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American Journal of Physiology.... Jun 2003
Topics: Animals; Atrial Natriuretic Factor; Enzyme Activation; Guanylate Cyclase; Mice; Muscle, Smooth, Vascular; Rats; Spleen; Vasoconstriction
PubMed: 12736171
DOI: 10.1152/ajpregu.00141.2003 -
Anesthesiology May 1990This study tested the hypothesis that the threshold for thermoregulatory vasoconstriction is lowered as isoflurane concentration increases, but the intensity of...
This study tested the hypothesis that the threshold for thermoregulatory vasoconstriction is lowered as isoflurane concentration increases, but the intensity of vasoconstriction, once triggered, is well preserved during isoflurane anesthesia. The thermoregulatory threshold was prospectively defined as the central temperature at which vasoconstriction occurred, and significant vasoconstriction was defined as a skin-surface temperature gradient (forearm-fingertip) greater than or equal to 4 degrees C. The threshold for thermoregulatory vasoconstriction and the intensity of vasoconstriction, measured as maximum skin-temperature gradient, was determined in six unpremedicated patients electively donating a kidney during isoflurane anesthesia, and in four healthy, awake volunteers. All anesthetized patients were deliberately cooled and became hypothermic. Vasoconstriction occurred in five of six at central temperatures between 35.3 and 32.4 degrees C, at end-tidal isoflurane concentrations between 0.74 and 1.65%. The patient who did not vasoconstrict received the highest isoflurane concentration (approximately 2.5%) and reached a central temperature of 31 degrees C. Unanesthetized volunteers also were exposed to cold and each vasoconstricted at a temperature near 37 degrees C. The threshold for thermoregulatory cutaneous vasoconstriction was inversely correlated with anesthetic dose, the thermoregulatory threshold decreasing approximately 3 degrees C/% isoflurane concentration. There were no statistically significant differences between maximum skin-surface temperature gradients in awake volunteers and patients given isoflurane, or between any of the groups when patients from previous studies given halothane or nitrous oxide/fentanyl anesthesia were included in the comparison. These data indicate that the intensity of vasoconstriction, once triggered, is similar during several different types of anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)
Topics: Adult; Anesthesia, Inhalation; Body Temperature Regulation; Female; Humans; Hyperthermia, Induced; Isoflurane; Kidney Transplantation; Male; Middle Aged; Tissue Donors; Vasoconstriction
PubMed: 2339798
DOI: 10.1097/00000542-199005000-00009 -
British Journal of Pharmacology Mar 19951. In anaesthetized dogs, intra-left atrial administration of 5-hydroxytryptamine (5-HT) and selected tryptamine analogues (5-carboxamidotryptamine, 5-CT; 5-methyl...
1. In anaesthetized dogs, intra-left atrial administration of 5-hydroxytryptamine (5-HT) and selected tryptamine analogues (5-carboxamidotryptamine, 5-CT; 5-methyl tryptamine, 5-MT; alpha-methyl 5-hydroxytryptamine, alpha-HT; sumatriptan, Sum) in the presence of ketanserin and MDL72222 (5-HT2 and 5-HT3 receptor antagonists, respectively), produced dose-related changes in carotid, coronary and renal vascular conductance mediated by vascular 5-HT1-like receptors. 2. In the carotid vascular bed, 5-HT, 5-MT, alpha-HT and Sum were vasoconstrictors with a rank order of potency (comparing ED50 values) of 5-HT = Sum > 5-MT > alpha-HT. By contrast in this vascular bed, 5-CT was a potent vasodilator. 3. In the coronary vascular bed, 5-HT, 5-CT, 5-MT and alpha-HT were vasodilators with a rank order of potency (comparing ED50 values) of 5-CT > 5-HT > 5-MT > alpha-HT. In this vascular bed, Sum was without effect. 4. In the renal vascular bed, 5-HT, 5-CT, 5-MT, alpha-HT and Sum were vasoconstrictors with a rank order of potency (comparing ED50 values) of 5-CT > 5-HT > Sum > 5-MT > alpha-HT. 5. The coronary (and carotid) vasodilator responses to 5-CT were antagonized by the 5-HT1-like receptor antagonists, spiperone (1 mg kg-1) and methiothepin (0.1 mg kg-1), whereas the renal vasoconstrictor responses to this tryptamine analogue were antagonized only by methiothepin. 6. It is concluded from these studies that agonist finger-printing in vivo, using tryptamine analogues,identifies and confirms the functional presence of at least two pharmacologically distinct subtypes of the 5-HT1-like receptor in the intact canine cardiovascular system. These two subtypes are located on the vascular smooth muscle and mediate direct vasoconstriction and vasodilatation responses in vivo.7. In addition, these studies confirm that the distribution of these subtypes within the major vascular beds, shows a marked heterogeneity. The carotid vascular responses to the tryptamine analogue sindicate the presence of both the vasodilator and the vasoconstrictor subtypes. The coronary vascular responses to these analogues are, however, consistent with presence of the vasodilator subtype, only. By contrast, the renal vascular responses to these analogues indicates only the presence of the vasoconstrictor subtype.
Topics: Animals; Cardiovascular Physiological Phenomena; Cardiovascular System; Carotid Arteries; Coronary Vessels; Dogs; Dose-Response Relationship, Drug; Male; Muscle, Smooth, Vascular; Receptors, Serotonin; Renal Circulation; Serotonin Antagonists; Serotonin Receptor Agonists; Tryptamines; Vasoconstriction; Vasodilation
PubMed: 7780651
DOI: 10.1111/j.1476-5381.1995.tb13298.x -
Critical Care (London, England) 2006In the current issue of Critical Care, Friesenecker and colleagues present a well-designed comparative study on the microvascular effects of arginine vasopressin (AVP)... (Comparative Study)
Comparative Study Review
In the current issue of Critical Care, Friesenecker and colleagues present a well-designed comparative study on the microvascular effects of arginine vasopressin (AVP) and norepinephrine (NE) in a physiological, unanesthetized hamster model. The authors clearly demonstrate that AVP, but not NE, has marked vasoconstrictive effects on large arterioles, whereas the impact on small arterioles is comparable for both vasopressors. However, it remains unclear if these results, per se, reflect a stronger vasopressive potential of AVP versus NE, as macrohemodynamic variables were not different between study groups. Since the authors did not investigate the effects of AVP and NE in vasodilatory shock states, the microcirculatory response in sepsis or systemic inflammatory response syndrome remains inconclusive. The same authors previously reported that AVP infusion in patients suffering from vasodilatory shock carries the risk for ischemic skin lesions. This in turn raises the question whether the quality of vasopressors should be judged by their potency.
Topics: Animals; Arginine Vasopressin; Humans; Norepinephrine; Vasoconstriction
PubMed: 16732898
DOI: 10.1186/cc4942 -
Journal of the American College of... Jan 1992
Topics: Acetylcholine; Angina Pectoris; Coronary Circulation; Humans; Vasoconstriction; Vasodilation
PubMed: 1729342
DOI: 10.1016/0735-1097(92)90047-q -
Autonomic Neuroscience : Basic &... Oct 2011Pilocarpine (cholinergic muscarinic agonist) injected peripherally may act centrally to produce pressor responses; in the present study, using c-fos immunoreactive...
Pilocarpine (cholinergic muscarinic agonist) injected peripherally may act centrally to produce pressor responses; in the present study, using c-fos immunoreactive expression, we investigated the forebrain and brainstem areas activated by pressor doses of intravenous (i.v.) pilocarpine. In addition, the importance of vasopressin secretion and/or sympathetic activation and the effects of lesions in the anteroventral third ventricle (AV3V) region in awake rats were also investigated. In male Holtzman rats, pilocarpine (0.04 to 4μmol/kg b.w.) i.v. induced transitory hypotension followed by long lasting hypertension. Sympathetic blockade with prazosin (1mg/kg b.w.) i.v. or AV3V lesions (1 day) almost abolished the pressor response to i.v. pilocarpine (2μmol/kg b.w.), whereas the vasopressin antagonist (10μg/kg b.w.) i.v. reduced the response to pilocarpine. Pilocarpine (2 and 4μmol/kg b.w.) i.v. increased the number of c-fos immunoreactive cells in the subfornical organ, paraventricular and supraoptic nuclei of the hypothalamus, organ vasculosum of the lamina terminalis, median preoptic nucleus, nucleus of the solitary tract and caudal and rostral ventrolateral medulla. These data suggest that i.v. pilocarpine activates specific forebrain and brainstem mechanisms increasing sympathetic activity and vasopressin secretion to induce pressor response.
Topics: Animals; Blood Pressure; Brain Stem; Male; Muscarinic Agonists; Pilocarpine; Prosencephalon; Rats; Rats, Sprague-Dawley; Vasoconstriction
PubMed: 21689994
DOI: 10.1016/j.autneu.2011.05.008 -
American Journal of Physiology. Cell... Oct 2010Hydrogen sulfide (H(2)S), an endogenous gaseous mediator, produces both vasorelaxation and vasoconstriction at different concentrations. We found in the present study...
Hydrogen sulfide (H(2)S), an endogenous gaseous mediator, produces both vasorelaxation and vasoconstriction at different concentrations. We found in the present study that NaHS, an H(2)S donor, produced stronger vasorelaxant and weaker vasoconstrictive effects in HEPES solution compared with those achieved in Krebs solution. We further screened the buffer components and found that bicarbonate (HCO(3)(-)) was the ion to influence the effect of H(2)S. After examining the vasorelaxant effects of acetylcholine, a vasodilator by releasing nitric oxide, and isoprenaline, a β-adrenoceptor agonist, in HEPES and Krebs buffers, we found the HCO(3)(-)-dependent effect was specific to H(2)S. Blockade of anion exchanger-2 activity with 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS) or with HCO(3)(-)-free solution abolished the vasoconstrictive effect of NaHS. Moreover, NaHS decreased nitric oxide level in the rat aorta in HCO(3)(-)-containing buffer, but this effect was abolished by HCO(3)(-)-free buffer or DIDS. In summary, we found for the first time that H(2)S stimulates anion exchanger to transport extracellular HCO(3)(-) in exchange for intracellular superoxide anions, which may further inactivate nitric oxide and induces vasoconstriction.
Topics: 1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt; 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid; Adrenergic beta-Agonists; Air Pollutants; Albuterol; Animals; Aorta; Bicarbonates; Buffers; Electrophysiology; Hydrogen Sulfide; Indicators and Reagents; Male; Nitric Oxide; Rats; Rats, Sprague-Dawley; Vasoconstriction; Vasodilation
PubMed: 20660164
DOI: 10.1152/ajpcell.00105.2010 -
Internal Medicine (Tokyo, Japan) 2016We encountered two patients with sumatriptan-induced reversible cerebral vasoconstriction syndrome (RCVS). The present patients were taking sumatriptan for the first... (Review)
Review
We encountered two patients with sumatriptan-induced reversible cerebral vasoconstriction syndrome (RCVS). The present patients were taking sumatriptan for the first time because they had been tentatively diagnosed with a migraine. On reviewing the literature, we found nine other cases of triptan-induced RCVS, predominantly among women aged 30 to 40 years. RCVS has been precipitated by triptan at the first ever use, after daily use, and even with long-term use at a normal dose. Patients with acute onset of severe headache should be thoroughly evaluated, and triptan should be administered appropriately. If triptan-induced RCVS is suspected, vascular imaging should be repeated after several days.
Topics: Adult; Female; Humans; Magnetic Resonance Imaging; Syndrome; Tomography, X-Ray Computed; Tryptamines; Vasoconstriction; Vasospasm, Intracranial
PubMed: 27904122
DOI: 10.2169/internalmedicine.55.7185 -
British Journal of Pharmacology Nov 2013Endothelin (ET)-1 and ET-2 cause potent long-lasting vasoconstrictions by tight binding to smooth muscle ETA receptors. We tested the hypotheses that different...
BACKGROUND AND PURPOSE
Endothelin (ET)-1 and ET-2 cause potent long-lasting vasoconstrictions by tight binding to smooth muscle ETA receptors. We tested the hypotheses that different mechanisms mediate initiation and maintenance of arterial contractile responses to ET-1 and ET-2 and that this differs among vascular beds.
EXPERIMENTAL APPROACH
Segments of rat mesenteric resistance artery (MRA) and basilar artery (BA) were studied in wire myographs with and without functional antagonists.
KEY RESULTS
Sensitivity and maximum of MRA contractile responses to ET-1 were not, or only moderately, reduced by stimulation of soluble GC, AC or K(+) -channels and by an inhibitor of receptor-operated ion channels. However, each of these reduced maintenance of ET-1 effects and relaxed ET-1-induced contractions in MRA. A calcium channel antagonist did not alter sensitivity, maximum and maintenance of ET-1 effects, but relaxed ET-1-induced contractions in MRA. A PLC inhibitor prevented contractile responses to ET-1 and ET-2 in MRA and BA, and relaxed ET-1- and ET-2-induced responses in MRA and ET-1 effects in BA. A Rho-kinase inhibitor did not modify sensitivity, maximum and maintenance of responses to both peptides in both arteries but relaxed ET-2, but not ET-1, effects in MRA and ET-1 effects in BA.
CONCLUSIONS AND IMPLICATIONS
PLC played a key role in arterial contractile responses to ETs, but ET-1 and ET-2 initiated and maintained vasoconstriction through different mechanisms, and these differed between MRA and BA. Selective functional antagonism may be considered for agonist- and vascular bed selective pharmacotherapy of ET-related diseases.
Topics: 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; Animals; Cerebral Arteries; Endothelin-1; Endothelin-2; Estrenes; Male; Mesenteric Arteries; Phosphodiesterase Inhibitors; Protein Kinase Inhibitors; Pyrrolidinones; Rats; Rats, Inbred WKY; Type C Phospholipases; Vasoconstriction; rho-Associated Kinases
PubMed: 23941276
DOI: 10.1111/bph.12332 -
Journal of Physiology and Pharmacology... Oct 2017Hydrogen sulfide (HS) has recently emerged as a biologically active gas with multiple effects on the cardiovascular system. We aimed to investigate the vasomotor actions...
Hydrogen sulfide (HS) has recently emerged as a biologically active gas with multiple effects on the cardiovascular system. We aimed to investigate the vasomotor actions of sodium sulfide (NaS), which forms HS and HS in solution, in human umbilical artery (HUA) and vein (HUV) rings. In addition, we examined by immunocytochemistry the expression and localization of cystathionine β-synthase (CBS), cystathionine lyase (CSE), and 3-mercaptopyruvate sulphurtransferase (MPST), the enzymes responsible for endogenous HS production. Human umbilical vessels were compared with chicken embryo umbilical vessels. HUA and HUV expressed a robust signal for CSE, CBS, and 3-MPST in both endothelial and smooth muscle cells. However, HUA rings did not respond to NaS (10-10) either at resting tone or during contraction evoked by serotonin or KCl. Similarly, the extraembryonic part of chicken allantoic artery did not respond to NaS. In contrast, NaS induced a concentration-dependent contraction in HUV rings under resting tone and a concentration-dependent relaxation when the HUV rings were contracted with serotonin (42 ± 5% relaxation) or KCl (12 ± 5% relaxation). NaS-induced contraction of HUV was impaired following removal of extracellular Ca, endothelial denudation, NO synthase inhibition (L-NAME), or soluble guanylate cyclase (sGC) inhibition (ODQ). NaS-induced relaxation of HUV was impaired by the K channel inhibitor glibenclamide. In conclusion, HS does not have vasomotor effects on HUA but induced contraction (mediated through inactivation of the NO/sGC axis) and relaxation (mediated through K channels) in HUV. Our data suggest a role for HS in the venous side of human umbilical circulation.
Topics: Animals; Chick Embryo; Dose-Response Relationship, Drug; Humans; Hydrogen Sulfide; Myocytes, Smooth Muscle; Organ Culture Techniques; Umbilical Arteries; Umbilical Cord; Umbilical Veins; Vasoconstriction; Vasodilation
PubMed: 29375049
DOI: No ID Found