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Am J Respir Cell Mol Biol. 2003 Sep;29(3 Pt 1):410-8. Epub 2003 Apr 24.
Adenosine receptors and phosphodiesterase inhibitors stimulate Cl- secretion in Calu-3 cells.
Cobb BR, Fan L, Kovacs TE, Sorscher EJ, Clancy JP.
Department of Human Genetics, Gregory Fleming James Cystic Fibrosis Research Center, University of Alabama at Birmingham, 35233, USA.
We investigated cystic fibrosis transmembrane conductance regulator (CFTR) activation by clinically used phosphodiesterase inhibitors (PDEis) in Calu-3 cell monolayers alone and in combination with A2B adenosine receptor stimulation. This receptor pathway has previously been shown to activate wild-type and mutant CFTR molecules. Several PDEis, including milrinone, cilostazol (Pletal), papaverine, rolipram, and sildenafil (Viagra), produced a short circuit current (Isc) that was glibenclamide-sensitive, achieving 20-85% of forskolin-stimulated Isc. Papaverine, cilostazol, and rolipram also augmented both the magnitude and the duration of Isc following low dose stimulation of adenosine receptors with Ado (0.1-1.0 microM, P < 0.01). Subsequent studies demonstrated that very low concentrations of cilostazol or papaverine (approximately 1/2 peak serum concentrations) were sufficient to activate Isc, and both agents markedly augmented Ado-stimulated Isc (1 microM, P < 0.01). Our results provide evidence that select PDEis, at concentrations achieved as part of systemic therapies, can activate CFTR-dependent Isc in Calu-3 cell monolayers. These studies also indicate that PDEis have the capacity to augment an endogenous CFTR-activating pathway in an "in vivo"-like model system, and supports future investigations of these agents relevant to cystic fibrosis.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12714375&dopt=Abstract sildenafil, Viagra
J Cardiovasc Pharmacol. 2003 May;41(5):734-43.
Effects of sildenafil (viagra) on human myocardial contractility, in vitro arrhythmias, and tension of internal mammaria arteries and saphenous veins.
Cremers B, Scheler M, Maack C, Wendler O, Schafers HJ, Sudkamp M, Bohm M.
Medizinische Klinik und Poliklinik, Innere Medizin III, Chirurgische Klinik und Poliklinik, Abteilung Thorax-und Herz-, Homburg, Germany,
Sildenafil (Viagra) has been proved effective in the therapy for erectile dysfunction. Cardiovascular adverse effects are a matter of continuous debate. The aim of the study was to investigate effects of sildenafil on isolated human cardiovascular tissue directly. Isometric force of contraction was determined in isolated, electrically stimulated (1 Hz, 37 degrees C) human right atrial and left ventricular muscle strips. Vascular tension was determined in rings of human internal mammaria arteries and saphenous veins. Sildenafil (0.0001-10 microM) neither in human atrium (n = 12) nor in failing (n = 8) or nonfailing (n = 5) ventricle exerted a significant inotropic response. Furthermore, no effect on isoprenaline-elicited arrhythmias was observed. Neither addition of isoprenaline (0.1 microM) nor addition of the nitric oxide donor S-nitroso-N-acetylpenicillamine (SNAP) (100 microM) affected myocardial contractility in the presence of sildenafil (10 microM). In precontracted arteries and veins, addition of sildenafil (0.1-10 microM) led to pronounced vasorelaxation (maximal 35.5 +/- 2.2% and 45.6 +/- 6.3%, respectively, in the presence of 10 microM sildenafil). In the presence of SNAP (0.03 microM), this effect was markedly increased in arteries (72.4 +/- 10.1%, n = 4, P < 0.02) as well as in veins (73.5 +/- 6.3%, n = 6, P < 0.02). Sildenafil exerts potent vasodilatory actions but has no direct influence on human myocardial contractility or proarrhythmic effects in vitro.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12717104&dopt=Abstract sildenafil, Viagra [PubMed - in process]
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