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Fritz R. Bühler - One of the best experts on this subject based on the ideXlab platform.
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Effects of peptide Vasoconstrictors on vessel structure.
The American journal of medicine, 1993Co-Authors: Alfred W. A. Hahn, Thérèse J. Resink, Eleanor J. Mackie, T. Scott-burden, Fritz R. BühlerAbstract:The peptide Vasoconstrictors angiotensin II and endothelin-1, originally described as being derived exclusively from the plasma renin-angiotensin system and vascular endothelium, respectively, have been demonstrated to be produced independently of these 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. There is increasing evidence that these locally produced vasoconstrictor peptides may contribute to blood vessel homeostasis, as well as the development of vascular pathologic conditions. Results obtained from pharmaceutical intervention in humans and animals of these systems strongly support this hypothesis. In addition to their vasoconstrictor properties, angiotensin II and endothelin-1 act as potent biologic effectors. In vitro, both vasoconstrictor peptides appear to modulate the activity of autocrine feedback loops in vascular smooth muscle cells. The activity of these feedback loops in vivo may represent a central mechanism for regulation and phenotypic differentiation of this cell type. The most well-established autocrine feedback loops of vascular smooth muscle cells are constituted by platelet-derived growth factor and transforming growth factor-beta, both of which are influenced by the action of angiotensin II and endothelin-1. The effects of the peptide Vasoconstrictors on the (auto-) regulated feedback loops are of long-term structural importance, since both Vasoconstrictors (via autocrine growth modulators) may influence the composition of the extracellular matrix of vascular smooth muscle cells. This includes effects on the synthesis and secretion of thrombospondin, fibronectin, tenascin, etc. The secretion of extracellular matrix glycoproteins themselves and incorporation into extracellular matrix in vitro appear to be linked to the activity of the autocrine feedback loops: e.g., stimulation of thrombospondin mRNA results in secretion of the glycoprotein only in the concomitant presence of exogenous platelet-derived growth factor, whereas the expression of fibronectin and tenascin may be directed by transforming growth factor-beta. The influence of angiotensin II and endothelin-1 on vascular smooth muscle cell surface receptor expression may represent a secondary mode of action of these vasoconstrictor peptides. Endothelin-1, for instance, can rapidly down-regulate platelet-derived growth factor-alpha receptor mRNA and both angiotensin II and endothelin-1, via induction of transforming growth factor-beta, may interrupt the platelet-derived growth factor based autocrine feedback loop. In vivo, the highly complex interactions between local and systemic vasoconstrictor production, autoregulated feedback loops, and extracellular matrix (which also serves as a reservoir for growth and differentiation modulators) are central to vessel homeostasis.(ABSTRACT TRUNCATED AT 400 WORDS)
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Peptide Vasoconstrictors, vessel structure, and vascular smooth-muscle proliferation.
Journal of Cardiovascular Pharmacology, 1993Co-Authors: Alfred W. A. Hahn, Thérèse J. Resink, Frances Kern, Fritz R. BühlerAbstract: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)
John A Yagiela - One of the best experts on this subject based on the ideXlab platform.
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randomized study of phentolamine mesylate for reversal of local anesthesia
Journal of Dental Research, 2008Co-Authors: M Laviola, S K Mcgavin, G A Freer, G Plancich, S C Woodbury, S Marinkovich, R Morrison, R B Rutherford, Al Reader, John A YagielaAbstract:Local anesthetic solutions frequently contain Vasoconstrictors to increase the depth and/or duration of anesthesia. Generally, the duration of soft-tissue anesthesia exceeds that of pulpal anesthesia. Negative consequences of soft-tissue anesthesia include accidental lip and tongue biting as well as difficulty in eating, drinking, speaking, and smiling. A double-blind, randomized, multicenter, Phase 2 study tested the hypothesis that local injection of the vasodilator phentolamine mesylate would shorten the duration of soft-tissue anesthesia following routine dental procedures. Participants (122) received one or two cartridges of local anesthetic/vasoconstrictor prior to dental treatment. Immediately after treatment, 1.8 mL of study drug (containing 0.4 mg phentolamine mesylate or placebo) was injected per cartridge of local anesthetic used. The phentolamine was well-tolerated and reduced the median duration of soft-tissue anesthesia in the lip from 155 to 70 min (p < 0.0001).
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Vasoconstrictors: indications and precautions.
Dental clinics of North America, 2002Co-Authors: Lenny W Naftalin, John A YagielaAbstract:Vasoconstrictors are useful additives to local anesthetic solutions. They can enhance the duration and quality of the anesthetic block while also decreasing surgical blood loss. Precautions must be taken, however, when using Vasoconstrictors with certain patients, especially those with cardiovascular disease. Several drug interactions must also be considered before administration of a local anesthetic with a vasoconstrictor, and special care must be taken when injecting such preparations in patients on nonspecific beta-adrenergic blockers, tricyclic antidepressants, catechol-O-methyltransferase inhibitors, cocaine, and certain general anesthetics. Lastly, in the patient with true sulfite allergy, local anesthetics without a vasoconstrictor should be used.
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Adverse drug interactions in dental practice: interactions associated with Vasoconstrictors. Part V of a series.
Journal of the American Dental Association, 1999Co-Authors: John A YagielaAbstract:BACKGROUND: Adrenergic Vasoconstrictors are commonly used by dentists to enhance the pain-relieving action of local anesthetics and to control local bleeding. Although normally considered safe for these applications, Vasoconstrictors can participate in drug interactions that potentially are harmful to patients. METHODS: The faculty of a March 1998 symposium entitled "Adverse Drug Interactions in Dentistry: Separating the Myths From the Facts" extensively reviewed the literature on drug interactions. They then established a significance rating of alleged adverse drug interactions pertaining to dentistry, based on the quality of documentation and severity of effect. The author of this article focused on the adrenergic Vasoconstrictors epinephrine and levonordefrin. RESULTS: Vasoconstrictor drug interactions involving tricyclic antidepressants, nonselective beta-adrenergic blocking drugs, certain general anesthetics and cocaine are well-documented in both humans and animals as having the potential for causing serious morbidity or death. Evidence for adverse interactions involving adrenergic neuronal blocking drugs, drugs with alpha-adrenergic blocking activity, local anesthetics and thyroid hormones is much less compelling, suggesting for the most part that clinically significant reactions may occur only when both the vasoconstrictor and the interacting drug are used in excessive doses. In the case of monoamine oxidase inhibitors, there is no credible evidence of a significant interaction with epinephrine or levonordefrin. CONCLUSIONS: Potentially serious adverse drug interactions involving adrenergic Vasoconstrictors can occur in dental practice. In most circumstances, careful administration of small doses of Vasoconstrictors and avoidance of gingival retraction cord containing epinephrine, coupled with monitoring of vita signs, will permit these drugs to be used with no risk or only minimally increased risk. Only in the case of cocaine intoxication must adrenergic Vasoconstrictors be avoided completely. CLINICAL IMPLICATIONS: For optimal patient safety, dentists must recognize potential drug interactions involving adrenergic Vasoconstrictors and modify their use of these agents accordingly.
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adverse drug interactions in dental practice interactions associated with Vasoconstrictors part v of a series
Journal of the American Dental Association, 1999Co-Authors: John A YagielaAbstract:ABSTRACT Background Adrenergic Vasoconstrictors are commonly used by dentists to enhance the pain-relieving action of local anesthetics and to control local bleeding. Although normally considered safe for these applications, Vasoconstrictors can participate in drug interactions that potentially are harmful to patients. Methods The faculty of a March 1998 symposium entitled “Adverse Drug Interactions in Dentistry: Separating the Myths From the Facts” extensively reviewed the literature on drug interactions. They then established a significance rating of alleged adverse drug interactions pertaining to dentistry, based on the quality of documentation and severity of effect. The author of this article focused on the adrenergic Vasoconstrictors epinephrine and levonordefrin. Results Vasoconstrictor drug interactions involving tricyclic antidepressants, nonselective β-adrenergic blocking drugs, certain general anesthetics and cocaine are well-documented in both humans and animals as having the potential for causing serious morbidity or death. Evidence for adverse interactions involving adrenergic neuronal blocking drugs, drugs with α-adrenergic blocking activity, local anesthetics and thyroid hormones is much less compelling, suggesting for the most part that clinically significant reactions may occur only when both the vasoconstrictor and the interacting drug are used in excessive doses. In the case of monoamine oxidase inhibitors, there is no credible evidence of a significant interaction with epinephrine or levonordefrin. Conclusions Potentially serious adverse drug interactions involving adrenergic Vasoconstrictors can occur in dental practice. In most circumstances, careful administration of small doses of Vasoconstrictors and avoidance of gingival retraction cord containing epinephrine, coupled with monitoring of vital signs, will permit these drugs to be used with no risk or only minimally increased risk. Only in the case of cocaine intoxication must adrenergic Vasoconstrictors be avoided completely. Clinical Implications For optimal patient safety, dentists must recognize potential drug interactions involving adrenergic Vasoconstrictors and modify their use of these agents accordingly.
Alfred W. A. Hahn - One of the best experts on this subject based on the ideXlab platform.
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Effects of peptide Vasoconstrictors on vessel structure.
The American journal of medicine, 1993Co-Authors: Alfred W. A. Hahn, Thérèse J. Resink, Eleanor J. Mackie, T. Scott-burden, Fritz R. BühlerAbstract:The peptide Vasoconstrictors angiotensin II and endothelin-1, originally described as being derived exclusively from the plasma renin-angiotensin system and vascular endothelium, respectively, have been demonstrated to be produced independently of these 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. There is increasing evidence that these locally produced vasoconstrictor peptides may contribute to blood vessel homeostasis, as well as the development of vascular pathologic conditions. Results obtained from pharmaceutical intervention in humans and animals of these systems strongly support this hypothesis. In addition to their vasoconstrictor properties, angiotensin II and endothelin-1 act as potent biologic effectors. In vitro, both vasoconstrictor peptides appear to modulate the activity of autocrine feedback loops in vascular smooth muscle cells. The activity of these feedback loops in vivo may represent a central mechanism for regulation and phenotypic differentiation of this cell type. The most well-established autocrine feedback loops of vascular smooth muscle cells are constituted by platelet-derived growth factor and transforming growth factor-beta, both of which are influenced by the action of angiotensin II and endothelin-1. The effects of the peptide Vasoconstrictors on the (auto-) regulated feedback loops are of long-term structural importance, since both Vasoconstrictors (via autocrine growth modulators) may influence the composition of the extracellular matrix of vascular smooth muscle cells. This includes effects on the synthesis and secretion of thrombospondin, fibronectin, tenascin, etc. The secretion of extracellular matrix glycoproteins themselves and incorporation into extracellular matrix in vitro appear to be linked to the activity of the autocrine feedback loops: e.g., stimulation of thrombospondin mRNA results in secretion of the glycoprotein only in the concomitant presence of exogenous platelet-derived growth factor, whereas the expression of fibronectin and tenascin may be directed by transforming growth factor-beta. The influence of angiotensin II and endothelin-1 on vascular smooth muscle cell surface receptor expression may represent a secondary mode of action of these vasoconstrictor peptides. Endothelin-1, for instance, can rapidly down-regulate platelet-derived growth factor-alpha receptor mRNA and both angiotensin II and endothelin-1, via induction of transforming growth factor-beta, may interrupt the platelet-derived growth factor based autocrine feedback loop. In vivo, the highly complex interactions between local and systemic vasoconstrictor production, autoregulated feedback loops, and extracellular matrix (which also serves as a reservoir for growth and differentiation modulators) are central to vessel homeostasis.(ABSTRACT TRUNCATED AT 400 WORDS)
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Peptide Vasoconstrictors, vessel structure, and vascular smooth-muscle proliferation.
Journal of Cardiovascular Pharmacology, 1993Co-Authors: Alfred W. A. Hahn, Thérèse J. Resink, Frances Kern, Fritz R. BühlerAbstract: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)
Paul E. Rolan - One of the best experts on this subject based on the ideXlab platform.
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Drug Interactions with Triptans
CNS Drugs, 2012Co-Authors: Paul E. RolanAbstract:The triptans are a group of compounds with high efficacy for the acute treatment of migraine and cluster headache. They have a relatively wide therapeutic index, and although a number of minor pharmacokinetic interactions have been observed, few are likely to be clinically significant. Given the differences in principal elimination pathways, potentially interacting drugs on a pharmacokinetic basis are not common across all compounds. Of more concern than pharmacokinetic interactions are pharmacodynamic interactions. Of most concern, additive vasoconstrictor effects are likely to occur with other Vasoconstrictors, especially the ergots used for migraine. Serotonin syndrome has been observed due to coadministration of triptans with selective serotonin reuptake inhibitors (SSRIs), but the absolute rate of such a clinical response to coadministration is probably low. Most patients can take triptans with other medications without dose alteration, although vigilance is required for pharmacodynamic interactions.
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drug interactions with triptans which are clinically significant
CNS Drugs, 2012Co-Authors: Paul E. RolanAbstract:The triptans are a group of compounds with high efficacy for the acute treatment of migraine and cluster headache. They have a relatively wide therapeutic index, and although a number of minor pharmacokinetic interactions have been observed, few are likely to be clinically significant. Given the differences in principal elimination pathways, potentially interacting drugs on a pharmacokinetic basis are not common across all compounds. Of more concern than pharmacokinetic interactions are pharmacodynamic interactions. Of most concern, additive vasoconstrictor effects are likely to occur with other Vasoconstrictors, especially the ergots used for migraine. Serotonin syndrome has been observed due to coadministration of triptans with selective serotonin reuptake inhibitors (SSRIs), but the absolute rate of such a clinical response to coadministration is probably low. Most patients can take triptans with other medications without dose alteration, although vigilance is required for pharmacodynamic interactions.
John C. Mcgiff - One of the best experts on this subject based on the ideXlab platform.
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Chloride anion concentration as a determinant of renal vascular responsiveness to vasoconstrictor agents.
British journal of pharmacology, 1993Co-Authors: Caroline P. Quilley, Yu‐shi R. Lin, John C. McgiffAbstract: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.
