Positive and negative contractile effects of neuropeptide Y on ventricular cardiomyocytes

1991 ◽  
Vol 261 (6) ◽  
pp. H1727-H1733 ◽  
Author(s):  
B. C. Millar ◽  
T. Weis ◽  
H. M. Piper ◽  
M. Weber ◽  
U. Borchard ◽  
...  
Keyword(s):  
Amino Acid ◽  
Neuropeptide Y ◽  
Pertussis Toxin ◽  
Contractile Response ◽  
Contractile Responses ◽  
Contractile Effect ◽  
Terminal Fragment ◽  
Ventricular Cardiomyocytes ◽  
K Current

The potency of neuropeptide Y (NPY) to cause negative and positive contractile responses in rat ventricular cardiomyocytes was investigated. In these cells, NPY was found to activate the transient outward K+ current (Ito) and the slow inward Ca2+ current (Isi). As reported before (H. M. Piper, B. C. Millar, and J. R. McDermott, Naunyn Schmiedeberg's Arch. Pharmacol. 340: 333-337, 1989), NPY attenuated the increase in the contractile response induced by isoprenaline (10(-7) M). This effect of NPY could be abolished by 1) the presence of the inhibitor of Ito, 4-aminopyridine (4-AP, 0.5 mM); 2) pretreatment of the cells with pertussis toxin (1 microgram/ml for 6 h); and 3) the presence of the 19-amino acid COOH-terminal fragment of NPY, NPY-(18-36) (10(-6) M). In the absence of isoprenaline, but in the presence of 4-AP, NPY exerted a stimulatory effect on the cardiomyocytes. This effect could be abolished 1) by using the inhibitor of the Isi, verapamil (10(-8) M), but not 2) by pretreatment with pertussis toxin, nor 3) by coincubation with NPY-(18-36). The results indicate that in the rat the antiadrenergic negative contractile effect of NPY results from its action on the Ito. Blockade of this current by 4-AP unmasks a positive contractile effect of NPY that is related to activation of the Isi.

Decreased vascular contractile and inositol phosphate responses in portal hypertensive rats

1995 ◽  
Vol 73 (3) ◽  
pp. 378-382 ◽  
Author(s):  
Yi-Tsau Huang ◽  
Chuang-Ye Hong ◽  
Pi-Chin Yu ◽  
Ming-Fang Lee ◽  
May C. M. Yang ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Contractile Response ◽  
Inositol Phosphates ◽  
Inositol Phosphate ◽  
Venous Pressure ◽  
Portal Vein Ligation ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Contractile Responses ◽  
Tail Artery

The purpose of this study was to investigate the vascular contractile and inositol phosphate responses in portal hypertensive rats. Portal hypertension was induced by partial portal vein ligation (PVL) in Sprague–Dawley rats. Sham-operated rats served as controls. Pressures, vasoconstrictor responses, and inositol phosphate responses were determined at 14 days after surgery. The portal venous pressure was significantly higher, while systemic arterial pressure and heart rate were lower, in PVL rats. Dose-dependent contractile responses were observed for both norepinephrine (1 × 10−8 – 3 × 10−6 M) and vasopressin (3 × 10−10 – 3 × 10−8 M) in the tail artery of both groups. The contractile response to norepinephrine was significantly decreased in PVL rats compared with controls at all doses. The contractile response to vasopressin was significantly decreased in PVL rats at higher doses. After myo-[3H]inositol incorporation in tail artery, the levels of 3H-labelled phosphatidylinositols (cpm/mg) were similar between the two groups. Norepinephrine (10−7 – 10−5 M) and vasopressin (10−10 – 10−8 M) dose dependently stimulated the 3H-labelled inositol phosphate production in the tail artery of both PVL and sham-operated rats. However, the response was significantly lower in PVL rats. The results suggested that the attenuation of vascular contractile responses in portal hypertension was reflected in the phosphoinositide messenger system.Key words: portal hypertension, inositol phosphates, phosphoinositide, tail artery, contractile response.

Pertussis toxin induces parallel loss of neuropeptide Y Y1 receptor dimers and Gi α subunit function in CHO cells

2008 ◽  
Vol 579 (1-3) ◽  
pp. 13-25 ◽  
Author(s):  
Steven L. Parker ◽  
Michael S. Parker ◽  
Renu Sah ◽  
Ambikaipakan Balasubramaniam ◽  
Floyd R. Sallee
Keyword(s):  
Neuropeptide Y ◽  
Pertussis Toxin ◽  
Cho Cells ◽  
Α Subunit ◽  
Y1 Receptor ◽  
Subunit Function ◽  
Receptor Dimers

Contractility and phenotype transitions in serosal thickening of obstructed rabbit bladder

1995 ◽  
Vol 78 (4) ◽  
pp. 1432-1441 ◽  
Author(s):  
M. Roelofs ◽  
A. J. Wein ◽  
F. C. Monson ◽  
G. Passerini-Glazel ◽  
V. E. Koteliansky ◽  
...  
Keyword(s):  
Contractile Response ◽  
Outlet Obstruction ◽  
Phenotypic Change ◽  
Related Protein ◽  
Neurofilament Proteins ◽  
Contractile Responses ◽  
Phenotypic Changes ◽  
Time Period ◽  
Rabbit Bladder ◽  
Alpha Actin

Partial outlet obstruction of rabbit bladder induces serosal thickening and smooth muscle (SM) cell hypertrophy that are accompanied by phenotypic changes in the expression of cytoskeletal and cytocontractile proteins. In the present study, we compare the observed progressive phenotypic changes with the contractile responses of strips of the thickened serosa. At 15 days after partial outlet obstruction, although cells in thickened serosa demonstrate the presence of nonmuscle (NM) myosin of A-like type, vimentin, and SM alpha-actin, no contractile responses of this tissue were noted. At later times (30 days), this tissue expressed in addition SM myosin, and this pattern was paralleled by the development of KCl-stimulated contractility. It is only after 60 days that the serosa demonstrated the expression of desmin, phosphoglucomutase (PGM)-related protein, and was locally negative for NM myosin, indicating a maturation toward adult SM cells. Concomitant to this phenotypic change, the response to KCl increased, and a bethanechol-stimulated contractile response developed. At no time period did the serosal layer react with anti-synaptophysin or anti-neurofilament proteins nor did the strips respond to field stimulation (via release of neurotransmitters), showing that SM cell differentiation and development of contractile responses during serosal thickening are independent of innervation.

Cloning of hok gene into anhydrotetracycline inducible pASK75 vector reveals potent antimicrobial effect of 19 amino acid long N‐terminal fragment of hok peptide

2020 ◽  
Vol 64 (11) ◽  
pp. 737-746
Author(s):  
Anit Kaur ◽  
Thungapathra Muthukumarappa ◽  
Poonam Kanta ◽  
Aaqib Zaffar Banday ◽  
Mohana Kumari Chidananda
Keyword(s):  
Amino Acid ◽  
Antimicrobial Effect ◽  
Terminal Fragment

Neuropeptide Y reduces macromolecule permeability of coronary endothelial monolayers

1996 ◽  
Vol 271 (5) ◽  
pp. H1878-H1883 ◽  
Author(s):  
T. Noll ◽  
A. Hempel ◽  
H. M. Piper
Keyword(s):  
Endothelial Cells ◽  
Neuropeptide Y ◽  
Pertussis Toxin ◽  
Maximum Effect ◽  
Maximal Effect ◽  
Dependent Manner ◽  
Camp Content ◽  
Endothelial Monolayers ◽  
Coronary Endothelial Cells ◽  
Oxide Synthase

The effect of neuropeptide Y (NPY) on cellular adenosine 3',5'-cyclic monophosphate (cAMP) contents and macromolecule permeability was studied in cultured monolayers of microvascular coronary endothelial cells from rat. Macromolecule permeability was continuously determined as passage of albumin across the monolayers. NPY (10(-10)-10(-7) M) decreased albumin flux and cellular cAMP content in a dose-dependent manner, with a half-maximal effect on albumin flux at 1.4 x 10(-9) M and on cAMP contents at 0.7 x 10(-9) M. A maximum effect of NPY was observed at 10(-7) M, decreasing albumin flux by 71 +/- 8% and cellular cAMP contents by 80 +/- 9% (mean +/- SD, n = 6, P < 0.05) compared with control. The effect of NPY on albumin flux was not altered in the presence of 10(-5) M indomethacin (an inhibitor of cyclooxygenase) and 10(-5) M NG-nitro-L-arginine (an inhibitor of nitric oxide synthase). NPY (10(-7) M) also antagonized the increase of albumin flux and cAMP content induced by 10(-6) M isoproterenol. Pretreatment of endothelial monolayers with pertussis toxin (1 microgram/ml for 2 h) abolished the effect of NPY on albumin flux and cAMP contents. This study shows that NPY can modulate macromolecule permeability of endothelial monolayers by reducing the cellular cAMP contents. Together with the effect of pertussis toxin, the data suggest that NPY exerts its antiadrenergic effect on cAMP metabolism and endothelial barrier function by receptors linked to adenylyl cyclase via an inhibitory guanosine-binding protein in coronary endothelial cells.

Comparison of two solid-phase peptide syntheses of a 32-amino acid carboxyl-terminal fragment of human parathyroid hormone, hPTH-(53–84)

1980 ◽  
Vol 199 (1) ◽  
pp. 286-296 ◽  
Author(s):  
Michael Rosenblatt ◽  
Geoffrey W. Tregear ◽  
Gary L. Shepard ◽  
George A. Tyler ◽  
Marta Veroni ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Amino Acid ◽  
Solid Phase ◽  
Human Parathyroid Hormone ◽  
Terminal Fragment ◽  
Carboxyl Terminal

Effects of pertussis and cholera toxins on α-adrenoceptor function in rat tail artery: differences in hypertension

1993 ◽  
Vol 71 (10-11) ◽  
pp. 791-799 ◽  
Author(s):  
Xiao-Fang Li ◽  
Christopher R. Triggle
Keyword(s):  
Cholera Toxin ◽  
Pertussis Toxin ◽  
Rat Tail Artery ◽  
Response Curves ◽  
Contractile Responses ◽  
Tail Artery ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
The Right ◽  
Rat Tail

The α1- and α2-adrenoceptor-stimulated contractile responses of rat tail artery rings were compared in Sprague–Dawley (SD), spontaneously hypertensive (SHR), and Wistar–Kyoto (WKY) rats that were untreated, treated with pertussis toxin, or treated with cholera toxin. The maximal responses, expressed as milligrams of tension, induced by clonidine (an α2-adrenoceptor agonist) and cirazoline (a selective (α1-adrenoceptor agonist) were significantly greater in SHR than in SD or WKY, and the tissues were more sensitive to the agonists in SHR or SD than in WKY. Yohimbine (0.1 μM), a selective α2-adrenoceptor antagonist, shifted the dose–response curves for clonidine to the right. The effects of yohimbine were greater in SD than in WKY or SHR, but not different between WKY and SHR. Prazosin (0.05 μM), a selective α1-adrenoceptor antagonist, shifted the dose–response curves of cirazoline to the right, but the effects of prazosin were not different among these three strains of rats. Nifedipine (0.05 μM) completely blocked the response to clonidine in SD and WKY; however, in SHR, approximately one-third of the response to clonidine was resistant to nifedipine. Nifedipine, at 0.05 μM, only partially inhibited responses to cirazoline in SD, SHR, and WKY, and no differences were noted between the strains. Pertussis toxin pretreatment (50 μg/kg, 3 days before experiment) almost completely blocked the responses to clonidine, but only partially inhibited those to cirazoline. After pertussis toxin pretreatment, the responses (maximal effects and EC50s) to clonidine and cirazoline were not significantly different in arteries from the three strains of rats. A combination of pertussis toxin and nifedipine resulted in an additive inhibition of the responses induced by cirazoline. cholera toxin pretreatment (0.3 mg/kg, 3 days before experiment), however, had no effects on the contractile responses induced by either clonidine or cirazoline, or on the inhibitory effects of nifedipine in SHR, SD, and WKY. These results indicate that (i) the maximal responses to α1- and α2-adrenoceptor agonists are enhanced in rat tail artery rings from SHR; (ii) tissues from SH and SD rats are also more sensitive to cirazoline and clonidine than are tissues from WKY; (iii) responses to clonidine, but not cirazoline, in tissues from the SHR are less sensitive to nifedipine than tissues from SD and WKY; (iv) a G-protein sensitive to pertussis but not cholera toxin is involved in the regulation of both α1 and α2-adrenoceptor signal transduction processes in rat tail artery smooth muscle; and (v) pretreatment with pertussis toxin reduces the enhanced response levels of SHR tissues so that the maximal contractile responses to both α1- and α2-adrenoceptor agonists are equivalent in arteries from the three strains of rats.Key words: pertussis toxin, cholera toxin, α1-adrenoceptor, α2-adrenoceptor, rat tail artery ring.

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