12.5 +/- 6.4 ml/min/100 ml. The percent increase of forearm blood flow during co-infusion of endothelin-1 and the highest dosage of nifedipine was significantly greater compared with nifedipine alone (1,204 +/- 531% vs 833 +/- 426%, p less than 0.05). The results demonstrate a dual action of luminally applied endothelin-1 in human resistance vessels in vivo (e.g., transient initial vasodilation followed by pronounced vasoconstriction) and suggest that blockade of voltage-operated calcium channels can effectively counteract the vasoconstrictor effects of endothelin-1.

Adult↗
PubMed1993

Pentoxifylline decreases cyclosporine-induced renal endothelin release and vasoconstriction.

Cyclosporine (CSA) causes an acute vasoconstriction of renal artery and a significant increase in renal endothelin release. Pentoxifylline, a vasodilator, has been suggested to prevent CSA toxicity. To study the effect of pentoxifylline treatment on CSA-related vasoconstriction and endothelin release, a model of renal autoperfusion in the dog was used. Oral pentoxifylline at the dose of 400 mg three times daily for 3 days was given to 15 dogs. Pure powder CSA (10 mg) was injected into the isolated renal artery perfused at constant flow; changes in perfusion pressure reflected variations in vascular resistance. In the pentoxifylline-treated group (15 dogs), the infusion of CSA caused an average increase of 27 +/- 8 mm Hg in renal perfusion pressure, compared with 60 +/- 10 mm Hg in a control group of 8 untreated animals (p < or = 0.05). Plasma concentration of endothelin in the renal vein increased from an average of 1.2 +/- 0.2 pg/mL before to 2.4 +/- 0.5 pg/mL after CSA administration (p < or = 0.05) in the control group, whereas it did not change significantly in the pentoxifylline-treated group. Thus, oral pretreatment with pentoxifylline significantly decreased the renal vasoconstriction and endothelin release due to CSA administration.

Animals↗
PubMed1992

Quantitative EEG changes due to cerebral vasoconstriction. Indomethacin versus hyperventilation-induced reduction in cerebral blood flow in normal subjects.

Hyperventilation leads to an increase in slow EEG activity as well as to a decrease in alpha activity. These effects may be considered a result of reduction in cerebral blood flow due to vasoconstriction, but metabolic factors, such as alkalosis and the increased formation of cerebral lactate, may also have to be taken into account. As indomethacin decreases cerebral blood flow it is possible to study cerebral vasoconstriction, without concomitant metabolic alkalosis or cerebral lactate formation. Two parallel groups of 12 healthy male subjects (age 20-25) were studied with quantitative EEG (qEEG) and cerebral blood flow velocity as parameters. In the first group the effect of 100 mg indomethacin was studied. In the parallel group a standardized hyperventilation procedure was performed. In the indomethacin group the blood flow velocity decreased to 60% of the initial value; the qEEG showed a 0.5 Hz slowing of the alpha peak frequency (P less than 0.01) and a decrease in the power of the alpha band without any change in the delta or theta band. In the hyperventilation group the blood flow velocity decreased to 63% of the initial value and the qEEG showed a marked increase in delta and theta activity (P less than 0.01), but a non-significant change in alpha peak frequency. Indomethacin and hyperventilation caused similar degrees of vasoconstriction; however, the increase in qEEG slow wave activity, which was observed only in the hyperventilation group, is apparently related to metabolic rather than haemodynamic factors.

Adult↗
PubMed1986

Antagonism by some ergot derivatives of 5-HT-induced vasoconstriction.

The ability of a number of ergot derivatives to inhibit 5-hydroxytryptamine (5-HT)-induced vasoconstriction was examined in the perfused rat mesenteric artery preparation. 5-HT produced an increase in perfusion pressure indicative of vasoconstriction. The ergot derivatives inhibited the 5-HT-induced vasoconstriction in a manner that was predominantly not competitive in nature. As 5-HT2 antagonists the ergot derivatives ranged in potency from CQ 32-084 which abolished the 5-HT2 receptor mediated response at a concentration of 10 nM to LY-141865 which was inactive up to a concentration of 10 microM.

Animals↗
PubMed1988

Adrenergic effect on the atrial natriuretic peptide secretion and vasoconstriction induced in the perfused rat heart by phorbol ester.

Infusion of a phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), known to stimulate protein kinase C, caused a gradual, sustained increase in perfusate immunoreactive atrial natriuretic peptide (IR-ANP) concentration and a more rapid increase in perfusion pressure in the isolated perfused rat heart. Administration of isoprenaline resulted in a rapid rise in IR-ANP release whereas methoxamine induced a sustained increase in IR-ANP secretion into the perfusion fluid. Methoxamine, when infused in combination with TPA, enhanced both IR-ANP secretion and the increase in perfusion pressure produced by phorbol ester. Isoprenaline also acted synergistically on TPA-induced IR-ANP release but attenuated the coronary vasoconstriction produced by phorbol ester. The TPA-induced increase in IR-ANP secretion was attenuated significantly by infusion of atenolol and slightly by infusion of prazosin, neither of which affected TPA-induced vasoconstriction. The vasoconstrictor response to infusion of phorbol ester was similar but the secretory response was attenuated in hearts from rats pretreated with reserpine. The results indicate that adrenoceptor stimulation interacts differentially with phorbol ester-induced ANP secretion and vasoconstriction in the perfused rat heart. Our results also suggest that the effect of TPA on perfusion pressure appears to be due to its direct action on vascular smooth muscle cells but that a part of the TPA effect on ANP secretion may be an indirect one.

Adrenergic alpha-Agonists↗
PubMed1990

Pindolol inhibits the development of hypoxic pulmonary vasoconstriction.

We examined the effects of beta-adrenoceptor antagonists, propranolol and pindolol, on hypoxic pulmonary vasoconstriction using isolated, blood-perfused dog lung lobes. Pindolol markedly inhibited the development of hypoxic pulmonary vasoconstriction, whereas propranolol had no effect. The different role of the drugs on hypoxic pulmonary vasoconstriction is discussed.

Airway Resistance↗
PubMed1993

Different mechanisms are involved in neuropeptide Y-induced pancreatic vasoconstriction and inhibition of insulin secretion.

We have studied the mechanisms whereby neuropeptide Y (NPY) inhibits insulin secretion and induces vasoconstriction in the isolated perfused rat pancreas. Neither prazosin (alpha 1-adrenoceptor antagonist; 6 microM) nor yohimbine (alpha 2-adrenoceptor antagonist; 0.6 microM) affected the effects of neuropeptide Y (1 nM). Also the Ca2+ channel antagonist, verapamil (5 microM), which itself decreased insulin output by 55%, could not affect the neuropeptide Y-induced inhibition of insulin secretion. However, verapamil impaired the neuropeptide Y-induced decrease in pancreatic outflow rate. Finally, neuropeptide Y (1 and 10 nM) suppressed the insulin secretion induced by dibutyryl cAMP (100 microM) and the cyclic nucleotide suppressed the neuropeptide Y-induced vasoconstriction. We conclude that the secretory and vascular effects of neuropeptide Y are mediated by different processes in the perfused rat pancreas: inhibition of insulin secretion seems mediated by a mechanism distal to and/or different from cAMP generation, whereas vasoconstriction seems to involve uptake of extracellular Ca2+ and to be sensitive to dibutyryl cAMP. Both effects occur independently of adrenoceptor receptors.

Adrenergic alpha-Antagonists↗
PubMed1988

Local measurements of thrombus induced vasoconstriction in vivo.

No data is available describing the local effect of thrombus formation on the vessel's diameter in vivo. As platelet or thrombus induced vasoconstriction seems to be of clinical importance in various diseases, it is desirable to get insight into the interrelation of thrombus formation and local vasoactivity. With a contactless photochemical process, endothelial cells can be damaged and thrombogenesis may be initiated in vivo. After first platelets stick to endothelial cells, a strong vasoconstriction is observed in arterioles. In venules, no vascular reaction can be observed. Constriction is most pronounced at the site of thrombus formation and decreases at growing distance. The thrombus is squeezed by the vascular constriction and thus mechanically held in place and squeezed out. A slight relaxation follows 30-80 min later, but the vessel remains constricted during the following three hours. Thrombus induced vasoconstrictions can be reduced by papaverine, EP 092 (a thromboxane A2 antagonist) and phentolamine in dose-dependent manner in vivo. Papaverine was most effective followed by EP 092, Phentolamine was less effective, showing the minor importance of alpha-receptor stimulation in this model.

Animals↗
PubMed1994

Comparison of the NPY receptors mediating vasoconstriction of the guinea-pig uterine artery and thoracic vena cava using a range of NPY analogues.

The ability of analogues of neuropeptide Y (NPY) to produce direct vasoconstriction, or to antagonize NPY constrictions, was examined in isolated segments of the thoracic vena cava and the uterine artery of guinea-pigs, where NPY mediates a slow phase of sympathetic vasoconstriction. [Leu31,Pro34]NPY, NPY(13-36) and NPY(18-36) all contracted the uterine artery and the vena cava. Contractions produced by [Leu31,Pro34]NPY were similar in time course to those produced by porcine NPY (pNPY), although contractions produced by NPY(13-36) or NPY(18-36) typically were slower than pNPY contractions. In both vessels the order of potency of the agonists was pNPY > or = [Leu31,Pro34]NPY > NPY(13-36) > NPY(18-36). High concentrations (10(-5)mol.l-1) of pNPY or [Leu31,Pro34]NPY produced desensitization of contractions of the uterine artery produced by NPY(13-36). The reported NPY receptor antagonists, PYX-1 and PYX-2 (5 x 10(-6)mol.l-1), slightly reduced (by 21-47%) the magnitude of constrictions produced by exogenous pNPY (1-3 x 10(-8) mol.l-1) in both the uterine artery and the vena cava. These results show that the NPY receptors mediating slow sympathetic vasoconstriction of both the uterine artery and the vena cava are likely to be predominantly Y1 receptors, despite differences between the adrenoceptors mediating sympathetic responses in the two blood vessels.

Animals↗
PubMed1990

Neuropeptide Y mimics a non-adrenergic component of sympathetic vasoconstriction in the bullfrog.

The effects of preganglionic sympathetic nerve stimulation and exogenous agents upon vascular tone were observed in hindlimb preparations of pithed adult bullfrogs. Repetitive electrical stimulation of the sympathetic C, but not the B, system elicited arterial vasoconstriction and reduced blood flow in vascular beds supplying the sartorius muscle and the skin. Close-arterial injections of epinephrine and neuropeptide Y each mimicked neurogenic vasoconstriction. After close-arterial injection of phentolamine, an alpha-adrenergic antagonist, the maximal effects of nerve stimulation were delayed in onset and reduced in magnitude, but not eliminated. Pretreatment with phentolamine blocked the vasoconstriction caused by injection of epinephrine, and produced a mild reduction in responses to neuropeptide Y. These observations demonstrate the vasomotor function of the sympathetic C system and they support the hypothesis that neuropeptide Y and epinephrine function as cotransmitters in postganglionic C neurons.

Animals↗