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Kaygısız Z. - One of the best experts on this subject based on the ideXlab platform.

  • Positive Inotropic, Positive chronotropic and coronary vasodilatory effects of rat amylin: mechanisms of amylin-induced Positive inotropy
    'Akademiai Kiado Zrt.', 2030
    Co-Authors: Kaygısız Z., Erkasap N., Ozden H., Koken T., Gunduz T., Ikizler M., Kural T.
    Abstract:

    Even though there are a few studies dealing with the cardiac effects of amylin, the mechanisms of amylin-induced Positive inotropy are not known well. Therefore, we investigated the possible signaling pathways underlying the amylin-induced Positive inotropy and compared the cardiac effects of rat amylin (rAmylin) and human amylin (hAmylin).Isolated rat hearts were perfused under constant flow condition and rAmylin or hAmylin was infused to the hearts. Coronary perfusion pressure, heart rate, left ventricular developed pressure and the maximum rate of increase of left ventricular pressure (+dP/dtmax) and the maximum rate of pressure decrease of left ventricle (−dP/dtmin) were measured.rAmylin at concentrations of 1, 10 or 100 nM markedly decreased coronary perfusion pressure, but increased heart rate, left ventricular developed pressure, +dP/dtmax and −dP/dtmin. The infusion of H-89 (50 μM), a protein kinase A (PKA) inhibitor did not change the rAmylin (100 nM)-induced Positive Inotropic effect. Both diltiazem (1 μM), an L-type Ca2+ channel blocker and ryanodine (10 nM), a sarcoplasmic reticulum (SR) Ca2+ release channel opener completely suppressed the rAmylin-induced Positive Inotropic effect, but staurosporine (100 nM), a potent protein kinase C (PKC) inhibitor suppressed it partially. hAmylin (1, 10 and 100 nM) had no significant effect on coronary perfusion pressure, heart rate and developed pressure, +dP/dtmax and -dP/dtmin. We concluded that rAmylin might have been produced vasodilatory, Positive chronotropic and Positive Inotropic effects on rat hearts. Ca2+ entry via L-type Ca2+ channels, activation of PKC and Ca2+ release from SR through ryanodine-sensitive Ca2+ channels may be involved in this Positive Inotropic effect. hAmylin may not produce any significant effect on perfusion pressure, heart rate and contractility in isolated, perfused rat hearts

  • The effect of adrenomedullin, amylin fragment8-37 and calcitonin gene-related peptide on contractile force, heart rate and coronary perfusion pressure in isolated rat hearts
    'Akademiai Kiado Zrt.', 2023
    Co-Authors: Kaygısız Z., Erkasap N., Uyar R., Kabadere S., Kabadere T.e., Dernek S.
    Abstract:

    The effect of human adrenomedullin, human amylin fragment8-37 and rat calcitonin gene-related pepted (CGRP)on contractile force, heart rate and coronary perfusion pressure has been investigated in the isolated perfused rat hearts. Adrenomedulllin (2x10-10, 2x10-9 and 2-10-8 M) produced a significant decrease in contractile force and perfusion pressure, but only the peptide caused a decline in heart rate at the highest dose. Amylin (10-9, 10-8 and 10-7 M) significantly increased and then decreased contractile force. Two doses of amylin (10-8 and 10-7 M) induced a significant increase in heart rate, however amylin did not change perfusion pressure in all the doses used. Rat aplha CGRP (10-8, 10-7 and 10-6 M) evoked a slight decline in contractile force following a significant increasing in contractile force induced by the peptide. CGRP in all the doses raised heart rate and lowered perfusion pressure. Our results suggest that adrenomedullin has negative Inotropic, negative chronotropic and coronary vasodilator actions. Amylin prduces a biphasic intropic effect and evokes a Positive chronotropy. CGRP causes Positive Inotropic, Positive chronotropic and vasodilatory effects in isolated rat hearts

Kural T. - One of the best experts on this subject based on the ideXlab platform.

  • Positive Inotropic, Positive chronotropic and coronary vasodilatory effects of rat amylin: mechanisms of amylin-induced Positive inotropy
    'Akademiai Kiado Zrt.', 2030
    Co-Authors: Kaygısız Z., Erkasap N., Ozden H., Koken T., Gunduz T., Ikizler M., Kural T.
    Abstract:

    Even though there are a few studies dealing with the cardiac effects of amylin, the mechanisms of amylin-induced Positive inotropy are not known well. Therefore, we investigated the possible signaling pathways underlying the amylin-induced Positive inotropy and compared the cardiac effects of rat amylin (rAmylin) and human amylin (hAmylin).Isolated rat hearts were perfused under constant flow condition and rAmylin or hAmylin was infused to the hearts. Coronary perfusion pressure, heart rate, left ventricular developed pressure and the maximum rate of increase of left ventricular pressure (+dP/dtmax) and the maximum rate of pressure decrease of left ventricle (−dP/dtmin) were measured.rAmylin at concentrations of 1, 10 or 100 nM markedly decreased coronary perfusion pressure, but increased heart rate, left ventricular developed pressure, +dP/dtmax and −dP/dtmin. The infusion of H-89 (50 μM), a protein kinase A (PKA) inhibitor did not change the rAmylin (100 nM)-induced Positive Inotropic effect. Both diltiazem (1 μM), an L-type Ca2+ channel blocker and ryanodine (10 nM), a sarcoplasmic reticulum (SR) Ca2+ release channel opener completely suppressed the rAmylin-induced Positive Inotropic effect, but staurosporine (100 nM), a potent protein kinase C (PKC) inhibitor suppressed it partially. hAmylin (1, 10 and 100 nM) had no significant effect on coronary perfusion pressure, heart rate and developed pressure, +dP/dtmax and -dP/dtmin. We concluded that rAmylin might have been produced vasodilatory, Positive chronotropic and Positive Inotropic effects on rat hearts. Ca2+ entry via L-type Ca2+ channels, activation of PKC and Ca2+ release from SR through ryanodine-sensitive Ca2+ channels may be involved in this Positive Inotropic effect. hAmylin may not produce any significant effect on perfusion pressure, heart rate and contractility in isolated, perfused rat hearts

Erkasap N. - One of the best experts on this subject based on the ideXlab platform.

  • Positive Inotropic, Positive chronotropic and coronary vasodilatory effects of rat amylin: mechanisms of amylin-induced Positive inotropy
    'Akademiai Kiado Zrt.', 2030
    Co-Authors: Kaygısız Z., Erkasap N., Ozden H., Koken T., Gunduz T., Ikizler M., Kural T.
    Abstract:

    Even though there are a few studies dealing with the cardiac effects of amylin, the mechanisms of amylin-induced Positive inotropy are not known well. Therefore, we investigated the possible signaling pathways underlying the amylin-induced Positive inotropy and compared the cardiac effects of rat amylin (rAmylin) and human amylin (hAmylin).Isolated rat hearts were perfused under constant flow condition and rAmylin or hAmylin was infused to the hearts. Coronary perfusion pressure, heart rate, left ventricular developed pressure and the maximum rate of increase of left ventricular pressure (+dP/dtmax) and the maximum rate of pressure decrease of left ventricle (−dP/dtmin) were measured.rAmylin at concentrations of 1, 10 or 100 nM markedly decreased coronary perfusion pressure, but increased heart rate, left ventricular developed pressure, +dP/dtmax and −dP/dtmin. The infusion of H-89 (50 μM), a protein kinase A (PKA) inhibitor did not change the rAmylin (100 nM)-induced Positive Inotropic effect. Both diltiazem (1 μM), an L-type Ca2+ channel blocker and ryanodine (10 nM), a sarcoplasmic reticulum (SR) Ca2+ release channel opener completely suppressed the rAmylin-induced Positive Inotropic effect, but staurosporine (100 nM), a potent protein kinase C (PKC) inhibitor suppressed it partially. hAmylin (1, 10 and 100 nM) had no significant effect on coronary perfusion pressure, heart rate and developed pressure, +dP/dtmax and -dP/dtmin. We concluded that rAmylin might have been produced vasodilatory, Positive chronotropic and Positive Inotropic effects on rat hearts. Ca2+ entry via L-type Ca2+ channels, activation of PKC and Ca2+ release from SR through ryanodine-sensitive Ca2+ channels may be involved in this Positive Inotropic effect. hAmylin may not produce any significant effect on perfusion pressure, heart rate and contractility in isolated, perfused rat hearts

  • The effect of adrenomedullin, amylin fragment8-37 and calcitonin gene-related peptide on contractile force, heart rate and coronary perfusion pressure in isolated rat hearts
    'Akademiai Kiado Zrt.', 2023
    Co-Authors: Kaygısız Z., Erkasap N., Uyar R., Kabadere S., Kabadere T.e., Dernek S.
    Abstract:

    The effect of human adrenomedullin, human amylin fragment8-37 and rat calcitonin gene-related pepted (CGRP)on contractile force, heart rate and coronary perfusion pressure has been investigated in the isolated perfused rat hearts. Adrenomedulllin (2x10-10, 2x10-9 and 2-10-8 M) produced a significant decrease in contractile force and perfusion pressure, but only the peptide caused a decline in heart rate at the highest dose. Amylin (10-9, 10-8 and 10-7 M) significantly increased and then decreased contractile force. Two doses of amylin (10-8 and 10-7 M) induced a significant increase in heart rate, however amylin did not change perfusion pressure in all the doses used. Rat aplha CGRP (10-8, 10-7 and 10-6 M) evoked a slight decline in contractile force following a significant increasing in contractile force induced by the peptide. CGRP in all the doses raised heart rate and lowered perfusion pressure. Our results suggest that adrenomedullin has negative Inotropic, negative chronotropic and coronary vasodilator actions. Amylin prduces a biphasic intropic effect and evokes a Positive chronotropy. CGRP causes Positive Inotropic, Positive chronotropic and vasodilatory effects in isolated rat hearts

Dernek S. - One of the best experts on this subject based on the ideXlab platform.

  • The effect of adrenomedullin, amylin fragment8-37 and calcitonin gene-related peptide on contractile force, heart rate and coronary perfusion pressure in isolated rat hearts
    'Akademiai Kiado Zrt.', 2023
    Co-Authors: Kaygısız Z., Erkasap N., Uyar R., Kabadere S., Kabadere T.e., Dernek S.
    Abstract:

    The effect of human adrenomedullin, human amylin fragment8-37 and rat calcitonin gene-related pepted (CGRP)on contractile force, heart rate and coronary perfusion pressure has been investigated in the isolated perfused rat hearts. Adrenomedulllin (2x10-10, 2x10-9 and 2-10-8 M) produced a significant decrease in contractile force and perfusion pressure, but only the peptide caused a decline in heart rate at the highest dose. Amylin (10-9, 10-8 and 10-7 M) significantly increased and then decreased contractile force. Two doses of amylin (10-8 and 10-7 M) induced a significant increase in heart rate, however amylin did not change perfusion pressure in all the doses used. Rat aplha CGRP (10-8, 10-7 and 10-6 M) evoked a slight decline in contractile force following a significant increasing in contractile force induced by the peptide. CGRP in all the doses raised heart rate and lowered perfusion pressure. Our results suggest that adrenomedullin has negative Inotropic, negative chronotropic and coronary vasodilator actions. Amylin prduces a biphasic intropic effect and evokes a Positive chronotropy. CGRP causes Positive Inotropic, Positive chronotropic and vasodilatory effects in isolated rat hearts

Ikizler M. - One of the best experts on this subject based on the ideXlab platform.

  • Positive Inotropic, Positive chronotropic and coronary vasodilatory effects of rat amylin: mechanisms of amylin-induced Positive inotropy
    'Akademiai Kiado Zrt.', 2030
    Co-Authors: Kaygısız Z., Erkasap N., Ozden H., Koken T., Gunduz T., Ikizler M., Kural T.
    Abstract:

    Even though there are a few studies dealing with the cardiac effects of amylin, the mechanisms of amylin-induced Positive inotropy are not known well. Therefore, we investigated the possible signaling pathways underlying the amylin-induced Positive inotropy and compared the cardiac effects of rat amylin (rAmylin) and human amylin (hAmylin).Isolated rat hearts were perfused under constant flow condition and rAmylin or hAmylin was infused to the hearts. Coronary perfusion pressure, heart rate, left ventricular developed pressure and the maximum rate of increase of left ventricular pressure (+dP/dtmax) and the maximum rate of pressure decrease of left ventricle (−dP/dtmin) were measured.rAmylin at concentrations of 1, 10 or 100 nM markedly decreased coronary perfusion pressure, but increased heart rate, left ventricular developed pressure, +dP/dtmax and −dP/dtmin. The infusion of H-89 (50 μM), a protein kinase A (PKA) inhibitor did not change the rAmylin (100 nM)-induced Positive Inotropic effect. Both diltiazem (1 μM), an L-type Ca2+ channel blocker and ryanodine (10 nM), a sarcoplasmic reticulum (SR) Ca2+ release channel opener completely suppressed the rAmylin-induced Positive Inotropic effect, but staurosporine (100 nM), a potent protein kinase C (PKC) inhibitor suppressed it partially. hAmylin (1, 10 and 100 nM) had no significant effect on coronary perfusion pressure, heart rate and developed pressure, +dP/dtmax and -dP/dtmin. We concluded that rAmylin might have been produced vasodilatory, Positive chronotropic and Positive Inotropic effects on rat hearts. Ca2+ entry via L-type Ca2+ channels, activation of PKC and Ca2+ release from SR through ryanodine-sensitive Ca2+ channels may be involved in this Positive Inotropic effect. hAmylin may not produce any significant effect on perfusion pressure, heart rate and contractility in isolated, perfused rat hearts