alpha-Adrenoceptors and cold-induced vasoconstriction in human finger skin

1988 ◽  
Vol 255 (5) ◽  
pp. H1000-H1003 ◽  
Author(s):  
L. Ekenvall ◽  
L. E. Lindblad ◽  
O. Norbeck ◽  
B. M. Etzell
Keyword(s):  
Laser Doppler ◽  
Local Cooling ◽  
Alpha Adrenoceptors ◽  
Alpha Adrenoceptor ◽  
Adrenoceptor Antagonist ◽  
Doppler Probe ◽  
Human Finger ◽  
Finger Skin

Experiments were designed to determine how cold-induced vasoconstriction is mediated in superficial vessels of human finger skin. alpha-Adrenoceptor antagonists were administered into the finger skin by iontophoresis, and local cooling was applied by a laser-Doppler probe supplied with Peltier elements. Cold-induced vasoconstriction was abolished after administration of the alpha 2-adrenoceptor antagonist rauwolscine but not after the alpha 1-adrenoceptor antagonist doxazosin. The results indicate that vasoconstriction on local cooling in human finger skin is mainly mediated by adrenoceptors of the alpha 2-subtype.

Laser Doppler Flow-Meter Assessment of Iontophoretically Applied Norepinephrine on Human Finger Skin Circulation

1986 ◽  
Vol 87 (5) ◽  
pp. 634-636 ◽  
Author(s):  
Lars Erik Lindblad ◽  
Lena Ekenvall ◽  
Klas Ancker ◽  
Håkan Rohman ◽  
P Åke Öberg
Keyword(s):  
Laser Doppler ◽  
Flow Meter ◽  
Laser Doppler Flow ◽  
Doppler Flow ◽  
Skin Circulation ◽  
Human Finger ◽  
Finger Skin

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

Nifedipine and alpha-adrenoceptor function in human finger skin vessels

1989 ◽  
Vol 37 (2) ◽  
pp. 107-110
Author(s):  
L. E. Lindblad ◽  
L. Ekenvall ◽  
B. -M. Etzell
Keyword(s):  
Alpha Adrenoceptor ◽  
Human Finger ◽  
Finger Skin

scholarly journals Mediation of contraction in rat cauda epididymidis by alpha-adrenoceptors

Reproduction ◽  
2002 ◽  
pp. 887-892 ◽  
Author(s):  
G Chaturapanich ◽  
S Maythaarttaphong ◽  
V Verawatnapakul ◽  
C Pholpramool
Keyword(s):  
Pressure Transducer ◽  
Systemic Effects ◽  
Alpha Adrenoceptors ◽  
Alpha Adrenoceptor ◽  
Adrenoceptor Antagonist ◽  
Alpha Adrenoceptor Agonists ◽  
Adrenoceptor Agonists ◽  
Cauda Epididymidis ◽  
Spontaneous Contractions

Subtypes of alpha-adrenoceptors responsible for contractions of the rat cauda epididymidis were studied in vivo by micropuncture using a servo-nulling pressure transducer system. Administration of both non-selective and selective alpha-adrenoceptor agonists in doses of 1-40 microg noradrenaline kg(-1) body weight (BW), 1-100 microg clonidine kg(-1) BW, or 100-800 mg methoxamine kg(-1) BW enhanced contractions of the proximal cauda epididymidis in a dose-response manner. The potency of the agonists were noradrenaline > or = clonidine>methoxamine. Pre-treatments with selective alpha(1)-adrenoceptor antagonist (prazosin) and alpha(2)-adrenoceptor antagonist (yohimbine) at the doses of 400 and 800 microg kg(-1) BW, respectively, had very little effect on spontaneous contractions, but effectively blocked the responses to the maximal doses of methoxamine and clonidine. The responses could not be explained by the systemic effects of agonists and antagonists. The results suggest that contraction of the proximal cauda epididymidis of rats is mediated by both alpha(1)- and alpha(2)-adrenoceptors. The latter appears to be more abundant.

Paraventricular hypothalamic adrenoceptors and energy metabolism in exercising rats

1990 ◽  
Vol 259 (3) ◽  
pp. R478-R484 ◽  
Author(s):  
A. J. Scheurink ◽  
A. B. Steffens ◽  
R. P. Gaykema
Keyword(s):  
Blood Glucose ◽  
Plasma Corticosterone ◽  
Plasma Norepinephrine ◽  
Alpha Adrenoceptors ◽  
Beta Adrenoceptor ◽  
Alpha Adrenoceptor ◽  
Glucose Levels ◽  
Adrenoceptor Antagonist ◽  
Exercise Induced ◽  
Induced Changes

The role of adrenoceptors in the paraventricular nucleus (PVN) in the exercise-induced changes in plasma norepinephrine (NE), epinephrine (E), corticosterone, free fatty acids (FFA), and blood glucose was investigated in rats. Exercise consisted of strenuous swimming against a countercurrent for 15 min. Before, during, and after swimming, blood samples were withdrawn through a permanent heart catheter for determination of E, NE, corticosterone, FFA, and glucose, In control rats receiving artificial cerebrospinal fluid through permanent bilateral cannulas into the PVN, the levels of all blood components increased during exercise. Infusion of the alpha-adrenoceptor antagonist phentolamine into the PVN completely reduced the exercise-induced increases in blood glucose and plasma corticosterone concentrations. Plasma NE, E, and FFA were not affected. Infusion of the beta-adrenoceptor antagonist timolol into the PVN reduced blood glucose and plasma NE concentrations. Plasma E, corticosterone, and FFA remained unchanged. It is concluded that alpha- and beta-adrenergic receptors in the PVN are involved in the central nervous regulation of blood glucose levels during exercise, partly by influencing sympathetic outflow. alpha-Adrenoceptors in the PVN play an important role in the release of corticosterone during exercise.

scholarly journals A Blunted Sympathetic Function and an Enhanced Nitrergic Activity Contribute to Reduce Mesenteric Resistance in Hyperthyroidism

2021 ◽  
Vol 22 (2) ◽  
pp. 570
Author(s):  
Laia Cros-Brunsó ◽  
Laura Camacho-Rodríguez ◽  
Ángel Martínez-González ◽  
Pablo Llévenes ◽  
Mercedes Salaices ◽  
...  
Keyword(s):  
Citrate Synthase ◽  
Purinergic Receptor ◽  
Body Weight Gain ◽  
Electrical Field Stimulation ◽  
Alpha Adrenoceptor ◽  
Adrenoceptor Antagonist ◽  
Sympathetic Function ◽  
Vasoconstrictor Response ◽  
Relevant Role ◽  
Male Wistar Rats

We aimed to determine whether an experimental model of hyperthyroidism could alter the function of sympathetic and nitrergic components of mesenteric innervation. For this purpose, male Wistar rats were divided into (1) control rats (CT) and (2) rats infused with L-Thyroxine (HT). Body weight gain and adipose tissue accumulation were lower in HT rats, while systolic blood pressure and citrate synthase activity in the soleus muscle were increased by HT. In segments from the superior mesenteric artery, the application of an electrical field stimulation (EFS) induced a vasoconstrictor response, which was lower in arteries from HT animals. The alpha-adrenoceptor antagonist phentolamine diminished EFS-induced vasoconstriction to a lower extent in HT arteries, while the purinergic receptor antagonist suramin reduced contractile response to EFS only in segments from CT. In line with this, noradrenaline release, tyrosine hydroxylase expression and activation and dopamine β hydroxylase expression were diminished in HT. The unspecific nitric oxide synthase (NOS) inhibitor L-NAME increased EFS-induced vasoconstriction more markedly in segments from HT rats. NO release was enhanced in HT, probably due to an enhancement in neuronal NOS activity, in which a hyperactivation of both PKC and PI3K-AKT signaling pathways might play a relevant role. In conclusion, perivascular mesenteric innervation might contribute to reduce the vascular resistance observed in hyperthyroidism.

Miniature Implantable Laser Doppler Probe Monitoring of Free Tissue Transfer

1988 ◽  
Vol 20 (5) ◽  
pp. 434-442 ◽  
Author(s):  
Barry Fernando ◽  
V Leroy Young ◽  
Samuel E. Logan
Keyword(s):  
Free Tissue Transfer ◽  
Laser Doppler ◽  
Doppler Probe ◽  
Tissue Transfer

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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