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PubMedDate not supplied

Deterioration of body oxygen metabolism by vasodilator and/or vasoconstrictor administration during cardiopulmonary bypass.

During cardiopulmonary bypass (CPB), tissue perfusion injury occurs even if perfusion pressure is maintained. Although a vasodilator and a vasoconstrictor are clinically administered if bypass flow is maintained, they may restore perfusion pressure without improving tissue perfusion. We evaluated the influence of vasodilators and vasoconstrictors on the whole body during CPB. Fifty-six patients with valvular disease who received moderately hypothermic CPB without blood transfusion were divided into four groups, depending upon whether a vasodilator and/or a vasoconstrictor was administered, and postoperative data were compared. Bypass flow and aortic pressure were maintained at 2.4 l/min/m and 5090 mm Hg. Body weight, dilution, hematocrit level, CPB, and aortic clamp duration, blood temperature, bypass flow, perfusion pressure, base excess levels during CPB, cardiac index, arterial and mixed venous oxygen pressure, and alveolar-arterial oxygen distribution after CPB were comparable among the four groups. However, the time to extubation was significantly longer. Blood lactate levels, measured for patients returned to the ward, were significantly higher in the agent-administered groups than in the no-agent group, whereas blood lactate levels on extubation and blood creatinine levels on postoperative day 1 were comparable among the groups. Vasodilator and/or vasoconstrictor administration during CPB may deteriorate the body oxygen metabolism, which might imply tissue perfusion and worsen the complications induced by hypoperfusion during CPB.

Aged↗

PubMed1999

Comparison of topical anesthetics and vasoconstrictors vs lubricants prior to nasogastric intubation: a randomized, controlled trial.

OBJECTIVE: To determine whether pre-treatment of the nose and throat with topical anesthetics and vasoconstrictors would reduce the pain associated with nasogastric (NG) intubation. METHODS: This was a prospective, randomized, controlled trial assessing the pain of NG intubation in patients pretreated with topical anesthetics and vasoconstrictors vs surgical lubricants alone. The subjects were 40 alert, cooperative adult patients requiring NG intubation without allergies to the study medications or contraindications to their use from a suburban university-based ED. The patients in the experimental group had phenylephrine 0.5% sprayed in their noses followed by instillation of 5 mL of 2% lidocaine jelly. Their throats were sprayed with 2% tetracaine and 14% benzocaine. The control patients received intranasal lubrication only. The primary outcome measured was pain of NG intubation on a 100-mm visual analog scale. Other outcomes included nasal pain, discomfort from gagging, and the incidences of vomiting, choking, and epistaxis. RESULTS: The mean age (+/-SD) was 54.8+/-22.3 years; 20 (50%) were female. The patients who had a combination of topical anesthetics and vasoconstrictors inserted prior to NG intubation experienced significantly less overall pain/ discomfort than did the control patients [28.6 mm (95% CI = 17.3 to 39.9 mm) vs 57.5 mm (95% CI = 44.9 to 70.1 mm), p = 0.001]. The patients in the experimental group also experienced significantly less nasal pain than did the patients in the control group [18.1 mm (95% CI = 8.0 to 28.2 mm) vs 44.4 mm (95% CI = 30.4 to 58.6 mm), p = 0.003] and significantly less discomfort from gagging than the patients receiving pretreatment with a lubricant alone [24.1 mm (95% CI = 11.1 to 37.1 mm) vs 50.9 mm (95% CI = 36.7 to 65.1 mm), p = 0.006]. There was no between-group difference in the frequencies of adverse effects. CONCLUSIONS: Use of topical lidocaine and phenylephrine for the nose and tetracaine with benzocaine spray for the throat prior to NG intubation results in significantly less pain and discomfort than use of a nasal surgical lubricant alone. Widespread use of topical anesthetics and vasoconstrictors prior to NG intubation is recommended.

Administration, Topical↗

PubMed1999

Vasoconstrictor effect of endothelin-1 in human skin: role of ETA and ETB receptors.

The aim of this project was to investigate the role of ETA and ETB receptors in the mediation of endothelin (ET)-1-induced vasoconstriction in human skin. This information should provide important insights into the design of pharmacological intervention against skin vasospasm induced by ET-1 in peripheral vascular disease or surgical trauma. Vasoconstriction in response to intra-arterial drug infusion in isolated perfused human skin flaps (8 x 18 cm) derived from dermolipectomy specimens was assessed by studying changes in skin perfusion and perfusion pressure under constant flow rate in each drug treatment (n = 4). It was observed that ET-1 (10(-10) to 10(-8) M) and norepinephrine (NE, 10(-8) to 10(-5) M) caused skin vasoconstriction in a concentration-dependent manner, with the vasoconstrictor potency of ET-1 approximately 200-fold higher than NE. The ETA-receptor antagonist BQ-123 but not the ETB-receptor antagonist BQ-788 blocked the vasoconstrictor effect of ET-1. This observation was confirmed by studying skin perfusion using the dermofluorometry technique. In addition, ETB-receptor agonists BQ-3020 and sarafotoxin S6c (10(-9) to 10(-6) M) did not evoke skin vasoconstriction. BQ-3020 also did not elicit skin vasoconstriction even in the presence of 10(-5) M of Nomega-nitro-L-arginine methyl ester and indomethacin. Furthermore, results from saturable and competitive ET-1 radioligand membrane receptor binding assays revealed that high-affinity and capacity binding sites are predominantly the ETA receptor subtype in endothelium-denuded skin arteries and veins of 0.5-1.5 mm diameter, with an ETA-to-ETB receptor ratio of 83:17 in arteries (n = 5) and 78:22 in veins (n = 7). Results from the present functional and radioligand receptor binding studies clearly indicate that ET-1 is a very potent vasoconstrictor in human skin and its vasoconstrictor effect is primarily mediated by ETA receptors, with no significant participation from ETB receptors.

Adult↗

PubMed1986

Role of the vasoconstrictor and antidiuretic activities of vasopressin in inhibition of renin secretion in conscious dogs.

The nature of the activity of vasopressin that is responsible for the inhibition of renin secretion was studied in normally hydrated conscious dogs using intravenous infusions of vasopressin and analogues of vasopressin with selective antidiuretic and vasoconstrictor activity. Vasopressin (1.0 ng . kg-1 . min-1) increased mean arterial pressure (MAP) from 106 +/- 2 to 115 +/- 3 mmHg (P less than 0.05) and decreased heart rate (HR) from 81 +/- 6 to 56 +/- 5 beats/min (P less than 0.001). Plasma renin activity (PRA) decreased from 4.4 +/- 1.1 to 2.4 +/- 0.8 ng . ml-1 . 3 h-1 (P less than 0.05). A specific antagonist of the vasoconstrictor activity of vasopressin, d(CH2)5MeTyrAVP (10 micrograms/kg), completely blocked the cardiovascular and renin responses to vasopressin. A selective vasoconstrictor agonist, 2-phenylalanine-8-ornithine oxytocin (1.0 ng . kg-1 . min-1), increased MAP from 112 +/- 4 to 128 +/- 6 mmHg (P less than 0.001) and decreased HR from 69 +/- 3 to 47 +/- 4 beats/min (P less than 0.001). PRA decreased from 5.5 +/- 1.1 to 2.7 +/- 0.2 ng . ml-1 X 3 h-1 (P less than 0.001). In contrast, a selective antidiuretic agonist, 1-deamino-8-D-arginine vasopressin (1.0 ng . kg-1 . min-1) did not alter PRA, MAP, or HR. These results demonstrate that the acute inhibition of renin secretion by vasopressin in normally hydrated conscious dogs is due to vasoconstrictor rather than antidiuretic activity.

Animals↗

PubMed1998

Perindopril treatment affects both preglomerular renal vascular lumen dimensions and in vivo responsiveness to vasoconstrictors in spontaneously hypertensive rats.

We have previously shown that chronic treatment with angiotensin-converting enzyme inhibition (ACEI) did not reverse hypertrophy of the renal arterial wall in spontaneously hypertensive rats (SHR). In this study we determined the effects of perindopril on the functional properties of the renal vasculature in vivo and on its resistance to flow at maximal dilatation in vitro, a measure of vessel lumen diameter. Two groups of SHR were studied: untreated or treated with perindopril (3 mg/kg per day) in their drinking water from 4 weeks of age. At 10 weeks, (1) vessel lumen characteristics were assessed using a maximally dilated in vitro isolated kidney perfusion and (2) the renal vasoconstrictor responses to bolus doses of vasoactive agents (angiotensin II and phenylephrine) administered into the renal artery were measured in vivo (anesthetized rats). Mean arterial pressure was significantly lower in conscious SHR treated with perindopril (132+/-2 versus 97+/-2 mm Hg, P<.001). In vitro, the pressure-flow relationship and the pressure-glomerular filtration rate relationship were both shifted significantly to the left (P<.001). The perindopril-treated kidneys began filtering at a significantly lower threshold perfusion pressure than nontreated controls (P<.001). In vivo, renal vasoconstrictor responses to increasing doses of both vasoconstrictor agents were significantly less marked in the perindopril-treated SHR than in untreated SHR (P<.05). Thus, chronic ACEI increased average renal vessel lumen diameter in SHR, predominantly in preglomerular vessels, and reduced renal vasoconstrictor responsiveness in vivo, findings compatible with remodeling of the preglomerular vasculature around a greater lumen.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1999

Effect of estrogen replacement on vasoconstrictor responses in rat mesenteric arteries.

Recent studies have shown that estrogen can increase endothelial nitric oxide synthase expression and/or activity and that nitric oxide may play a role in attenuating vasoconstrictor responses. Yet there are still controversies in this field. Our hypothesis was that the role of nitric oxide in modulating vasoconstrictor responses in estrogen-replaced animals depends on the agonist. The aim of the study was to determine the effect of long-term estrogen replacement on vascular reactivity of resistance-sized mesenteric arteries in ovariectomized rats with the use of a variety of vasoconstrictors. Female Sprague-Dawley rats were ovariectomized at 11 weeks of age. 17beta-estradiol pellets (0.5 mg/pellet) were implanted in the estrogen-replaced group (n=9) for 4 weeks; placebo pellets were used in the ovariectomized group (n=10). Resistance-sized mesenteric arteries were dissected and mounted onto a dual-chamber arteriograph system. Estradiol replacement did not alter the response of mesenteric arteries to either arginine vasopressin or the thromboxane mimetic U46619. Inhibition of nitric oxide synthase with N(G)-monomethyl-L-arginine (100 micromol/L) did not modulate these vasoconstrictor responses in either group of rats. In contrast, the dose-response curve of the adrenergic agonist phenylephrine was significantly attenuated for the estradiol-replaced rats compared with the ovariectomized group (EC(50)=0.90+/-0.17 vs 0.44+/-0.08 micromol/L, P<0.05). After incubation with N(G)-monomethyl-L-arginine, the EC(50) of phenylephrine significantly decreased in both groups, but a significant difference remained between the 2 groups (EC(50)=0.41+/-0.08 vs 0.28+/-0.02 micromol/L, P<0.05). Importantly, Western immunoblotting demonstrated that the expression of alpha(1)-adrenergic receptors was significantly suppressed by estradiol replacement. We conclude that estrogen may have a specific effect on adrenergic vasoconstriction by modulating its receptors.

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

PubMed2004

Peptidergic innervation of the vasoconstrictor muscle of the abdominal aorta in Aplysia kurodai.

The arterial system of the marine mollusc Aplysia consists of three major arteries. One of them, the abdominal aorta, has a sphincter (the vasoconstrictor muscle) at the base of the artery. Contraction of this muscle reduces the blood flow into the abdominal aorta, thereby, playing a role in the regulation of the blood distribution in Aplysia. Here, we show the contractility of the vasoconstrictor muscle is modulated by three types of endogenous peptides, Aplysia mytilus inhibitory peptide-related peptides (AMRP), enterin and NdWFamide. Immunohistochemistry showed that putative neuronal processes containing the three peptides exist in the vasoconstrictor muscle. Enterin inhibited the muscle contraction elicited by the nerve stimulation or the application of a putative excitatory transmitter, acetylcholine (ACh). Enterin hyperpolarized the resting potential of the muscle and decreased the amplitude of the excitatory junction potential (EJP). AMRP also inhibited the nerve-evoked contraction although its action on the ACh-induced contraction was variable. AMRP also reduced the size of EJP, but had no effect on the resting potential of the muscle. NdWFamide enhanced the nerve-evoked contraction but not the ACh-induced contraction. NdWFamide augmented EJP without affecting the resting potential of the muscle. These results suggest that AMRP, enterin and NdWFamide are endogenous modulators of the contractile activity of the vasoconstrictor muscle, and that the peptidergic innervations of this muscle contribute to fine tuning of the blood distribution in Aplysia.

Animals↗

PubMed1998

Effect of amezinium metilsulfate on the finger skin vasoconstrictor response to cold stimulation and venoconstrictor response to noradrenaline.

Orthostatic hypotension can be caused by an inadequate vasoconstrictor response. The effects of amezinium on vasoconstrictor response to sympathetic stimulation and to exogenous noradrenaline were investigated and compared with those of midodrine. In 8 healthy men, the following experiments were performed after a single oral dose of 10mg of amezinium, 2mg of midodrine or a placebo. First, finger-tip blood flow (FTBF) was recorded using a laser Doppler flowmeter before and during the contralateral hand cooling and a reduction ratio of FTBF was calculated as an index of the vasoconstrictor response. Second, dose-response curves to increasing doses (1-512ng/min) of noradrenaline infused locally to the dorsal hand vein were determined using a linear variable differential transformer. The reduction ratio of FTBF was significantly increased (p<0.05) by amezimium [placebo, 75.9 +/- 9.8(mean +/- SD)%; amezinium, 85.1 +/- 7.9%; midodrine, 78.1 +/- 9.3%]. The infusion rate of noradrenaline producing a half-maximum venoconstriction was significantly decreased (p<0.05) by amezinium (placebo, 40.6 +/- 33.9 ng/min; amezinium, 21.0 +/- 21.3 ng/min; midodrine, 33.2 +/- 31.5 ng/min). These findings indicate that amezinium increases the vasoconstrictor response to sympathetic stimulation and to noradrenaline in normal subjects, and this mechanism might contribute to the improvement by amezinium of the symptoms of orthostatic hypotension.

Adrenergic alpha-Agonists↗

PubMedDate not supplied

One year follow-up of patients with rhinitis medicamentosa after vasoconstrictor withdrawal.

The aim of the study was to systematically follow-up 10 patients with rhinitis medicamentosa for at least 1 year after vasoconstrictor withdrawal. During withdrawal of the decongestants the patients used budesonide nasal spray, 400 micrograms/day, for 6 weeks. The thickness of the nasal mucosa, the decongestive effect of oxymetazoline, and the histamine sensitivity were measured with rhinostereometry during the period. The thickness of the nasal mucosa and the symptom scores of nasal stuffiness were reduced considerably 6 and 12 months after vasoconstrictor withdrawal. The histamine sensitivity reflecting nasal hyperreactivity was still increased after 6 months, but not after 1 year. The decongestive effect of oxymetazoline increased after 6 months, indicating reversible tolerance. We conclude that when given adequate treatment and information about nose-drop overuse, all patients were able to stop using the vasoconstrictors and no one relapsed into a daily long-term overuse of vasoconstrictors during the 1-year follow-up period.

Administration, Intranasal↗

PubMed1986

Evaluation of angiotensins II and III as vasoconstrictors in the hepatic and hindlimb vasculatures of dogs.

Previous work has demonstrated that intravenously administered angiotensin II is more potent than angiotensin III as a systemic vasopressor agent. We tested the hypothesis that this difference in potency is caused at least partially by angiotensin II being more potent than angiotensin III as a vasoconstrictor in the hindlimb and hepatic vasculatures. The effects of angiotensins II and III on hindlimb and hepatic blood flow were evaluated in 14 dogs anesthetized with pentobarbital. Blood flows were measured electromagnetically. Graded doses of angiotensins II and III were administered as bolus injections directly into the arterial supply of the hindlimb and liver. On the basis of duration and graphic integration of the flow responses, but not on the basis of absolute changes in amplitude, angiotensin II was significantly more potent than angiotensin III as a vasoconstrictor in the hindlimb vasculature. In the hepatic circulation the flow changes produced by angiotensin II and angiotensin III were not significantly different on the basis of duration, graphic integration, or amplitude. We conclude that (i) differential vasoconstrictor responses of the hindlimb, but not the hepatic circulation, to angiotensins II and III contribute to the difference in systemic vasopressor potency between these two peptides, and (ii) because flow responses are an integral event with duration and constantly varying amplitude, evaluation of vasoconstrictor potency based only upon amplitude of the flow changes can be misleading.

Angiotensin II↗

PubMedDate not supplied

[Local-regional dental anesthesia without vasoconstrictors].

Since Braun in 1905 first associated adrenalin with Einhorn's novocaine (procaine) to augment anaesthetic action, many attempts have been made to replace this vasoconstrictor because of the often severe inconveniences it can cause (cardiovasculopathic, arteriosclerotic, etc.). Reduction in dosimetry is recalled in brief: 1-corbasil; vasopressin; nor-adrenalin. It is personally considered that none of these measures ever successfully replaced adrenalin, nor did they prove to be so harmless as was originally believed. Finally, the refinement of biochemical research enabled more powerful and less toxic locoregional anaesthetics to be marketed and these provided ideal anaesthesia without vasoconstrictors. Pure carbocaine has been personally used exclusively for more than four years, with the two-fold advantage of practically completely avoiding any general inconvenience, particularly in cardionephrotics, diabetics, etc. and, in plexic (or terminal) injections, avoiding the threat of ischaemia which is the most frequent cause of alveolitis and of secondary haemorrhage. This locoregional anaesthetic without vasoconstrictor is therefore recommended, while the vast majority of clinics continue to use anaesthetics associated wtih non-indispensable and dangerous vasoconstrictors.

Adult↗

PubMed1991

Effect of endothelin-1 on responses of isolated blood vessels to vasoconstrictor agonists.

The effect of endothelin-1 (ET-1) on vasoconstrictor responses of the endothelium-denuded perfused rabbit ear artery to 5-hydroxytryptamine (5-HT), histamine, and vasopressin (VP) was studied. In low concentrations with no vasoconstrictor action (0.1 and 0.3 nM), and in a concentration that increased the perfusion pressure by 70 mm Hg (1 nM), ET-1 significantly enhanced responses to the agonists studied; this enhancement was apparently mediated by an increased influx of extracellular calcium through voltage-operated channels, as it was abolished by the calcium channel antagonist nicardipine (10 nM). In contrast, higher concentrations of ET-1 (3 and 10 nM) inhibited responses to VP and 5-HT and this inhibitory effect was accentuated in the presence of nicardipine. The possible mechanism by which ET-1 exerts this inhibitory effect on vasoconstrictor responses is discussed. Because ET-1 is released from endothelial cells that are immediately adjacent to vascular smooth muscle cells, these modulatory effects of ET-1 on responses to endogenously present vasoconstrictors may play a role in vascular function.

Animals↗

PubMed1989

Effects of exogenous vasoconstrictors on coronary vascular resistance and prostacyclin production of the quiescent heart: the inhibitory effect of aspirin.

The in situ heart is exposed to blood-borne vasoconstrictor agents (e.g., vasopressin) which, if unopposed, may cause radically increased coronary vascular resistance (CVR). Release of endogenous vasodilator, such as prostacyclin (PGI2), is a possible mitigating mechanism. We investigated the ability of the heart to maintain CVR within a narrow range when exposed to exogenous vasoconstrictors. The isolated rat heart was perfused at constant flow rate (5-6 ml/min) with oxygenated Krebs-Ringer bicarbonate solution (37 degrees C, pH 7.4), and was rendered quiescent by a local injection of lidocaine to the atrio-ventricular node. Changes of perfusion pressure, indicating changes of CVR, were monitored and the cardiac effluent was collected for analysis of 6-keto PGF1 alpha and thromboxane B2 (stable metabolites of PGI2 and thromboxane A2, respectively) by radioimmunoassay. Hearts were infused with four different vasoconstrictors (i.e., serotonin, vasopressin, angiotensin II and the thromboxane A2/PGH2 mimetic, U46619). There was a linear relationship between the dose-dependent increase in CVR and PGI2 production in serotonin, U46619 and vasopressin-infused quiescent heart. Vasoconstriction induced by angiotensin II was not dose-dependent and was unrelated to PGI2 production. Thus, PGI2 is produced in response to coronary vessel constriction, presumably to mitigate the constriction. No detectable thromboxane B2 was released by any of these vasoconstrictors. Partial inhibition (approximately 50%) of PGI2 production by aspirin (5.6 microM) treatment resulted in a paradoxically decreased vasoconstriction except at the lowest level of serotonin and vasopressin. Aspirin (1 mM) greatly reduced PGI2 production (approximately 90%) but the fall in CVR persisted.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗

PubMed1983

Impairment of tissue defenses by vasoconstrictors in vaginal hysterectomies.

This paper examines the role of vasoconstrictors, specifically epinephrine, as an etiologic factor in the impairment of the host's defense mechanism. One hundred patients were injected circumferentially around the cervix with a dilute solution of epinephrine before vaginal hysterectomy; these patients were compared to a control group of 100 patients injected in the same manner with a normal saline solution. This randomized prospective study shows that vasoconstrictors significantly predisposed the vaginal cuff surgical site to infection compared to the matched control group. This study shows also that the use of a vasoconstrictor did not significantly reduce blood loss. Based on these data, it is recommended that a locally injected vasoconstrictor not be used during vaginal hysterectomy.

Abscess↗

PubMed1984

[Peridural anesthesia with etidocaine. Clinical studies on the effect of vasoconstrictors on sensory and motor blockade].

In a randomized double-blind study etidocaine 1.5% without a vasoconstrictor (n = 10), with adrenaline 1:200,000 (n = 10) and with ornipressine 1 IU/10 ml (n = 10) were administered epidurally to 30 orthopaedic patients. Sensory blockade was tested with electric pain stimuli; motor blockade was assessed with dynamometry during isometric plantar flexion of the foot and with the Bromage score; the intraoperative analgesia was determined as well. The development of sensory and motor blockade became faster and more intensive by addition of the two vasoconstrictors. The intraoperative analgesia, insufficient without vasoconstrictors, however, not to full satisfaction. Adrenaline improved the effects of etidocaine more than did ornipressine . The sole use of etidocaine without and with vasoconstrictors is not recommended for epidural anaesthesia for surgery of the lower extremities. It is the local anaesthetic of choice for intensifying motor blockade during already achieved analgesia.

Acetanilides↗

PubMed1992

Vasoconstrictors in local anesthesia for dentistry.

Addition of a vasoconstrictor to a local anesthetic may have several beneficial effects: a decrease in the peak plasma concentration of the local anesthetic agent, increase in the duration and the quality of anesthesia, reduction of the minimum concentration of anesthetic needed for nerve block, and decrease of blood loss during surgical procedures. The addition of a vasoconstrictor to a local anesthetic may also have detrimental effects. A review of the literature indicates that vasoconstrictor concentrations in local anesthetics marketed for dental use in the United States are not always optimal to achieve the purposes for which they are added. In most cases, a reduced concentration of vasoconstrictor could achieve the same goal as the marketed higher concentration, with less side-effect liability.

Amides↗

PubMed1997

[The differences of the cerebral and spinal vessels in sensitivity to PaCO2 and vasoconstrictors].

We investigated the differences in the response to arterial CO2 tension and vasoconstrictors between the cerebral and spinal vasculatures using cranial and spinal window technique which provided the direct observation of pial vessels. Pentobarbital anesthetized dogs (n = 18) (CO2 tension; n = 6 and vasoconstrictor; n = 12) were instrumented for measurement of pial vessel diameters by intravital microscopy in the cranial and spinal window preparation simultaneously. We achieved hypocarbia (20-25 mmHg) followed by adjusting CO2 levels for normocarbia (35-40 mmHg) and for hypercarbia (55-60 mmHg) using CO2 gas addition. After obtaining the desired PaCO2, the measurements were made. In the next experiment, we administered 2 different concentrations of epinephrine or phenylephrine solutions (1:2 x 10(6), 1:2 x 10(5)) through the window, and the measurement was made sequentially. The response of cerebral and spinal vasculature to change in PaCO2 was almost similar. Topical application of both drugs produced a significant constriction of spinal pial arterioles compared with the cerebral ones, while epinephrine but not phenylephrine constricted cerebral pial venules compared with spinal ones. These results suggest that the responses to vasoconstrictor of cerebral and spinal pial vessels are not similar, and high sensitivity of spinal arterioles to vasoconstrictors may possibly contribute to a risk of ischemic damage of the spinal cord.

Animals↗

PubMed1997

Vasoconstrictor-mediated increase in muscle resting thermogenesis is inhibited by membrane-stabilizing agents.

Norepinephrine and angiotensin II are potent vasoconstrictors and stimulate thermogenesis (oxygen uptake) as well as lactate and glycerol efflux in the constant-flow perfused rat hind limb at rest. However, the mechanism by which oxygen uptake (VO2) is increased is unknown, and it is not clear whether vasoconstriction is required for the increase in VO2 by the hind limb. In the present study the association between vasoconstriction and VO2 was further investigated, and a chance observation that high-dose propranolol selectively blocked vasoconstrictor-induced increase in VO2 was further explored. The norepinephrine-mediated increase in VO2 was totally blocked by either 50 microM (+)-propranolol or 50 microM (-)-propranolol (active beta-blocking enantiomer), but only (+)-propranolol reduced the vasoconstriction. Similarly, 100 microM (+/-)-propranolol (a dose likely to cause plasma membrane stabilizing effects involving interruption and (or) prevention of action potentials) blocked increases in VO2, lactate, and glycerol efflux by 5 nM angiotensin II (a nonadrenergic vasoconstrictor) with only marginal effects on pressure development. (+/-)-Propranolol (100 microM) had no effect on postequilibration red blood cell washout mediated by angiotensin II, a putative indicator of vasoconstrictor-induced redistribution of flow. Quinidine (260 microM) (an antiarrhythmic agent with membrane-stabilizing activity) inhibited only the increase in VO2, but neither nadolol (300 microM) nor atenolol (300 microM) (beta-blockers without membrane-stabilizing activity) inhibited VO2 or perfusion pressure increases produced by 5 nM angiotensin II. Veratridine (a membrane labilizer that is capable of evoking plasma membrane depolarization by maintaining voltage-gated Na+ channels in their open state) increased VO2 without vasoconstriction, and the increase in VO2 was blocked by 100 microM (+/-)-propranolol. It is concluded that the increase in hind-limb VO2 results from a destabilization of skeletal muscle plasma membranes. This can be achieved directly by veratridine or indirectly by angiotensin II, involving vasoconstriction and redistribution of flow. The findings suggest a novel mechanism for resting muscle thermogenesis.

Adrenergic beta-Antagonists↗