Inhibitory effect of a selective kappa receptor agonist, U-50, 488H, on methamphetamine-elicited ipsilateral circling behavior in rats with unilateral nigral lesions

1989 ◽  
Vol 97 (2) ◽  
pp. 219-221 ◽  
Author(s):  
Masuo Ohno ◽  
Tsuneyuki Yamamoto ◽  
Showa Ueki
Keyword(s):  
Receptor Agonist ◽  
Inhibitory Effect ◽  
Circling Behavior ◽  
Kappa Receptor

Adenosine A1 receptor-mediated inhibition of vasopressin action in inner medullary collecting duct

1994 ◽  
Vol 266 (5) ◽  
pp. F791-F796 ◽  
Author(s):  
R. M. Edwards ◽  
W. S. Spielman
Keyword(s):  
Receptor Agonist ◽  
Collecting Duct ◽  
Basolateral Membrane ◽  
Inhibitory Effect ◽  
Dependent Manner ◽  
Camp Accumulation ◽  
Concentration Dependent Manner ◽  
Cgs 21680 ◽  
Camp Generation ◽  
A1 Receptor

We examined the effects of adenosine and adenosine analogues on arginine vasopressin (AVP)-induced increases in osmotic water permeability (Pf; micron/s) and adenosine 3',5'-cyclic monophosphate (cAMP) accumulation in rat inner medullary collecting ducts (IMCDs). When added to the bath, the A1 receptor agonist N6-cyclohexyladenosine (CHA) produced a rapid and reversible inhibition of AVP-stimulated (10 pM) Pf (1,781 +/- 195 to 314 +/- 85 microns/s at 0.3 microM CHA; n = 9). The inhibitory effect of CHA was concentration dependent, with a 50% inhibitory concentration of 10 nM. The effect of CHA was inhibited by prior exposure of IMCDs to the A1 receptor antagonist 1,3-dipropylxanthine-8-cyclopentylxanthine (DP-CPX; 1 microM) or by preincubation with pertussis toxin. CHA had no effect on cAMP-induced increases in Pf. In addition to CHA, adenosine and the nonselective agonist 5'-(N-ethylcarboxamido)-adenosine (NECA) inhibited AVP-dependent Pf by > or = 70%, whereas the A2 receptor agonist CGS-21680 had no effect. Luminal adenosine (0.1 mM) had no effect on basal or AVP-stimulated Pf. CHA, NECA, and adenosine but not CGS-21680 inhibited AVP-stimulated cAMP accumulation in a concentration-dependent manner (50% inhibitory concentrations 0.1–300 nM). The inhibitory effect of CHA on AVP-stimulated cAMP accumulation was attenuated by DPCPX. We conclude that adenosine, acting at the basolateral membrane, inhibits AVP action in the IMCD via interaction with A1 receptors. The inhibition occurs proximal to cAMP generation and likely involves an inhibitory G protein.

Identification of opioid receptors on gastric muscle cells by selective receptor protection

1991 ◽  
Vol 260 (1) ◽  
pp. G103-G107 ◽  
Author(s):  
J. R. Grider ◽  
G. M. Makhlouf
Keyword(s):  
Opioid Receptors ◽  
Receptor Agonist ◽  
Muscle Cells ◽  
Mu Opioid Receptors ◽  
Mu Opioid ◽  
Selective Antagonist ◽  
Receptor Agonists ◽  
Mu Receptor ◽  
Gastric Muscle ◽  
Kappa Receptor

Opioid receptors on isolated gastric smooth muscle cells were characterized pharmacologically by a technique in which synthetic selective opioid agonists and antagonists were used to protect and thus enrich a specific receptor type while all other receptors were inactivated by N-ethylamaleimide. Treatment of the cells with the selective mu-receptor agonist DAGO or antagonist CTAP preserved only the response to DAGO; treatment with the selective delta-receptor agonist DPDPE or antagonist naltrindole preserved only the response to DPPE; and treatment with the selective kappa-receptor agonist U50,488H or antagonist nor-binaltorphimine preserved only the response to U50,488H. The results established the presence of distinct kappa-, delta-, and mu-opioid receptors capable of mediating contraction of isolated gastric muscle cells. The pattern of interaction of endogenous opioid peptides with protected receptors implied that dynorphin-(1-13) and Met-enkephalin were selective agonists for kappa- and delta-opioid receptors, respectively, and Leu-enkephalin a preferential agonist of mu-opioid receptors. The results were confirmed by a reverse approach in which opioid receptors were inactivated by site-directed irreversible antagonists. beta-Funaltrexamine, a mu-selective antagonist, abolished the response to mu-receptor agonists, whereas beta-chlornaltrexamine, a mu- and kappa-selective antagonist, abolished the response to mu-receptor agonists and partially inhibited the response to kappa-receptor agonists.

ATP stimulates Ca2+ mobilization by a nucleotide receptor in glomerular endothelial cells

1994 ◽  
Vol 266 (2) ◽  
pp. F210-F217 ◽  
Author(s):  
V. A. Briner ◽  
F. Kern
Keyword(s):  
Endothelial Cells ◽  
Receptor Agonist ◽  
Rank Order ◽  
P2y Receptors ◽  
Inhibitory Effect ◽  
P2x Receptor ◽  
Dependent Manner ◽  
Nucleotide Receptor ◽  
Pyrimidine Nucleotide ◽  
Glomerular Endothelial Cells

The present study investigates ATP effects on Ca2+ mobilization in bovine glomerular endothelial cells (GEC) and the receptors mediating ATP response. Extracellular ATP stimulated a rise in inositol 1,4,5-trisphosphate and cytosolic free Ca2+ concentration ([Ca2+]i) in a dose-dependent manner. Extracellular Ca2+ depletion did not prevent [Ca2+]i rise. ATP effects were not mediated by P1, P2x, and P2t purinoceptors, since the P1 receptor agonist adenosine and the P2x receptor agonist [alpha,beta-CH2]ATP had no effect on inositol 1-monophosphate (IP) formation and Ca2+ mobilization and ATP does not activate P2t receptors. The P2y receptor antagonist reactive blue (10(-3) M) had little inhibitory effect on ATP (10(-5) M)-stimulated IP formation (15.6 +/- 4.2%) and Ca2+ rise (7.0 +/- 3.0%). According to the classification of purinoceptors, ATP is less potent than 2-methylthioadenosine 5'-triphosphate (2-MeS-ATP) in stimulating P2y receptors. In GEC, however, the rank order of potency in stimulating IP and [Ca2+]i rise was ATP > 2-MeS-ATP > ADP. The pyrimidine nucleotide UTP (10(-3) M) induced maximal IP formation (653 +/- 37%) and Ca2+ mobilization (591 +/- 22 nM) similar to ATP (IP 647 +/- 27%; [Ca2+]i 583 +/- 15 nM). At submaximal (10(-5) M) but not at maximal (10(-3) M) doses ATP and UTP effects were additive. ATP and UTP induced specific cross-desensitization. It is concluded that the purinergic nucleotide ATP and pyrimidine nucleotide UTP mediate their effects by a common nucleotide receptor. This receptor differs from P2z and P2y1 receptors, since by definition UTP does not activate these receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

The Inhibitory Effect of S-777469, a Cannabinoid Type 2 Receptor Agonist, on Skin Inflammation in Mice

Pharmacology ◽  
2017 ◽  
Vol 99 (5-6) ◽  
pp. 259-267 ◽  
Author(s):  
Takayo Haruna ◽  
Masahiko Soga ◽  
Yasuhide Morioka ◽  
Kinichi Imura ◽  
Yoko Furue ◽  
...  
Keyword(s):  
Receptor Agonist ◽  
Skin Inflammation ◽  
Inhibitory Effect

scholarly journals Inhibitory effect of D1-like and D3 dopamine receptors on norepinephrine-induced proliferation in vascular smooth muscle cells

2008 ◽  
Vol 294 (6) ◽  
pp. H2761-H2768 ◽  
Author(s):  
Zhen Li ◽  
Changqing Yu ◽  
Yu Han ◽  
Hongmei Ren ◽  
Weibin Shi ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Adrenergic Receptor ◽  
Receptor Agonist ◽  
Thymidine Incorporation ◽  
Inhibitory Effect ◽  
Vsmc Proliferation

The sympathetic nervous system plays an important role in the regulation of blood pressure. There is increasing evidence for positive and negative interactions between dopamine and adrenergic receptors; the activation of the α-adrenergic receptor induces vasoconstriction, whereas the activation of dopamine receptor induces vasorelaxation. We hypothesize that the D1-like receptor and/or D3 receptor also inhibit α1-adrenergic receptor-mediated proliferation in vascular smooth muscle cells (VSMCs). In this study, VSMC proliferation was determined by measuring [3H]thymidine incorporation, cell number, and uptake of 3-(4,5-dimethylthiazol-2-yl)-diphenyltetrazolium bromide (MTT). Norepinephrine increased VSMC number and MTT uptake, as well as [3H]thymidine incorporation via the α1-adrenergic receptor in aortic VSMCs from Sprague-Dawley rats. The proliferative effects of norepinephrine were attenuated by the activation of D1-like receptors or D3 receptors, although a D1-like receptor agonist, fenoldopam, and a D3 receptor agonist, PD-128907, by themselves, at low concentrations, had no effect on VSMC proliferation. Simultaneous stimulation of both D1-like and D3 receptors had an additive inhibitory effect. The inhibitory effect of D3 receptor was via protein kinase A, whereas the D1-like receptor effect was via protein kinase C-ζ. The interaction between α1-adrenergic and dopamine receptors, especially D1-like and D3 receptors in VSMCs, could be involved in the pathogenesis of hypertension.

scholarly journals Urocortin 2 acts centrally to delay gastric emptying through sympathetic pathways while CRF and urocortin 1 inhibitory actions are vagal dependent in rats

2006 ◽  
Vol 290 (3) ◽  
pp. G511-G518 ◽  
Author(s):  
József Czimmer ◽  
Mulugeta Million ◽  
Yvette Taché
Keyword(s):  
Gastric Emptying ◽  
Receptor Agonist ◽  
Inhibitory Action ◽  
Delayed Gastric Emptying ◽  
Inhibitory Effect ◽  
Corticotropin Releasing Factor ◽  
Phenol Red ◽  
Sympathetic Blockade ◽  
Intracisternal Injection ◽  
Urocortin 1

We characterized the influence of the selective corticotropin-releasing factor 2 (CRF2) receptor agonist human urocortin 2 (Ucn 2), injected intracisternally, on gastric emptying and its mechanism of action compared with intracisternal CRF or urocortin (Ucn 1) in conscious rats. The methylcellulose phenol red solution was gavaged 20 min after peptide injection, and gastric emptying was measured 20 min later. The intracisternal injection of Ucn 2 (0.1 and 1 μg) and Ucn 1 (1 μg) decreased gastric emptying to 37.8 ± 6.9%, 23.1 ± 8.6%, and 21.6 ± 5.9%, respectively, compared with 58.4 ± 3.8% after intracisternal vehicle. At lower doses, Ucn 2 (0.03 μg) and Ucn 1 (0.1 μg) had no effect. The CRF2 antagonist astressin2-B (3 μg ic) antagonized intracisternal Ucn 2 (0.1 μg) and CRF (0.3 μg)-induced inhibition of gastric emptying. Vagotomy enhanced intracisternal Ucn 2 (0.1 or 1 μg)-induced inhibition of gastric emptying compared with sham-operated group, whereas it blocked intracisternal CRF (1 μg) inhibitory action (45.5 ± 8.4% vs. 9.7 ± 9.7%). Sympathetic blockade by bretylium prevented intracisternal and intracerebroventricular Ucn 2-induced delayed gastric emptying, whereas it did not influence intravenous Ucn 2-, intracisternal CRF-, and intracisternal Ucn 1-induced inhibition of gastric emptying. Prazosin abolished the intracisternal Ucn 2 inhibitory effect, whereas yohimbine and propranolol did not. None of the pretreatments modified basal gastric emptying. These data indicate that intracisternal Ucn 2 induced a central CRF2-mediated inhibition of gastric emptying involving sympathetic α1-adrenergic mechanisms independent from the vagus contrasting with the vagal-dependent inhibitory actions of CRF and Ucn 1.

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