The Experts below are selected from a list of 138 Experts worldwide ranked by ideXlab platform

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

  • Effects of the Phosphodiesterase-IV Inhibitor EMD 95832/3 on tumour growth and cachexia in rats bearing the Yoshida AH-130 ascites hepatoma.
    Cancer letters, 2002
    Co-Authors: Bas Meijsing, Neus Carbó, Francisco J López-soriano, Josep M Argilés
    Abstract:

    Administration of the Phosphodiesterase-IV Inhibitor EMD 95832/3 (Merck KGaA, Darmstadt, Germany) to rats bearing the ascites hepatoma Yoshida AH-130, a highly cachectic tumour, could not prevent either the anorexia nor the massIVe weight loss (affecting both adipose and skeletal muscle tissues) present in the tumour-bearing animals. This compound did not have any effects on the fractional rates of protein turnover in skeletal muscle, and did not affect circulating triacylglycerols or lipoprotein lipase actIVity in adipose tissue. Although the administration of EMD 95832/3 did not influence tumour growth either, it did increase the number of tumour cells undergoing apoptosis. It is concluded that the drug is unable to reverse the cachectic state in this particular experimental tumour model.

  • effects of the Phosphodiesterase IV Inhibitor emd 95832 3 on tumour growth and cachexia in rats bearing the yoshida ah 130 ascites hepatoma
    Cancer Letters, 2002
    Co-Authors: Bas Meijsing, Neus Carbó, Francisco J Lopezsoriano, Josep M Argilés
    Abstract:

    Administration of the Phosphodiesterase-IV Inhibitor EMD 95832/3 (Merck KGaA, Darmstadt, Germany) to rats bearing the ascites hepatoma Yoshida AH-130, a highly cachectic tumour, could not prevent either the anorexia nor the massIVe weight loss (affecting both adipose and skeletal muscle tissues) present in the tumour-bearing animals. This compound did not have any effects on the fractional rates of protein turnover in skeletal muscle, and did not affect circulating triacylglycerols or lipoprotein lipase actIVity in adipose tissue. Although the administration of EMD 95832/3 did not influence tumour growth either, it did increase the number of tumour cells undergoing apoptosis. It is concluded that the drug is unable to reverse the cachectic state in this particular experimental tumour model.

Bas Meijsing - One of the best experts on this subject based on the ideXlab platform.

  • Effects of the Phosphodiesterase-IV Inhibitor EMD 95832/3 on tumour growth and cachexia in rats bearing the Yoshida AH-130 ascites hepatoma.
    Cancer letters, 2002
    Co-Authors: Bas Meijsing, Neus Carbó, Francisco J López-soriano, Josep M Argilés
    Abstract:

    Administration of the Phosphodiesterase-IV Inhibitor EMD 95832/3 (Merck KGaA, Darmstadt, Germany) to rats bearing the ascites hepatoma Yoshida AH-130, a highly cachectic tumour, could not prevent either the anorexia nor the massIVe weight loss (affecting both adipose and skeletal muscle tissues) present in the tumour-bearing animals. This compound did not have any effects on the fractional rates of protein turnover in skeletal muscle, and did not affect circulating triacylglycerols or lipoprotein lipase actIVity in adipose tissue. Although the administration of EMD 95832/3 did not influence tumour growth either, it did increase the number of tumour cells undergoing apoptosis. It is concluded that the drug is unable to reverse the cachectic state in this particular experimental tumour model.

  • effects of the Phosphodiesterase IV Inhibitor emd 95832 3 on tumour growth and cachexia in rats bearing the yoshida ah 130 ascites hepatoma
    Cancer Letters, 2002
    Co-Authors: Bas Meijsing, Neus Carbó, Francisco J Lopezsoriano, Josep M Argilés
    Abstract:

    Administration of the Phosphodiesterase-IV Inhibitor EMD 95832/3 (Merck KGaA, Darmstadt, Germany) to rats bearing the ascites hepatoma Yoshida AH-130, a highly cachectic tumour, could not prevent either the anorexia nor the massIVe weight loss (affecting both adipose and skeletal muscle tissues) present in the tumour-bearing animals. This compound did not have any effects on the fractional rates of protein turnover in skeletal muscle, and did not affect circulating triacylglycerols or lipoprotein lipase actIVity in adipose tissue. Although the administration of EMD 95832/3 did not influence tumour growth either, it did increase the number of tumour cells undergoing apoptosis. It is concluded that the drug is unable to reverse the cachectic state in this particular experimental tumour model.

I A Reid - One of the best experts on this subject based on the ideXlab platform.

  • stimulation of renin secretion by the Phosphodiesterase IV Inhibitor rolipram
    Journal of Pharmacology and Experimental Therapeutics, 1996
    Co-Authors: N Chiu, Ina U. Park, I A Reid
    Abstract:

    It is now generally accepted that the renin secretory response to beta adrenoceptor stimulation is mediated by increased formation of cAMP in the juxtaglomerular cells. It is also known that renin secretion is increased when cAMP metabolism is decreased by Phosphodiesterase Inhibitors such as theophylline, but it is not known which isoforms of Phosphodiesterase are involved. In the present study, we investigated the effect on renin secretion of the Phosphodiesterase IV Inhibitor rolipram in conscious rabbits. The i.v. administration of rolipram in a dose of 25 microgram/kg followed by infusion at 5 microgram/kg/min in eight rabbits increased mean arterial pressure from 82 +/- 5 to 93 +/- 6 mm Hg (P<.05), decreased HR from 242 +/- 7 to 204 +/- 10 bpm (P<.05) and increased plasma renin actIVity (PRA) from 6.9 +/- 1.3 to 29.0 +/- 4.2 ng/ml/2 h (P<.01). In a second series of experiments, i.v. infusion of isoproterenol at 0.05 microgram/kg/min increased PRA from 4.1 +/- 0.9 to 9.9 +/- 1.2 ng/ml/2 h (P<.01). Administration of rolipram again increased PRA, and infusion of isoproterenol in the presence of rolipram increased PRA from 30.2 +/- 7.0 to 58.9 +/- 12.6 ng/ml/2 h (P<.01), an increase significantly greater (P<.05) than that produced by isoproterenol alone. Rolipram also prolonged the PRA and HR responses to isoproterenol. These results demonstrate that inhibition of Phosphodiesterase IV increases renin secretion and potentiates the renin secretory response to beta adrenoceptor stimulation, thus providing evidence for a role of Phosphodiesterase IV in the regulation of renin secretion.

  • Stimulation of renin secretion by the Phosphodiesterase IV Inhibitor rolipram.
    The Journal of pharmacology and experimental therapeutics, 1996
    Co-Authors: N Chiu, Ina U. Park, I A Reid
    Abstract:

    It is now generally accepted that the renin secretory response to beta adrenoceptor stimulation is mediated by increased formation of cAMP in the juxtaglomerular cells. It is also known that renin secretion is increased when cAMP metabolism is decreased by Phosphodiesterase Inhibitors such as theophylline, but it is not known which isoforms of Phosphodiesterase are involved. In the present study, we investigated the effect on renin secretion of the Phosphodiesterase IV Inhibitor rolipram in conscious rabbits. The i.v. administration of rolipram in a dose of 25 microgram/kg followed by infusion at 5 microgram/kg/min in eight rabbits increased mean arterial pressure from 82 +/- 5 to 93 +/- 6 mm Hg (P

Neus Carbó - One of the best experts on this subject based on the ideXlab platform.

  • Effects of the Phosphodiesterase-IV Inhibitor EMD 95832/3 on tumour growth and cachexia in rats bearing the Yoshida AH-130 ascites hepatoma.
    Cancer letters, 2002
    Co-Authors: Bas Meijsing, Neus Carbó, Francisco J López-soriano, Josep M Argilés
    Abstract:

    Administration of the Phosphodiesterase-IV Inhibitor EMD 95832/3 (Merck KGaA, Darmstadt, Germany) to rats bearing the ascites hepatoma Yoshida AH-130, a highly cachectic tumour, could not prevent either the anorexia nor the massIVe weight loss (affecting both adipose and skeletal muscle tissues) present in the tumour-bearing animals. This compound did not have any effects on the fractional rates of protein turnover in skeletal muscle, and did not affect circulating triacylglycerols or lipoprotein lipase actIVity in adipose tissue. Although the administration of EMD 95832/3 did not influence tumour growth either, it did increase the number of tumour cells undergoing apoptosis. It is concluded that the drug is unable to reverse the cachectic state in this particular experimental tumour model.

  • effects of the Phosphodiesterase IV Inhibitor emd 95832 3 on tumour growth and cachexia in rats bearing the yoshida ah 130 ascites hepatoma
    Cancer Letters, 2002
    Co-Authors: Bas Meijsing, Neus Carbó, Francisco J Lopezsoriano, Josep M Argilés
    Abstract:

    Administration of the Phosphodiesterase-IV Inhibitor EMD 95832/3 (Merck KGaA, Darmstadt, Germany) to rats bearing the ascites hepatoma Yoshida AH-130, a highly cachectic tumour, could not prevent either the anorexia nor the massIVe weight loss (affecting both adipose and skeletal muscle tissues) present in the tumour-bearing animals. This compound did not have any effects on the fractional rates of protein turnover in skeletal muscle, and did not affect circulating triacylglycerols or lipoprotein lipase actIVity in adipose tissue. Although the administration of EMD 95832/3 did not influence tumour growth either, it did increase the number of tumour cells undergoing apoptosis. It is concluded that the drug is unable to reverse the cachectic state in this particular experimental tumour model.

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

  • stimulation of renin secretion by the Phosphodiesterase IV Inhibitor rolipram
    Journal of Pharmacology and Experimental Therapeutics, 1996
    Co-Authors: N Chiu, Ina U. Park, I A Reid
    Abstract:

    It is now generally accepted that the renin secretory response to beta adrenoceptor stimulation is mediated by increased formation of cAMP in the juxtaglomerular cells. It is also known that renin secretion is increased when cAMP metabolism is decreased by Phosphodiesterase Inhibitors such as theophylline, but it is not known which isoforms of Phosphodiesterase are involved. In the present study, we investigated the effect on renin secretion of the Phosphodiesterase IV Inhibitor rolipram in conscious rabbits. The i.v. administration of rolipram in a dose of 25 microgram/kg followed by infusion at 5 microgram/kg/min in eight rabbits increased mean arterial pressure from 82 +/- 5 to 93 +/- 6 mm Hg (P<.05), decreased HR from 242 +/- 7 to 204 +/- 10 bpm (P<.05) and increased plasma renin actIVity (PRA) from 6.9 +/- 1.3 to 29.0 +/- 4.2 ng/ml/2 h (P<.01). In a second series of experiments, i.v. infusion of isoproterenol at 0.05 microgram/kg/min increased PRA from 4.1 +/- 0.9 to 9.9 +/- 1.2 ng/ml/2 h (P<.01). Administration of rolipram again increased PRA, and infusion of isoproterenol in the presence of rolipram increased PRA from 30.2 +/- 7.0 to 58.9 +/- 12.6 ng/ml/2 h (P<.01), an increase significantly greater (P<.05) than that produced by isoproterenol alone. Rolipram also prolonged the PRA and HR responses to isoproterenol. These results demonstrate that inhibition of Phosphodiesterase IV increases renin secretion and potentiates the renin secretory response to beta adrenoceptor stimulation, thus providing evidence for a role of Phosphodiesterase IV in the regulation of renin secretion.

  • Stimulation of renin secretion by the Phosphodiesterase IV Inhibitor rolipram.
    The Journal of pharmacology and experimental therapeutics, 1996
    Co-Authors: N Chiu, Ina U. Park, I A Reid
    Abstract:

    It is now generally accepted that the renin secretory response to beta adrenoceptor stimulation is mediated by increased formation of cAMP in the juxtaglomerular cells. It is also known that renin secretion is increased when cAMP metabolism is decreased by Phosphodiesterase Inhibitors such as theophylline, but it is not known which isoforms of Phosphodiesterase are involved. In the present study, we investigated the effect on renin secretion of the Phosphodiesterase IV Inhibitor rolipram in conscious rabbits. The i.v. administration of rolipram in a dose of 25 microgram/kg followed by infusion at 5 microgram/kg/min in eight rabbits increased mean arterial pressure from 82 +/- 5 to 93 +/- 6 mm Hg (P