ArticleBritish journal of pharmacology2002
Alpha-1 adrenoceptor up-regulation induced by prazosin but not KMD-3213 or reserpine in rats.
Article in British journal of pharmacology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 24 citations in OpenAlex.
- The Role of the Paraventricular-Coerulear Network on the Programming of Hypertension by Prenatal Undernutrition.International journal of molecular sciences · 2022Review
- Biased antagonism of CXCR4 avoids antagonist tolerance.Science signaling · 2018Article
- Repeated stress down-regulates β(2)- and α (2C)-adrenergic receptors and up-regulates gene expression of IL-6 in the rat spleen.Cellular and molecular neurobiology · 2010Article
- Protein tyrosine phosphatase 1B, a major regulator of leptin-mediated control of cardiovascular function.Circulation · 2009Article
- Modelling of alpha1-adrenoceptor-mediated temporal dynamics of inotropic response in rat heart to assess ligand binding and signal transduction parameters.British journal of pharmacology · 2009Article
- Alpha-1D adrenoceptors are involved in reserpine-induced supersensitivity of rat tail artery.British journal of pharmacology · 2004Article
- Pharmacological characterization of unique prazosin-binding sites in human kidney.Naunyn-Schmiedeberg's archives of pharmacology · 2003Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. We have investigated the effects of chronic administration of prazosin (a subtype-nonspecific alpha-1 AR antagonist), KMD-3213 (an alpha-1A AR subtype-specific antagonist) and reserpine (a catecholamine depletor) on the density of alpha-1 AR subtypes in various rat tissues (liver, kidney, submaxillary gland, heart and spleen). 2. Administration of prazosin (2 mg kg(-1) day(-1), i.p.) for 2 weeks did not affect K(D) values for [(3)H]-prazosin or [(3)H]-KMD-3213 of alpha-1 ARs in five rat tissues tested. However, it caused 52% up-regulation of alpha-1B AR in the spleen, and 84% and 107% up-regulation of alpha-1A- and alpha-1B ARs, respectively, in the heart. Although major subtypes of alpha-1 AR are alpha-1A AR in the submaxillary gland, alpha-1B AR in the liver, and alpha-1A and alpha-1B ARs in the kidney, these tissues showed no up-regulation. The mRNA levels of alpha-1 AR subtypes were not affected by prazosin administration in any tissue tested. 3. Neither administration of KMD-3213 (2 mg kg(-1) day(-1), i.p.) nor reserpine (0.5 - 1 mg kg(-1) day(-1), i.p.) for 2 weeks caused any change in either the binding affinity for [(3)H]-prazosin or [(3)H]-KMD-3213 or the density of the alpha-1 AR subtypes in the five rat tissues. 4. Neither prazosin nor KMD-3213 treatment reduced the noradrenaline content in the five rat tissues, in contrast to reserpine treatment, which markedly reduced it. 5. The findings of the present study demonstrated that up-regulation of alpha-1 AR is selectively caused by prazosin treatment in some tissues but neither by KMD-3213 treatment nor by chemical denervation with reserpine. These results suggest that up-regulation of alpha-1 ARs is not caused by a simple blockade of sympathetic tone.
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