scholarly journals Action of Cleistanthins A and B on Alpha Adrenoceptors in Rats

2016 ◽  
Vol 8 (3) ◽  
pp. 177-185
Author(s):  
Mageshwaran Lakshmanan ◽  
Zachariah Bobby ◽  
Raveendran Ramasamy
Keyword(s):  
Alpha Adrenoceptors

Alpha-adrenoceptors in the vessels of human finger skin

1986 ◽  
Vol 128 (2) ◽  
pp. 219-222 ◽  
Author(s):  
L. E. LINDBLAD ◽  
L. EKENVALL
Keyword(s):  
Alpha Adrenoceptors ◽  
Human Finger ◽  
Finger Skin

scholarly journals Pathogenesis of Arterial Lesions Induced by Dopaminergic Compounds in the Rat

1989 ◽  
Vol 17 (1_part_2) ◽  
pp. 203-213 ◽  
Author(s):  
William D. Kerns ◽  
Emanuel Arena ◽  
Richard A. Macia ◽  
Peter J. Bugelski ◽  
William D. Matthews ◽  
...  
Keyword(s):  
Arterial Injury ◽  
Mesenteric Arteries ◽  
Receptor Subtypes ◽  
Alpha Adrenoceptors ◽  
Beta Adrenoceptor ◽  
Alpha Adrenoceptor ◽  
Alpha Adrenoceptor Agonists ◽  
Arterial Lesions ◽  
Vascular Beds ◽  
Renal Vascular

Fenoldopam mesylate (FM), a selective post-junctional dopaminergic (DA1) vasodilator, causes lesions of large caliber splanchnic arteries (100–800 μm) in the rat characterized by necrosis of medial smooth muscle cells and hemorrhage. FM does not induce lesions in other vascular beds of the rat, or in dogs or monkeys. Dopamine, like FM, causes hemorrhagic lesions of large caliber splanchnic arteries in the rat, as well as fibrinoid necrosis of small caliber arteries (<100 μm) of the splanchnic, cerebral, coronary and renal vascular beds. Dopamine is an alpha- and beta-adrenoceptor and a dopaminergic receptor agonist. Because these arterial lesions are thought to result from the pharmacologic activity of these 2 compounds, we sought to ascertain the presence of DA1 receptors in mesenteric arteries of the rat and to determine the role of these or other vascular receptor subtypes in lesion induction. We also studied the process of repair after arterial injury caused by FM or dopamine. The presence of DA1 receptors was confirmed in isolated perfused mesenteric arteries by standard pharmacologic techniques; stimulation by FM resulted in vasodilation which was inhibited by the DA1 receptor antagonist SK&F 83566-C. Likewise, SK&F 83566-C prevented the induction of hemorrhagic lesions of large caliber arteries in rats upon infusion of FM or dopamine. In rats co-exposed to the alpha-adrenoreceptor antagonist phenoxybenzamine (PBZ) and either FM or dopamine, the incidence and severity of hemorrhagic lesions of large caliber arteries were increased, but PBZ prevented the formation of dopamine-induced fibrinoid lesions in arteries of small caliber. Rats exposed concurrently to dopamine, phenoxybenzamine, and SK&F 83566-C were free of all arterial lesions. Thus, the induction of splanchnic arterial lesions in the rat by dopamine and FM is caused by stimulation of, and interaction between, alpha-adrenoceptors and dopaminergic DA1 receptors. Fibrinoid lesions of small arteries (alpha-adrenoceptor-mediated) were repaired, as observed morphologically by 14 d after exposure to dopamine. Hemorrhagic lesions of large caliber arteries (DA1 receptor-mediated) had undergone significant repair by 28 d after exposure to FM but these arteries possessed a thicker media surrounded by adventitial fibrosis. Thus, morphologically distinct receptor-mediated splanchnic arterial lesions induced by dopaminergic and alpha-adrenoceptor agonists follow a markedly different course of repair. Arterial lesions induced by FM or dopamine by activation of post-junctional dopaminergic DA1 receptors may represent a model of polyarteritis nodosa.

Alpha-adrenoceptors in human resistance arteries from colon, pericardial fat, and skeletal muscle

1991 ◽  
Vol 261 (3) ◽  
pp. H762-H767 ◽  
Author(s):  
H. Nielsen ◽  
J. M. Hasenkam ◽  
H. K. Pilegaard ◽  
F. V. Mortensen ◽  
M. J. Mulvany
Keyword(s):  
Skeletal Muscle ◽  
Potassium Chloride ◽  
Isometric Contractions ◽  
Resistance Arteries ◽  
Pericardial Fat ◽  
Alpha Adrenoceptors ◽  
Selective Antagonist ◽  
Alpha Adrenoceptor ◽  
Selective Agonist

Human resistance arteries (144-332 microns diam) from colon, pericardial fat, and skeletal muscle were mounted in a myograph for measurements of isometric contractions under conditions of partial depolarization by potassium chloride. In all preparations, both phenylephrine (alpha 1-selective agonist) and B-HT 933 (alpha 2-selective agonist) evoked concentration-dependent contractions that were antagonized by the alpha 1-selective antagonist prazosin (10(-8) M) and the alpha 2-selective antagonist yohimbine (10(-7) M), respectively. The affinities (expressed as pKB values) of prazosin for the receptor mediating the responses to phenylephrine were 8.88-9.41, whereas the affinities of yohimbine for the receptor mediating the responses to B-HT 933 were 7.71-7.97. Norepinephrine (mixed alpha 1-agonist/alpha 2-agonist) also elicited concentration-dependent responses that were modestly, but significantly, antagonized by prazosin alone and yohimbine alone at the above-mentioned concentrations. The two antagonists in combination, however, effectively antagonized the responses to this agonist. These findings strongly suggest the presence of functional, postjunctional alpha 1- and alpha 2-adrenoceptors in isolated human resistance arteries from colon, pericardial fat, and skeletal muscle and that responses to norepinephrine in these vessels are mediated by both alpha-adrenoceptor subtypes.

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