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PubMed1998

Vasoconstrictors and the heart.

The use of vasoconstrictors in local anesthetics, as topical hemostatic agents, and in gingival retraction cord, remains controversial although data exists from which to formulate reasonable guidelines. The value of such vasoconstrictors to increase local anesthetic efficacy and reduce systemic uptake is unquestioned. Elevated blood levels of epinephrine can occur with their use but do not generally appear to be associated with any significant cardiovascular effects in healthy patients or those with mild to moderate heart disease. Reduced dosages or local anesthetics without vasoconstrictors are indicated for patients with more significant disease, and epinephrine-impregnated retraction cord should be used cautiously or avoided in certain situations. Endogenous epinephrine released in dental treatment-associated stress may also reach significant blood levels and make it difficult to determine causation of cardiovascular adverse events. The safety record of dental local anesthetics and their vasoconstrictors has been impressive and will remain so with continued judicious use of these agents.

Adrenergic beta-Antagonists↗

PubMed2003

The skin vasoconstrictor assay does not correlate significantly to airway or systemic responsiveness to inhaled budesonide in asthmatic patients.

OBJECTIVE: The responsiveness to inhaled corticosteroid varies among individual asthmatic patients. It is not known, however, whether the effects of corticosteroids on one bodily tissue reflect the response in another in a given individual. The aim was to a assess whether skin vasoconstrictor assay might predict airway and systemic tissue responsiveness to inhaled budesonide in patients with asthma. METHODS: Twenty-two patients with mild to moderate persistent asthma previously enrolled in a dose-response study assessing the effects of inhaled budesonide on airway bronchial challenge testing, exhaled nitric oxide and blood cortisol and eosinophil count were recalled for assessment of vasoconstrictor response to topical budesonide. The MacKenzie vasoconstrictor assay was performed by applying tenfold dilutions from 10(-2) g/ml to 10(-8) g/ml budesonide and visually assessing the degree of skin blanching after 18 h at each concentration. RESULTS: There was a significant overall dose-response effect for the degree of skin blanching at each concentration. There was no significant correlation between the effects on the skin and measures of anti-asthmatic efficacy or systemic effect after 3 weeks of 400 microg/day inhaled budesonide. There was a significant correlation with the overall dose-cutaneous response effect versus the overall dose-response effect with adenosine monophosphate (r=-0.53) but not methacholine bronchial challenge testing or serum cortisol. CONCLUSION: It may not be possible to use the McKenzie vasoconstrictor assay to predict which patients are most or least susceptible to inhaled corticosteroids for anti-asthmatic efficacy or systemic adverse effects.

Administration, Inhalation↗

PubMed1989

Relation of atrial natriuretic factor to vasoconstrictor hormones and regional blood flow in congestive heart failure.

Plasma levels of both atrial natriuretic factor (ANF) and vasoconstrictor neurohormones are often increased in patients with congestive heart failure (CHF). It has been speculated that ANF is a counterregulatory hormone that influences regional blood flow and sodium balance in human patients by either direct vasorelaxation or by inhibiting the release of other vasoconstrictor neurohormones. The exact relation of increased ANF levels to regional vascular resistance and vasoconstrictor neurohormones has not previously been documented. Thus, we examined the relation between plasma ANF levels, levels of vasoconstrictor neurohormones, and forearm, splanchnic and renal blood flow in 20 normal subjects and in 17 patients with chronic CHF. The plasma ANF level was directly correlated with the plasma norepinephrine concentration (r = 0.83, p less than 0.01), plasma epinephrine concentration (r = 0.46, p less than 0.01), plasma renin activity (r = 0.50, p less than 0.01), plasma angiotensin II concentration (r = 0.79, p less than 0.01) and plasma vasopressin concentrations (r = 0.65, p less than 0.01). Positive correlations existed between plasma ANF levels and the calculated vascular resistances, i.e., between ANF and forearm vascular resistance (r = 0.41, p less than 0.05), splanchnic vascular resistance (r = 0.74, p less than 0.01) and renal vascular resistance (r = 0.66, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

Endothelin-1 enhances vasoconstrictor responses to exogenously administered and neurogenically released ATP in rabbit isolated perfused arteries.

Vasoconstrictor responses to ATP were enhanced in a concentration-dependent-manner by endothelin-1 (0.1-1 nM) in isolated perfused segments of rabbit ear artery. Higher concentrations of endothelin-1 (3-10 nM) also enhanced vasoconstrictor responses to ATP. The enhancement of ATP responses by endothelin-1 (0.1-10 nM) was not affected by nicardipine (10 nM). The ATP-mediated component of the vasoconstrictor response to perivascular nerve stimulation in the rabbit jejunal artery was enhanced by endothelin-1 to a similar extent as that to exogenously administered ATP. The enhancement of vasoconstrictor responses to neurogenic ATP was also not affected by nicardipine.

Adenosine Triphosphate↗

PubMed1980

Inhibition of vasoconstrictor responses by 6-keto-PGE1 in the feline mesenteric vascular bed.

The effects of 6-keto-PGE1 on vascular resistance and vascular responses to sympathetic nerve stimulation and vasoconstrictor hormones were investigated in the feline mesenteric vascular bed. Infusions of 6-keto-PGE1 into the superior mesenteric artery dilated the mesenteric vascular bed and markedly inhibited vasoconstrictor responses to sympathetic nerve stimulation, norepinephrine and angiotensin II. The effects of 6-keto-PGE1 and PGE1 on vascular resistance and vasoconstrictor responses were quite similar and both substances inhibited responses to nerve stimulation and pressor hormones in a reversible manner. Responses to nerve stimulation, norepinephrine and angiotensin II were inhibited to a similar extent during infusion of 6-keto-PGE1 and PGE1. Results of these studies suggest that 6-keto-PGE1, a newly identified prostaglandin metabolite, and PGE1 possess the ability to inhibit the vasoconstrictor effects of sympathetic nerve stimulation and pressor hormones by a non-specific action on vascular smooth muscle in the feline small intestine.

6-Ketoprostaglandin F1 alpha↗

PubMedDate not supplied

Changes of reflexes in vasoconstrictor neurons supplying the cat hindlimb following chronic nerve lesions: a model for studying mechanisms of reflex sympathetic dystrophy?

The generic term 'reflex sympathetic dystrophy' describes a clinical syndrome which sometimes develops after traumata at the extremities with lesions of nerves or --more rarely--after other events. The syndrome consists of the following components: pain (hyperpathia, allodynia), trophic changes of skin and deep tissues, dysregulation of sweating and cutaneous blood flow of the extremity concerned. It is assumed that all symptoms are produced by abnormal sympathetic activity. Interruption of the sympathetic activity to the affected extremity abolishes most of the pain and may lead to remission of the trophic changes. The hypothesis is that the trauma with lesion of the primary afferent axons leads subsequently to an abnormal state of the primary afferent neurons and to distorted processing of information in the spinal cord. As a consequence of this abnormal central state the activity in the sympathetic (vasomotor and sudomotor) supply to the affected extremity is distorted. The results are pain, trophic changes and dysregulations of autonomic effector organs. In some yet unknown way a vicious circle between periphery and spinal cord is established (afferent leads to spinal cord leads to sympathetic leads to afferent). This hypothesis was the starting point for analysis of the reflex pattern in postganglionic vasoconstrictor neurons supplying the cat hindlimb after chronic nerve lesions performed in the same limb (cutting and ligating a skin nerve; suturing the central stump of a skin nerve to the peripheral stump of a muscle nerve). The results obtained show that the reciprocity of the reflex pattern which is normally observed between cutaneous and muscle vasoconstrictor neurons is lost in many animals. Cutaneous vasoconstrictor neurons are very similar to muscle vasoconstrictor neurons in their reactions to stimulation of arterial baroreceptors and chemoreceptors. If the same sequence of events also occurs in patients with reflex sympathetic dystrophy, it could explain the dysregulation of blood flow through skin and also the occurrence of trophic changes in the limb.

Animals↗

PubMed1987

Characterization of the vasoconstrictor activity of indomethacin in the mesenteric vascular bed of the cat.

The effects of indomethacin on vascular resistance were investigated in the feline mesenteric vascular bed under conditions of constant blood flow. Indomethacin produced mesenteric vasoconstriction that was dose-dependent but was less active than U46619, the thromboxane mimic, angiotensin II, PGF2 alpha and norepinephrine. The vasoconstrictor response to indomethacin was not altered by meclofenamate and phenoxybenzamine. Indomethacin, in a dose that blocked the systemic vasodepressor response to arachidonic acid, did not alter mesenteric vasoconstrictor responses to sympathetic nerve stimulation, norepinephrine, angiotensin II, U46619, and U44069. The present data suggest that in the feline intestinal vascular bed indomethacin has marked vasoconstrictor activity that occurs independent of activation of alpha-adrenoceptors and formation of cyclooxygenase products possessing pressor activity. The present data suggest that cyclooxygenase products do not modulate vasoconstrictor responses as well as the sympathetic nervous system in the intestinal vascular bed of the cat.

Angiotensin II↗

PubMedDate not supplied

Enhancement of the vasoconstrictor response to KCL by nitric oxide synthesis inhibition: a comparison with noradrenaline.

The role of the vascular endothelium in the response to a vasoconstrictor agent acting through a non-receptorial mechanism, such as KCl, was tested in the isolated mesenteric vascular bed of the rat. It was confirmed that the vasoconstrictor response evoked by stimulation of sympathetic terminals was unaffected by 100 microM NG-nitro-D-arginine methyl ester (D-NAME), but was significantly potentiated by 100 microM NG-nitro-L-arginine methyl ester (L-NAME) and by removal of endothelium. Responses to exogenous noradrenaline (1-100 microM) were also enhanced by treatment with 100 microM NG-monomethyl-L-arginine (L-NMMA) and with L-NAME, but not with D-NAME. The potentiating effect of NO synthesis inhibitors was reversed by 1 mM L-arginine. Moreover, the noradrenaline-induced vasoconstriction was significantly increased by endothelium-deprivation. Potassium chloride (80 mM) induced a vasoconstrictor response which was not modified by pretreatment with prazosin (0.1 microM) and yohimbine (0.1 microM). The response to KCl was unaffected by D-NAME (100 microM) but the L-stereoisomer induced a significant increase in the perfusion pressure. In endothelium-denuded preparations the vasoconstrictor response to KCl was greater than in control conditions and was quantitatively similar to that observed in L-NAME-treated preparations. The responses to electrical field stimulation, noradrenaline and KCl in endothelium-denuded preparations were not modified by L-NAME. The results suggest that an increase in vascular tone, per se, may represent a trigger for the release of endothelium-derived relaxing factor from endothelial cells.

Amino Acid Oxidoreductases↗

PubMed2005

Measurement of skin vasoconstrictor response in healthy subjects.

OBJECTIVES: Laser Doppler flowmetry enables non-invasive quantification of skin blood flow and its sympathetically mediated change. Four different maneuvers were performed in 60 healthy subjects aged 20-78 years to investigate their variability, reproducibility and to determine the influence of gender, age and height. MATERIAL AND METHODS: Skin blood flow was measured on the pulp of both index fingers using laser Doppler flowmetry. Vasoconstriction was induced by deep inspiratory gasp, arm dependency, acoustic stimulation and a modified cold pressor test. RESULTS: More than 95% of normal subjects showed a vasoconstrictor response to cold pressure test and 100% to inspiratory gasp. In all other maneuvers vasoconstrictor response was less reliable. The magnitude of vasoconstrictor responses decreased with age in all maneuvers, while latencies remained unchanged. Only during inspiratory gasp men showed more pronounced vasoconstrictor response compared with women. Body height influenced latencies if peripheral stimuli were applied like in the cold pressor and arm dependency tests. CONCLUSIONS: Inspiratory gasp and the modified cold pressor test were found to be more suitable maneuvers for routine clinical testing than arm dependency and acoustic stimulation. Normal data also for side differences are provided as a base for routine clinical testing in systemic and unilateral neurological disorders.

Acoustic Stimulation↗

PubMed2005

Relationship of inspiratory flow rate and volume on digit tip skin and ulnar artery vasoconstrictor responses in healthy adults.

Reflex vasoconstrictive responses are commonly used to assess sympathetic nerve function of the extremities. A regularly used reflex trigger is deep and rapid inspiration. However, little is known about the relationship between respiratory effort and the magnitude of the resultant vasoconstrictor response. This study investigates the association of inspiratory flow rate and volume to the level of vasoconstrictor reflexes in the 4th digit tip skin and the ulnar artery in 12 healthy volunteers (age range 21-65, mean 38.1 years). The effects of Peak Inspiratory Flow (PIF) and Forced Inspiratory Vital Capacity (FIVC) on blood flow were measured at three levels of respiratory effort: low (PIF < 1.0 l/min; FIVC < 1.0 l), medium (PIF = 1.0-1.5 l/min; FIVC = 1.0-1.5 l), and high (PIF > 1.5 l/min; FIVC > 1.5 l) at two separate occasions. Ulnar vasoconstrictor responses showed good correlation with all levels of respiratory effort. Skin digit tip responses showed good correlation at medium and high levels but not at low respiratory effort. Repeatability of both tests was good. Correlation of inspiratory flow rate to vasoconstriction was consistently better than with inspiratory volume. Both digit tip and ulnar vasoconstrictor responses were maximal with greatest respiratory effort.

Adult↗

PubMed1999

Role of basal nitric oxide synthesis in vasoconstrictor hyporeactivity in the perfused rat hindlimb after myocardial infarction: effect of captopril.

OBJECTIVES: The contribution of vascular changes to the development of heart failure is largely unknown. In the present study, we evaluated endothelial and vascular contractile function in the rat hindlimb vascular bed after myocardial infarction (MI), including the modulatory role of basal nitric oxide (NO) production and the effects of treatment with the angiotensin converting enzyme inhibitor captopril on vascular function. METHODS: MI was induced in male Wistar rats by ligation of the left coronary artery. Acetylcholine-induced dilatations were assessed in the ex vivo perfused hindlimb at various time points. At 2 and 5 weeks post-MI, vascular contractile function in the perfused hindlimb was assessed from resistance changes induced by 35 mM and 125 mM potassium (K+) and the maximum increase in resistance (delta Rmax, 125 mM K+ and 3 mg phenylephrine). Basal NO synthesis was blocked for 2 weeks with L-nitro-arginine methylester (L-NAME) in sham and MI rats and similar contractility experiments were performed. The effect of captopril treatment from 2 to 5 weeks post-MI on vasoconstrictor responses was also tested. RESULTS: Acetylcholine-induced dilatations in the presence of 10 microM indomethacin were not different between sham and MI rats. Vasoconstrictor responses to K+ and delta Rmax were reduced at 2 weeks after MI. This reduction in vasoconstrictor ability was similar to that seen in L-NAME-treated sham rats, while chronic L-NAME treatment did not affect vasoconstrictor reactivity in MI rats. Similarly, L-NAME induced an increase in mean arterial pressure in sham rats, but not in MI rats. At 5 weeks after MI, vasoconstriction to 125 mM K+ and delta Rmax were still reduced in MI rats; this response was however partially restored after captopril treatment. CONCLUSION: The development of vascular contractile hyporeactivity in the rat hindlimb after MI may be due to reduced basal NO production. Delayed treatment with captopril improves peripheral vascular contractile function in this setting.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1997

Skin blood flow abnormalities in a rat model of neuropathic pain: result of decreased sympathetic vasoconstrictor outflow?

Loose ligation of a sciatic nerve in rats provokes signs and symptoms like those observed in human conditions of neuropathic pain. Some of these have been associated with sympathetic dysfunction. Since the skin microcirculation in the rat is strongly influenced by sympathetic tone, abnormalities in skin blood flow may be used as an indirect measure of sympathetic dysfunction. We measured, by means of laser Doppler flowmetry, skin blood flow at the plantar surface of the rat hind paw before and after ipsilateral loose sciatic nerve ligation. We assessed basal skin blood flow as well as the vasoconstrictor response which follows cooling of the rat abdomen. The effectiveness of this response may be used as a measure of sympathetic vasoconstrictor outflow. As compared to the values obtained before ligation (= 100%): (1) the vasoconstrictor response was impaired (65%, P < 0.01) from day 1 onwards, whereas (2) basal skin blood flow was increased (171%; P < 0.01) from day 3 until day 5, and decreased (51%, P < 0.0001) from day 7 until day 28. At day 28, blockade of impulse propagation in the loosely ligated sciatic nerve (by means of lidocaine) did not increase the lowered level of skin blood flow. These findings suggest that in the chronic construction injury model loose ligation of a sciatic nerve reduces sympathetic vasoconstrictor outflow, which, in turn may induce supersensitivity of skin microvessels to catecholamines.

Animals↗

PubMed2000

Conditions permitting suppression of stretch-induced and vasoconstrictor tone by basal nitric oxide activity in porcine cerebral artery.

This study examined the ability of basal nitric oxide activity to suppress intrinsic and vasoconstrictor tone in isolated rings of porcine cerebral artery. Following stretch of approximately 1 g, N(G)-nitro-L-arginine methyl ester (L-NAME, 100 microM) produced a rise in tone in endothelium-containing but not endothelium-denuded rings. Thus, intrinsic tone was present and was powerfully suppressed by basal nitric oxide activity. Nevertheless, when concentration-response curves were constructed to U46619 and 5-hydroxytryptamine (5-HT), no endothelium-dependent depression of vasoconstriction was observed. It therefore appeared that basal nitric oxide activity was able to suppress intrinsic but not vasoconstrictor tone in these vessels. Stretch-tension curves generated following the application of stretch over the range 0 - 5. 5 g on endothelium-denuded rings showed that tension was stretch-induced. Experiments conducted in the presence of L-NAME (100 microM) revealed that the level of tone present in endothelium-containing rings was substantially higher than in endothelium-denuded rings across the entire range of stretch. When endothelium-containing and endothelium-denuded rings were set at similar levels of stretch-induced tone, rather than similar levels of stretch, the presence of the endothelium now depressed significantly vasoconstrictor responses to U46619 and 5-HT. Thus, when endothelium-containing and endothelium-denuded rings of porcine cerebral artery are set at similar points along their respective stretch-tension curves, rather than at similar levels of stretch, basal nitric oxide activity can be seen to inhibit both stretch-induced and vasoconstrictor tone.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed1994

Atrial natriuretic factor potentiates the human forearm vasoconstrictor response to sympathetic stimulation.

1. Atrial natriuretic factor has been suggested to affect human sympathetic nervous system activity. The interaction between atrial natriuretic factor and the sympathetic nervous system has not been fully elucidated yet, but may occur at different sites. We studied this modulator effect at the level of the forearm vascular bed: the forearm vasoconstrictor response was examined after alpha-adrenergic sympathetic stimulation in healthy subjects during the locoregional administration of atrial natriuretic factor, sodium nitroprusside and placebo. As a sympathetic stimulation test, the technique of the lower body negative pressure (-20 mmHg) was used. 2. Lower body negative pressure increased the forearm vascular resistance by +37 +/- 8% during concomitant intra-arterial infusion of placebo (n = 10). During a predilator state achieved by infusion of atrial natriuretic factor (10 ng min-1 100 ml-1 forearm volume) into the brachial artery, lower body negative pressure subsequently induced a forearm vasoconstrictor response of +153 +/- 22% (P < 0.05 versus placebo), whereas this was +64 +/- 14% when predilatation was achieved by infusion of an equipotent vasodilator dose of sodium nitroprusside (P > 0.1 versus placebo; P < 0.05 versus atrial natriuretic factor). The potentiation of the forearm vasoconstrictor response to lower body negative pressure by atrial natriuretic factor only occurred in the experimental and not in the contralateral arm. According to calculations on simultaneously sampled arterial and venous plasma catecholamine concentrations, the augmented forearm vasoconstrictor response seemed not to be caused by an increased release of noradrenaline.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1999

Differential blocking effects of tetrodotoxin on double-peaked vasoconstrictor responses to periarterial nerve stimulation in canine isolated, perfused splenic artery.

1. In the present study, we investigated the effects of progressive inhibition of neuronal sodium channels by increasing concentrations of tetrodotoxin (TTX; 1-30 nmol/L) on the double-peaked vasoconstrictor responses to electrical periarterial nerve stimulation in the canine isolated and perfused splenic artery. 2. Double-peaked vasoconstrictions (biphasic vasoconstrictor responses) were consistently observed in following electrical stimulation with 30 s trains of pulses at 1-10 Hz. At low frequencies of stimulation (1-3 Hz), a submaximal concentration of 3 nmol/L TTX had no effect on the first phase of the contractile response, but almost completely inhibited the second-phase response. At high frequencies (6-10 Hz), the two vasoconstrictor phases were almost equally inhibited by 50% by 3 nmol/L TTX. A three-fold increase in the concentration of TTX used (10 nmol/L) abolished the second-phase vasoconstriction at all stimulation frequencies tested, whereas this concentration of TTX failed to block the first-phase response. Further increasing the concentration of TTX to 30 nmol/L completely blocked the remaining first-phase response. 3. Treatment with 0.1 mumol/L prazosin did not modify the first-phase response to any of the stimulation frequencies in the presence of 3 nmol/L TTX. Moreover, 0.1 mumol/L prazosin had no affect on the second-phase response at low frequencies (1-3 Hz), while at high frequencies (6-10 Hz) it slightly, but significantly inhibited the second-phase response. The vasoconstrictor responses that persisted after 3 nmol/L TTX and 0.1 mumol/L prazosin were completely suppressed by subsequent application of 1 mumol/L alpha, beta-methylene ATP at all stimulation frequencies (1-10 Hz). 4. In conclusion, progressive inhibition of sodium channels by increasing the concentration of TTX may exert a more preferential inhibition on adrenergic rather than purinergic components, suggesting that TTX-sensitive sodium channels may have a more important role in determining the adrenergic rather than purinergic transmission of sympathetic nerves.

Adenosine Triphosphate↗

PubMed1989

Endothelin-like pulmonary vasoconstrictor peptide release by alpha-thrombin.

The endothelial cells lining the vessel wall can modulate vasomotor tone by releasing vasoactive factors, such as endothelial-derived constricting factors. We observed that alpha-thrombin, but not catalytically inactivated alpha-thrombin, mediated the release of two pulmonary vasoconstrictor peptides into the venous effluent of guinea pig lungs. These peptides elicited a slow-onset, long-lasting pulmonary vasoconstriction similar to the effect of endothelin, an endothelial-derived 21-amino acid vasoconstrictor peptide previously isolated from cells in culture. One of the isolated peptides coelutes with endothelin upon reverse-phase HPLC with an acetonitrile gradient and has a molecular weight comparable to endothelin as determined by gel-permeation HPLC. The other vasoconstrictor peptide elutes earlier than endothelin on reverse-phase HPLC and exhibits a lower molecular weight. The studies show the release of endothelin-like pulmonary vasoconstrictor peptides in the intact lung by alpha-thrombin, a central regulatory enzyme in hemostasis.

Animals↗

PubMed1997

Galpha16 mimics vasoconstrictor action to induce smooth muscle alpha-actin in vascular smooth muscle cells through a Jun-NH2-terminal kinase-dependent pathway.

Prolonged exposure of vascular smooth muscle cells (VSMC) to vasoconstrictors such as vasopressin or angiotensin II induces hypertrophy and increases expression of muscle-specific genes including smooth muscle alpha-actin (SM-alpha-actin). These vasoconstrictors signal through G-proteins, including members of the Gq family. To further investigate the role of Gq family members, VSMC were transfected with a constitutively active mutant of a Gq family member, Galpha16 (Galpha16Q212L). Stable expression of Galpha16Q212L persistently stimulated phospholipase C, resulting in increased basal levels of inositol phosphates. These cells were hypertrophied and expressed elevated levels of SM-alpha-actin compared with wild-type VSMC or cells transfected with a control plasmid (Neo). SM-alpha-actin promoter activity was markedly increased in cells stably or transiently expressing Galpha16Q212L. Basal c-Jun-NH2-terminal kinase (JNK) activity was increased 3-9-fold in cells stably expressing Galpha16Q212L, while basal activity of the p42/44 mitogen-activated protein kinases (ERKs) was unaffected. Transient expression of a kinase inactive JNK kinase partially inhibited induction of SM-alpha-actin promoter activity in response to vasoconstrictors or expression of Galpha16Q212L. These results indicate that expression of constitutively active Galpha16 in VSMC mimics the effects of vasoconstrictors on hypertrophy and muscle-specific gene expression, and activation of JNK may play a role in these responses.

Actins↗

PubMed1988

Involvement of vascular endothelium in the potentiation of vasoconstrictor responses by neuropeptide Y.

Although neuropeptide Y is not a potent vasoconstrictor in many vascular beds, nanomolar concentrations of this peptide can potentiate the response of isolated blood vessels to sympathetic stimulation or exogenous vasoconstrictors. Potentiation of the response to field stimulation was observed in superfused ring segments of rabbit ear artery or canine saphenous vein, provided that the endothelium was not mechanically damaged. The ability of neuropeptide Y to potentiate the constrictor response to noradrenaline in the ear artery was also dependent on the presence of an intact endothelium. The release of an endothelial-derived vasoconstrictor substance, as yet unidentified, by neuropeptide Y may explain its ability to potentiate the responses to both nerve stimulation and a variety of exogenous vasoconstrictors.

Animals↗