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PubMed2002

Relation between sympathetic vasoconstrictor activity and pain and hyperalgesia in complex regional pain syndromes: a case-control study.

BACKGROUND: Complex regional pain syndromes can be relieved by sympathetic blockage. The mechanisms of sympathetically maintained pain (SMP) are unclear. We aimed to establish the effect of physiological sympathetic cutaneous vasoconstrictor activity on pain and hyperalgesia in patients with complex regional pain syndromes. METHODS: High and low cutaneous vasoconstrictor activity was produced by whole-body cooling and warming (thermal suit) in 13 patients with type I disease and in ten controls. The degree of cutaneous vasoconstrictor discharge was monitored by measurement of skin blood flow and temperature at the arm and leg. Local skin temperature at the affected region was fixed at 35 degrees C. Pain was quantified during high and low cutaneous vasoconstrictor activity (intensity of spontaneous pain, area of mechanical hyperalgesias, heat-pain thresholds). Furthermore, pain was measured before and after diagnostic sympathetic blockage to identify patients with SMP and sympathetically independent pain. FINDINGS: In patients with SMP, intensity of spontaneous pain significantly increased, by 22%, and spatial distribution of mechanical dynamic and punctate hyperalgesia increased by 42% and 27%, respectively, during high sympathetic activity compared with low activity. Heat-pain thresholds did not differ during high and low cutaneous vasoconstrictor activity (cold and warm state, 43.6 degrees C vs 44.6 degrees C). Pain relief after sympathetic blockage correlated with augmentation of spontaneous pain after experimental stimulation of cutaneous vasoconstrictor activity (r=0.6, p=0.0244). INTERPRETATION: We have shown that in complex regional pain syndromes with SMP, physiological activation of cutaneous vasoconstrictor neurons projecting to the painful arm or leg enhances spontaneous pain and hyperalgesia. We postulate that there is a pathological interaction between sympathetic and afferent neurons within the skin.

Adult↗

PubMed1994

Effects of preoptic warming on subretrofacial and cutaneous vasoconstrictor neurons in anaesthetized cats.

1. Sympathetic and subretrofacial neuron responses to preoptic warming were studied in chloralose- or Saffan-anaesthetized, paralysed cats. 2. Warming a thermode in the preoptic region inhibited the activity of cutaneous vasoconstrictor fibres supplying hairy skin. Muscle vasoconstrictor fibre activity recorded at the same time was either unaffected or raised. 3. Small injections of sodium glutamate (5 nl, 0.1 M) were made into the region of the subretrofacial nucleus in the ventrolateral medulla. The part of that region where glutamate injections evoked brisk increases in cutaneous vasoconstrictor fibre activity was chosen for further study. 4. Extracellular single unit recordings were made in that area from seventy-seven subretrofacial neurons, which were identified by their barosensitivity (inhibition by carotid blind sac inflation). Forty-seven of them were antidromically activated by stimulation in the spinal cord. 5. The activity of twenty subretrofacial neurons (twelve proven bulbospinal) was significantly reduced by periods of preoptic warming. Cutaneous vasoconstrictor activity recorded at the same time also fell. Forty-nine subretrofacial neurons (thirty-five proven bulbospinal) were unaffected or excited by periods of preoptic warming that inhibited cutaneous vasoconstrictor fibres. The response of eight neurons was unclear. 6. No difference in either mean firing rate or axonal conduction velocity was found between neurons inhibited by preoptic warming and other subretrofacial neurons. 7. The subretrofacial neurons inhibited by warming were found intermingled with those unaffected or excited. Marked recording sites of warm-inhibited neurons were clustered around the ventromedial border of the subretrofacial nucleus. 8. In two cats, bilateral inhibition of subretrofacial neurons by surface application of 1 M glycine reduced cutaneous vasoconstrictor fibre activity to 32 and 44% of control levels. 9. The results suggest that specific cutaneous vasoconstrictor premotor neurons exist in the subretrofacial nucleus. These apparently provide most of the background excitatory drive to cutaneous vasomotor neurons. Central warming stimuli may act, at least in part, by withdrawing that drive.

Anesthesia↗

PubMed1988

Inhibitory effects of diltiazem on vasoconstrictor responses in the cat.

The effect of diltiazem on vasoconstrictor responses was investigated in the feline mesenteric vascular bed under conditions of controlled blood flow. Diltiazem inhibited vasoconstrictor responses to sympathetic nerve stimulation, tyramine and norepinephrine suggesting that responses to both nerve-released and exogenous norepinephrine are dependent in part on an extracellular source of calcium. The calcium entry antagonist inhibited vasoconstrictor responses to alpha 1 and to alpha 2 adrenoceptor agonists over a wide range of concentration. Diltiazem also inhibited mesenteric vasoconstrictor responses to angiotensin II, vasopressin, prostaglandin F2 alpha and KCl. The inhibitor effects of diltiazem on vasoconstrictor responses to nerve stimulation and the pressor agents were reversible, and all responses returned to control value 30 to 45 min after the infusion of the calcium entry antagonist. The present data suggest that the inhibitory effects of diltiazem on responses to sympathetic nerve stimulation are postjunctional in nature, as responses to nerve-released and exogenous norepinephrine and nonadrenergic pressor agents are reduced to a similar extent. The present results suggest that vasoconstrictor responses to neuronally released and exogenous norepinephrine, as well as agents which activate membrane receptors or depolarize vascular smooth muscle in the feline mesenteric vascular bed, are dependent in part on an extracellular source of calcium. The inhibitory effects of diltiazem on vasoconstrictor responses to sympathetic nerve stimulation and pressor hormones may be relevant to the antihypertensive actions of this calcium entry antagonist.

Adrenergic alpha-Agonists↗

PubMed2001

Vasoconstrictors in erectile physiology.

The erectile response of the penis depends on a balance between vasoconstrictor agents which cause cavernosal smooth muscle to contract limiting blood inflow, and vasodilators which relax cavernosal smooth muscle leading to increased blood inflow and erection. This review emphasizes the role of vasoconstrictors in the penis and shows that both endothelin-1 (ET-1) and the alpha-adrenergic agonist, methoxamine (METHOX) exert strong vasoconstrictor actions in the cavernosal circulation. We recently reported the vasoconstrictor actions of exogenous ET-1 and METHOX to be mediated by the RhoA/Rho-kinase pathway in the cavernosal circulation. While it is widely held that the nitric oxide-cyclic GMP-protein kinase G (NO-cGMP-PKG) pathway mediates vasorelaxation and penile erection, the interaction between this pathway and the vasoconstrictor process remains to be fully elucidated. Our studies also have shown that, during erection, the vasoconstrictor action of METHOX and ET-1 are inhibited and that NO is likely responsible for this inhibition. We hypothesize that the NO-cGMP-PKG pathway controls erection by acting in two distinct ways-by lowering intracellular levels of calcium leading to vasorelaxation and by inhibiting Rho-kinase mediated vasoconstriction.

Adrenergic alpha-Agonists↗

PubMed1989

Alpha 2-adrenoceptor agonists enhance responses to certain other vasoconstrictor agonists in the rat tail artery.

1. The effects of the alpha2-adrenoceptor agonists clonidine, rilmenidine, TL99 and UK14304 on the vasoconstrictor response to sympathetic nerve stimulation and on the concentration-response curves to noradrenaline and phenylephrine were compared in two isolated, perfused vascular tissues: the rat tail artery (which has both postjunctional alpha 1- and alpha 2-adrenoceptors), and the rabbit ear artery (in which only alpha 1-adrenoceptors are present postjunctionally). 2. In the rabbit ear artery, the first observable effect of alpha 2-adrenoceptor agonists was inhibition of vasoconstrictor responses to sympathetic nerve stimulation. This occurred with concentrations of the alpha 2-adrenoceptor agonists which were far below those producing vasoconstriction. Responses to noradrenaline were not affected. 3. In contrast, in the rat isolated perfused tail artery, alpha 2-adrenoceptor agonists, in concentrations that produced no other observable effects, enhanced the vasoconstrictor responses to sympathetic nerve stimulation and to noradrenaline. Much higher concentrations of alpha 2-adrenoceptor agonists produced vasoconstriction in most preparations and only then reduced the response to sympathetic nerve stimulation. The enhancing effect of alpha 2-adrenoceptor agonists was blocked by idazoxan, but not by prazosin. 4. Vasoconstrictor responses in the rat tail artery to the relatively selective alpha 1-adrenoceptor agonist phenylephrine were enhanced by alpha 2-adrenoceptor agonists. The enhancement of the response to phenylephrine was greater than that to the mixed alpha 1- and alpha 2-adrenoceptor agonist noradrenaline. 5. Vasoconstrictor responses in the rat tail artery to vasopressin, ATP and KCl, like those to alpha 1-adrenoceptor agonists, were enhanced by alpha 2-adrenoceptor agonists.2+owever, vasoconstrictor responses to

Adrenergic alpha-Agonists↗

PubMed1993

Chloride anion concentration as a determinant of renal vascular responsiveness to vasoconstrictor agents.

1. The role of chloride concentration in modulating vasoconstrictor responses of the rat isolated kidney, perfused with Krebs-Henseleit solution, to angiotensin II (AII), arginine vasopressin (AVP) and phenylephrine (PE) was investigated. 2. Reduction of perfusate chloride from a high (117 mM) to low (87 mM) concentration, by substitution of sodium chloride with a mixture of sodium salts of propionate, acetate and methanesulphonate, reduced responsiveness to all three vasoconstrictors, the change for AII being most pronounced. 3. For AII, reduced vasoactivity with low chloride was evident both in terms of the threshold dose and on the linear part of the dose-response curve but not for the maximum response. This attenuating effect of low chloride on the vasoconstrictor response to AII was reversed when perfusion with high chloride was reinstituted. Continuous perfusion with high chloride progressively increased the vasoconstrictor effect of low doses of AII for successive dose-response curves. 4. In addition to reducing responses on the linear part of the dose-response curve for both AVP and PE, low chloride also reduced the maximum vasoconstrictor response to PE, whereas the threshold dose for the two agonists was unchanged. In contrast to the enhanced pressor response to AII, during continuous perfusion with high chloride, tachyphylaxis occurred with AVP and PE. 5. The ability of chloride to modify renal responsiveness to vasoconstrictor agents may contribute to the increase in renal vascular resistance and decrease in glomerular filtration rate (GFR) which occurs during infusion of hyperchloremic solutions into the renal artery and explain the need for chloride as the anion accompanying sodium in salt-sensitive hypertensive models.

Angiotensin II↗

PubMed2006

Vasoconstrictor administration during cardiopulmonary bypass affects acid-base balance in infants and children.

BACKGROUND: In experimental reports, blood flow redistribution occurred during cardiopulmonary bypass (CPB) and perfusion pressure was restored by vasoconstrictor administration without improving splanchnic perfusion. The influence of vasoconstrictor administration during CPB was clinically examined. MATERIALS AND METHODS: Twenty-two consecutive pediatric CPB cases of ventricular septal defect without blood transfusion were divided into two groups, depending upon whether a vasoconstrictor was administered during CPB or not (n = 7 vs. 15). Bypass flow and systemic perfusion pressure during CPB were maintained at 2.5 L/m(2)/min and not lower than 30 mm Hg by vasoconstrictor administration, respectively. RESULTS: Although preoperative state and CPB conditions were comparable between the two groups, more sodium bicarbonate was administered (P < 0.05); duration from the operation to extubation was longer (P < 0.05); and bowel movement occurred later in the vasoconstrictor-administered group than in the control group. CONCLUSIONS: Vasoconstrictor administration during CPB may deteriorate the acid-base balance and the postoperative state in infants and children.

Acid-Base Equilibrium↗

PubMed1990

A comparison of peripheral vasoconstrictor responses and cardiovascular autonomic function tests in diabetic patients.

Venous occlusion plethysmography has been used to measure sympathetic vasoconstrictor responses in the feet and hands to a deep breath and body cooling and to assess blood flow variability. Measurements were made in 14 non-diabetic control subjects and 52 diabetic patients, 30 of whom had evidence of peripheral neuropathy. All the measurements were significantly reduced in the feet of patients with neuropathy. Vasoconstrictor responses were not significantly impaired in the hands of these patients. Cardiovascular autonomic function was assessed in the same subjects by standard tests of reflex heart rate responses and compared to sympathetic vasoconstrictor function as determined by the response to a deep breath. Eighteen of the 30 diabetic patients with peripheral neuropathy had impairment of both cardiovascular and sympathetic vasoconstrictor function. Five had normal vasoconstrictor but impaired cardiovascular responses and two had normal cardiovascular but impaired vasoconstrictor function. It may therefore be important to assess both systems in diabetic patients.

Blood Pressure↗

PubMed1983

Reflex activation of postganglionic vasoconstrictor neurones supplying skeletal muscle by stimulation of arterial chemoreceptors via non-nicotinic synaptic mechanisms in sympathetic ganglia.

Postganglionic sympathetic neurones supplying skeletal muscle and skin can be activated from the preganglionic site via cholinergic nicotinic, muscarinic and noncholinergic synaptic mechanisms. The experiments described in this paper were designed in order to show that postganglionic vasoconstrictor neurones supplying skeletal muscle can be activated by the naturally occurring discharge pattern in preganglionic axons when the nicotinic transmission is blocked. For this purpose, the activity was recorded simultaneously from postganglionic vasoconstrictor axons supplying skeletal muscle and vasoconstrictor axons supplying hairy skin. The preganglionic neurones were driven reflexly by stimulation of the arterial chemoreceptors. 1) During blockade of nicotinic transmission muscle vasoconstrictor neurones were activated via the CNS during stimulation of arterial chemoreceptors. This activation is either generated by muscarinic action of released acetylcholine or by a noncholinergic synaptic mechanism. 2) Postganglionic cutaneous vasoconstrictor neurones were inhibited during stimulation of arterial chemoreceptors. During blockade of cholinergic nicotinic transmission these neurones were not activated reflexly by stimulation of arterial chemoreceptors although they received inputs via cholinergic muscarinic and noncholinergic synaptic mechanisms. 3) The results illustrate that postganglionic vasoconstrictor neurones supplying skeletal muscle can not only be activated via non-nicotinic synaptic mechanisms through synchronous repetitive electrical stimulation of preganglionic axons but also by the discharge pattern produced in preganglionic neurones during stimulation of arterial chemoreceptors.

Animals↗

PubMed1990

Influence of SQ 29,548 on vasoconstrictor responses in the mesenteric vascular bed of the cat.

The effects of SQ 29,548 on vasoconstrictor responses were investigated in the feline mesenteric vascular bed. Injections of the thromboxane (TX) A2 mimics, U46619 and U44069, caused dose-related increases in mesenteric arterial perfusion pressure. After administration of SQ 29,548, 0.5 mg/kg i.v, vasoconstrictor responses to U46619 and U44069 were reduced markedly whereas responses to prostaglandin (PG) F2 alpha, angiotensin II, vasopressin and BAY K 8644, an agent which enhances calcium entry, were not altered. The duration of the TXA2 receptor blockade was greater than 2 h and SQ 29,548 had no significant effect on mesenteric vasodilator responses to PGE2, isoproterenol, nitroglycerin, acetylcholine or bradykinin. SQ 29,548, at a dose of 0.5 mg/kg i.v., significantly reduced the response to TXB2, which had modest vasoconstrictor activity in the mesenteric vascular bed. However, when the dose of SQ 29,548 was reduced to 0.05 mg/kg i.v., responses to TXB2 were not altered, whereas responses to U46619 were significantly decreased. SQ 29,548 had no significant effect on vasoconstrictor responses to norepinephrine or to sympathetic nerve stimulation. The TXA2 receptor antagonist blocked the vasoconstrictor component of the biphasic response to the PG precursor, arachidonic acid, and the endoperoxide, PGH2. The results of these studies suggest that SQ 29,548 is a specific TX receptor antagonist in the mesenteric vascular bed, that the vasoconstrictor component of the biphasic response to arachidonic acid and PGH2 is due to formation of TXA2, and that endogenously formed TXA2 does not modulate adrenergic responses in the mesenteric circulation of the cat.

Angiotensin II↗

PubMed1993

Responses of lumbar vasoconstrictor neurons supplying different vascular beds to graded baroreceptor stimuli in the cat.

Lumbar sympathetic vasoconstrictor neurons supplying skeletal muscle, hairy skin and pelvic organs were tested for their responses to carotid baroreceptor stimulation in chloralose-anaesthetized cats. Using single- and few-fibre recordings, the responses of the different types of vasoconstrictor neuron to graded steps of non-pulsatile pressure ranging from 110 to 260 mmHg in a vascularly isolated carotid sinus were analyzed quantitatively during the first 10 s of stimulation. The activity in all postganglionic muscle vasoconstrictor (MVC) neurons, preganglionic visceral vasoconstrictor (VVC) neurons and one third of the postganglionic cutaneous vasoconstrictor (CVC1) neurons was strongly depressed by maximal baroreceptor stimulation. Moreover, quantitative analysis revealed no significant differences of the baroreceptor sensitivity of MVC and CVC1 neurons as compared with VVC neurons at all levels of carotid sinus pressure. In contrast, two-thirds of the postganglionic cutaneous vasoconstrictor (CVC2) neurons exhibited a significantly weaker barosensitivity. The functional implications are discussed.

Animals↗

PubMed1996

Reflex sympathetic dystrophy: skin blood flow, sympathetic vasoconstrictor reflexes and pain before and after surgical sympathectomy.

To examine the pathophysiological mechanisms of vascular disturbances and to assess the role of the sympathetic nervous system, 12 patients with reflex sympathetic dystrophy (RSD) of the hand were studied using laser Doppler flowmetry. Cutaneous blood flow, skin resistance and skin temperature were measured at the affected and contralateral hands. Sympathetic vasoconstrictor reflexes were induced bilaterally by deep inspiration. Four patients were treated with unilateral surgical sympathectomy and pain and vascular changes were documented in follow-up investigations. (1) After acclimatization in cold environment (< or = 18 degrees C) blood flow and skin temperature were considerably lower on the affected side in 10 patients. No additional vasoconstrictor reflexes could be elicited. (2) After acclimatization in warm environment (22-24 degrees C) blood flow and skin temperature demonstrated no side differences in all cases. Vasoconstrictor responses were the same on both sides. (3) After sympathectomy vasoconstrictor reflexes were absent. Skin resistance was considerably higher on the affected side. In the first 4 weeks the affected hand was warmer and blood flow was higher compared with the healthy side. Thereafter, skin temperature and perfusion slowly decreased and the affected hand turned from warm to cold. Very regular high amplitude vasomotion waves occurred unilaterally. There were no signs of reinnervation. Two patients had long-term pain relief. We conclude as follows. (1) Side differences in skin temperature and blood flow are no static descriptors in RSD. They are dynamic values depending critically on environmental temperature. Therefore, they have to be interpreted with care when defining reliable diagnostic criteria. (2) Vascular disturbances in RSD are not due to constant overactivity of sympathetic vasoconstrictor neurons. Changes in vascular sensitivity to cold temperature and circulating catecholamines may be responsible for vascular abnormalities. Alternatively, RSD may be associated with an abnormal (side different) reflex pattern of sympathetic vasoconstrictor neurons due to thermoregulatory and emotional stimuli generated in the central nervous system. (3) After sympathectomy, denervation supersensitivity of blood vessels and intense vasomotion may be associated with recurrence of pain in some patients.

Adult↗

PubMed2004

Rostral ventromedial medulla and the control of cutaneous vasoconstrictor activity following i.c.v. prostaglandin E(1).

Neurones within the rostral ventromedial medulla project to the intermediolateral cell column of the spinal cord where they may influence sympathetic preganglionic neuronal activity controlling cutaneous vascular beds. Here we assess whether such neurones contribute to cutaneous sympathetic vasoconstrictor activity in a fever-like state induced by i.c.v. injection of E-series prostaglandin. In urethane-anaesthetised rats, we recorded population sympathetic activity to the tail (an index of vasoconstrictor discharge regulating cutaneous thermoregulatory circulations). A survey of the effects of GABA microinjections (200 mM; 60-80 nl; 111 sites in 57 rats) demonstrated that those into the rostral ventromedial medulla (in the region of raphe pallidus and magnus; approximately bregma -10 to -12 mm) markedly decreased (51%-100%) population sympathetic cutaneous vasoconstrictor activity during "normothermic control." In contrast, injections at sites dorsal and lateral to this region tended to produce either a smaller decrease or have no effect. In heat-clamp (nine animals: body temperature 40-41 degrees C) cutaneous vasoconstrictor activity was decreased by 83+/-5%. I.c.v. prostaglandin E(1) (100 ng and above) restored activity to, or above, control levels in these animals and where body temperature was maintained at control levels (12 animals: body temperature 35.5-36.5 degrees C). The depressant action of GABA was sustained in both conditions. GABA did not significantly influence concurrently recorded splanchnic nerve activity and heart rate in any condition although both were increased following i.c.v. prostaglandin E(1) (500 ng). This study is the first to demonstrate that inhibition of neuronal activity within the rostral ventromedial medulla decreases sympathetic cutaneous vasoconstrictor activity during normothermic control and following i.c.v. prostaglandin E(1) (both with and without heat-clamp). Therefore, sympathetic premotor neurones in this area contribute to vasoconstrictor drive in these conditions. In contrast, we were unable to demonstrate that the same area had a substantial involvement in the control of splanchnic nerve activity or heart rate, even when these were enhanced following i.c.v. prostaglandin E(1).

Action Potentials↗

PubMed2003

Occurrence of the spinal reflex due to skin pressure in sudomotor and cutaneous vasoconstrictor nerve system of humans.

The effects of skin pressure applied to one side of the waist on sudomotor and vasoconstrictor nerve activity were compared with the effects on sweating and cutaneous blood flow in humans. The sweat rate and cutaneous blood flow were measured on left and right dorsal feet. Skin sympathetic nerve activity (SSNA) was recorded by microneurography from a microelectrode inserted in left and right peroneal nerves. Skin pressure was applied in a supine position to the area over the left or right anterior superior iliac spine under warm (T(a): 30-36 degrees C) and cool (T(a): 19-23 degrees C) conditions. Sudomotor and vasoconstrictor bursts were identified for quantitative analysis. The skin pressure increased the contralateral/ipsilateral ratio of the sweat rate. It also increased the contralateral/ipsilateral ratio of the cutaneous blood flow and the contralateral/ipsilateral ratio of the sudomotor burst amplitude. However, skin pressure did not induce any significant changes in the contralateral/ipsilateral ratio of the vasoconstrictor burst amplitude. The results indicate that an asymmetrical reflex effect of skin pressure on vasoconstrictor nerve activity was absent, suggesting that, whereas the ipsilateral suppression of sweating elicited by skin pressure was mediated by the sudomotor nerve system, the ipsilateral suppression of cutaneous blood flow was not mediated by the vasoconstrictor nerve system. Thus, the occurrence of the spinal reflex due to skin pressure is not uniform between the sudomotor and the vasoconstrictor nerve systems, which represent different organizations at the level of spinal cord.

Adult↗

PubMed1993

Peptide vasoconstrictors, vessel structure, and vascular smooth-muscle proliferation.

The peptide vasoconstrictors angiotensin II (Ang II) and endothelin-1 (ET-1), originally thought to derive exclusively from the plasma renin-angiotensin system and vascular endothelium, respectively, have been demonstrated to be produced independently of such sources. Local tissue angiotensin-generating systems are well documented, and endothelin production has been demonstrated for a variety of nonendothelial cells, including vascular smooth-muscle cells (VSMC). There is increasing evidence from in vitro studies that local production of these vasoconstrictor peptides may contribute to blood vessel homeostasis and the development of vascular pathologies. Results obtained from pharmaceutical intervention in humans and animals of these systems strongly support this hypothesis. In addition to their vasoconstrictor properties, Ang II and ET-1 act as potent biological effectors. In vitro, both vasoconstrictor peptides appear to modulate the activity of autocrine feedback loops in VSMC. The activity of these feedback loops in vivo may represent a central mechanism for regulation and phenotypic differentiation of this cell type. The best-recognized autocrine feedback loops of VSMC are constituted by platelet-derived growth factor and transforming growth factor-beta, both of which are influenced by the action of Ang II and ET-1. Because both vasoconstrictors (via their induction of autocrine growth modulators) may influence the composition of the extracellular matrix of VSMC, the effects of the peptide vasoconstrictors on the (auto-) regulated feedback loops are of long-term structural importance. Ang II and ET-1 promote the synthesis and secretion of the glycoproteins thrombospondin, fibronectin, and tenascin.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗

PubMed1999

Pharmacological analysis of vasoconstrictor responses to periarterial purinergic nerve stimulation.

1. Periarterial electrical nerve stimulation at a low frequency (1 Hz) readily induced a vasoconstrictor response of the canine splenic artery in a pulse number-related manner (1-30 pulses of trains). The vasoconstrictor response to trains of up to 10 pulses at 1 Hz of stimulation appeared to be monophasic, whereas it became clearly distinguished into two phases at a longer train of 30 pulses. 2. The monophasic vasoconstrictor responses to trains of 1, 3 or 10 pulses were not modified by an alpha1-adrenoceptor blocking agent, prazosin (0.1 microM), but were completely inhibited by the P2X receptor desensitization with alpha,beta-methylene adenosine 5'-triphosphate (alpha,beta-methylene ATP; 1 microM). The 1st phase of vasoconstriction induced by a train length of 30 pulses was not influenced by the treatment with prazosin, but was abolished by alpha,beta-methylene ATP. The 2nd phase response was markedly inhibited by prazosin, and the remaining response of this phase was blocked by alpha,beta-methylene ATP. 3. Rauwolscine (0.3 microM), an alpha2-adrenoceptor antagonist, enhanced the vasoconstrictor responses to trains of 1, 3 or 10 pulses. Particularly at 10 pulses of electrical stimulation, the vasoconstrictor responses were significantly potentiated. The blockade of neuronal uptake of noradrenaline with imipramine (1 microM) did not affect the vasoconstrictor responses to trains of 1, 3 or 10 pulses. 4. It is concluded that short pulse trains of stimulation at a low frequency may selectively activate a purinergic component of sympathetic cotransmission, and the prejunctional alpha2-adrenergic feedback mechanism may tonically participate into the modulation of ATP release. Imipramine-sensitive neuronal uptake mechanism may not play an important role in regulating vascular responses to periarterial purinergic nerve stimulation.

Adenosine Triphosphate↗

PubMedDate not supplied

Selective antagonism of humoral versus neural vasoconstrictor responses by nisoldipine.

The effects of nisoldipine administration on vascular reactivity to humoral and neural vasoconstrictor stimuli were examined in the intact rat. For these experiments, rats were instrumented with miniaturized pulsed Doppler flow probes to allow continuous measurement of renal, mesenteric, and hindquarters blood flow. In conscious and anesthetized rats, intravenous doses of angiotensin II (75 and 150 ng/kg), norepinephrine (0.6 and 1.2 microgram/kg), and epinephrine (0.6 and 1.2 microgram/kg) caused dose-dependent increases in arterial pressure and renal and mesenteric vascular resistance. Nisoldipine (0.7 microgram/min) administration significantly attenuated (p less than 0.05) the pressor and regional vasoconstrictor actions of all three circulating pressor agents; however, nisoldipine infusion had little effect on neurally mediated regional vasoconstrictor responses elicited by electrical stimulation of the posterior hypothalamus or greater splanchnic nerve. These data indicate that nisoldipine depressed vascular responsiveness to humoral vasoconstrictor agents, while neural vasoconstrictor responses were unaffected. Thus nisoldipine appears to exert preferential antagonistic effects on humoral rather than on neural vasoconstrictor stimuli.

Angiotensin II↗

PubMed2002

[Effect of admixture of commercially available corticosteroid ointments and/or creams on vasoconstrictor activity].

A commonly used admixture of commercially available ointments and/or creams was selected from the prescribed sheets in our hospital, and questionnaire to dermatologists. To assess the relationship between permeability of corticosteroid through murine skin and clinical effects in human, we attempted to investigate the vasoconstrictor activity of these admixtures of topical corticosteroid by double-blind controlled study. Test samples were occluded at random on the back of 20 healthy volunteers for 4 hours. The vasoconstrictor activity of corticosteroid creams (Lidomex) alone was significantly large as compared with that of ointments alone. The vasoconstrictor activity of corticosteroid in the admixture of Lidomex ointment and urea ointments or heparinoid ointment was 1.5-2 fold significantly larger than that from ointments alone. The extent of the stability of the emulsion after mixing was related to the vasoconstrictor activity. These experiments demonstrated a close relationship between the vasoconstrictor activity of human skin and permeability of hairless mice skin. These results suggested that the vasoconstrictor activity of topical corticosteroids mixed with commercially available ointments and/or creams depends upon their physicochemical characteristics.

Adrenal Cortex Hormones↗