Novel arylpiperazines were identified as alpha 1-adrenoceptor (AR) subtype-selective antagonists by functional in vitro screening. 3-[4-(ortho-Substituted phenyl)piperazin-1-yl]propylamines were derivatized with N,N-dimethyl anthranilamides, nicotinamides, as well as carboxamides of quinoline, 1,8-naphthyridine, pyrazolo[3,4-b]pyridine, isoxazolo[3,4-b]pyridine, imidazo[4,5-b]pyridine, and pyrazolo[1,5-a]pyrimidines. Strips of rabbit bladder neck were employed as a predictive assay for antagonism in the human lower tract. Rings of rat aorta were used as a "negative screen" for the test antagonists. Binding to alpha 1-ARs was relatively sensitive to size and electronic features of the arylpiperazine portion of the antagonists and permissive to these features on the heteroaryl carboxamide side. These structure-affinity findings were exploited to produce nicotinamides (e.g. 13ii and 25x) and pyrazolo[3,4-b]pyridines (e.g. 37f and 37y) ligands with nanomolar affinity at the alpha 1-AR subtype prevalent in the human lower urinary tract(pA2 values: 8.8, 10.7, 9.3, and 9.9, respectively) and displaying 2-3 orders of magnitude selectivity over the alpha 1D-AR.
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Am J Physiol Heart Circ Physiol
February 2025
Department of Basic Medical Sciences, University of Arizona College of Medicine, Phoenix, Arizona, United States.
Autonomic dysfunction is associated with cardiovascular and neurological diseases, including hypertension, heart failure, anxiety, and stress-related disorders. Prior studies demonstrated that late gestation exposure to dexamethasone (DEX) resulted in female-biased increases in stress-responsive mean arterial pressure (MAP) and heart rate (HR), suggesting a role for glucocorticoid-mediated programming of autonomic dysfunction. The present study investigated the influence of sympathetic (SYM) or parasympathetic (PS) blockade on cardiovascular function in male and female rat offspring of mothers injected with DEX in utero [ (GD) -].
View Article and Find Full Text PDFPlatelets
December 2024
Department of Clinical Sciences, Danderyd Hospital, Division of Cardiovascular Medicine, Karolinska Institutet, Stockholm, Sweden.
Drugs blocking the renin-angiotensin-aldosterone system may offer benefit on endothelial function, inflammation, and hemostasis in addition to the effects of reducing blood pressure. We have shown antithrombin effects by treatment with the angiotensin converting enzyme (ACE) inhibitor ramipril. As thrombin is a key inducer of platelet aggregation, we hypothesized that treatment with ramipril could modulate platelet reactivity and endothelial glycocalyx (eGCX) function.
View Article and Find Full Text PDFJ Smooth Muscle Res
November 2024
First Department of Pharmacology, School of Pharmaceutical Sciences, Kyushu University of Medical Science, Nobeoka, Miyazaki 882-8508, Japan.
Although naloxone is an antagonist of the opioid µ receptor, its effect on the peripheral sympathetic nerve function in the blood vessels has not yet been definitively elucidated. Therefore, we examined the effects of naloxone on vasoconstriction of the vascular smooth muscle of rats. Isolated rat mesenteric vascular-intestinal loop preparations were treated with either endogenous or exogenous α adrenoceptor agonists followed by prazosin, a selective antagonist of the α adrenoceptor, or naloxone, and noradrenaline overflow was measured.
View Article and Find Full Text PDFNeurogastroenterol Motil
January 2025
Department of Cell Biology, Physiology and Immunology, Universitat Autònoma de Barcelona, Barcelona, Spain.
Background: Inhibitory neuromuscular transmission in the gastrointestinal tract is mediated by intrinsic nitrergic and purinergic neurons. Purines activate G protein-coupled receptor P2Y receptors, increasing intracellular Ca that activates small conductance calcium-activated potassium (SK) channels. Little is known about the effect of adrenergic receptor activation on intestinal smooth muscle.
View Article and Find Full Text PDFBiol Pharm Bull
September 2024
Department of Clinical Pharmacology, Faculty of Pharmaceutical Sciences, Josai University.
The co-mitogenic effects of the α-adrenoceptor agonist phenylephrine on S-allyl-L-cysteine (SAC)-induced hepatocyte proliferation were examined in primary cultures of adult rat hepatocytes. The combination of phenylephrine (10-10 M) and SAC (10 M) exhibited a significant dose-dependent increase in the number of hepatocyte nuclei and viable cells compared to SAC alone. This combination also increased the progression of hepatocyte nuclei into the S-phase.
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