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Identification of endothelial H1, vascular H2 and cardiac presynaptic H3 receptors in the pithed rat.
Naunyn Schmiedebergs Arch Pharmacol. 1993 Jan; 347(1):55-60.NS

Abstract

In pithed and vagotomized rats the effects of the H3 receptor agonist R-(-)-alpha-methylhistamine, the H1 receptor agonist 2-(2-thiazolyl)ethylamine and the H2 receptor agonist dimaprit on basal diastolic blood pressure, basal heart rate and the electrically induced rise in heart rate were examined. Basal diastolic blood pressure was not altered by low, but increased by high doses of R-(-)-alpha-methylhistamine; the latter effect was not affected by selective H1, H2 or H3 receptor antagonists and by prazosin, but was attenuated by rauwolscine. Rauwolscine also unmasked a vasodepressor response to R-(-)-alpha-methylhistamine not affected by the H3 receptor antagonist thioperamide, but counteracted by the H1 receptor antagonist dimetindene or the H2 receptor antagonist ranitidine. The vasodepressor responses to 2-(2-thiazolyl)ethylamine and dimaprit were antagonized by dimetindene and ranitidine, respectively. The vasodepressor response to 2-(2-thiazolyl)ethylamine was not altered by indomethacin, but reduced by an inhibitor of endothelial nitric oxide synthase, N omega-nitro-L-arginine methyl ester (which, by itself, markedly increased blood pressure). Both drug tools did not alter the effect of dimaprit. Basal heart rate was not affected by 2-(2-thiazolyl)ethylamine (examined after administration of propranolol), dimaprit and R-(-)-alpha-methylhistamine. The electrically induced increase in heart rate (studied in animals which had received rauwolscine) was decreased by R-(-)-alpha-methylhistamine but not affected by 2-(2-thiazolyl)ethylamine and dimaprit. The effect of R-(-)-alpha-methylhistamine was abolished by thioperamide. R-(-)-alpha-methylhistamine did not influence the increase in heart rate produced by isoprenaline.(

ABSTRACT

TRUNCATED AT 250 WORDS)

Authors+Show Affiliations

Institut für Pharmakologie und Toxikologie, Rheinische Friedrich-Wilhelms-Universität Bonn, Federal Republic of Germany.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

8383300

Citation

Malinowska, B, and E Schlicker. "Identification of Endothelial H1, Vascular H2 and Cardiac Presynaptic H3 Receptors in the Pithed Rat." Naunyn-Schmiedeberg's Archives of Pharmacology, vol. 347, no. 1, 1993, pp. 55-60.
Malinowska B, Schlicker E. Identification of endothelial H1, vascular H2 and cardiac presynaptic H3 receptors in the pithed rat. Naunyn Schmiedebergs Arch Pharmacol. 1993;347(1):55-60.
Malinowska, B., & Schlicker, E. (1993). Identification of endothelial H1, vascular H2 and cardiac presynaptic H3 receptors in the pithed rat. Naunyn-Schmiedeberg's Archives of Pharmacology, 347(1), 55-60.
Malinowska B, Schlicker E. Identification of Endothelial H1, Vascular H2 and Cardiac Presynaptic H3 Receptors in the Pithed Rat. Naunyn Schmiedebergs Arch Pharmacol. 1993;347(1):55-60. PubMed PMID: 8383300.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Identification of endothelial H1, vascular H2 and cardiac presynaptic H3 receptors in the pithed rat. AU - Malinowska,B, AU - Schlicker,E, PY - 1993/1/1/pubmed PY - 1993/1/1/medline PY - 1993/1/1/entrez SP - 55 EP - 60 JF - Naunyn-Schmiedeberg's archives of pharmacology JO - Naunyn Schmiedebergs Arch Pharmacol VL - 347 IS - 1 N2 - In pithed and vagotomized rats the effects of the H3 receptor agonist R-(-)-alpha-methylhistamine, the H1 receptor agonist 2-(2-thiazolyl)ethylamine and the H2 receptor agonist dimaprit on basal diastolic blood pressure, basal heart rate and the electrically induced rise in heart rate were examined. Basal diastolic blood pressure was not altered by low, but increased by high doses of R-(-)-alpha-methylhistamine; the latter effect was not affected by selective H1, H2 or H3 receptor antagonists and by prazosin, but was attenuated by rauwolscine. Rauwolscine also unmasked a vasodepressor response to R-(-)-alpha-methylhistamine not affected by the H3 receptor antagonist thioperamide, but counteracted by the H1 receptor antagonist dimetindene or the H2 receptor antagonist ranitidine. The vasodepressor responses to 2-(2-thiazolyl)ethylamine and dimaprit were antagonized by dimetindene and ranitidine, respectively. The vasodepressor response to 2-(2-thiazolyl)ethylamine was not altered by indomethacin, but reduced by an inhibitor of endothelial nitric oxide synthase, N omega-nitro-L-arginine methyl ester (which, by itself, markedly increased blood pressure). Both drug tools did not alter the effect of dimaprit. Basal heart rate was not affected by 2-(2-thiazolyl)ethylamine (examined after administration of propranolol), dimaprit and R-(-)-alpha-methylhistamine. The electrically induced increase in heart rate (studied in animals which had received rauwolscine) was decreased by R-(-)-alpha-methylhistamine but not affected by 2-(2-thiazolyl)ethylamine and dimaprit. The effect of R-(-)-alpha-methylhistamine was abolished by thioperamide. R-(-)-alpha-methylhistamine did not influence the increase in heart rate produced by isoprenaline.(ABSTRACT TRUNCATED AT 250 WORDS) SN - 0028-1298 UR - https://www.unboundmedicine.com/medline/citation/8383300/Identification_of_endothelial_H1_vascular_H2_and_cardiac_presynaptic_H3_receptors_in_the_pithed_rat_ L2 - https://www.lens.org/lens/search/patent/list?q=citation_id:8383300 DB - PRIME DP - Unbound Medicine ER -