Az ATP-fuggo K+-csatorna-(K+(ATP))-aktivalo pinacidil pre- es poszt- szinaptikus hatasa nyul pulmonaris arterian

Translated title of the contribution: Pre- and post-synaptic action of ATP-dependent K+-channel-(K+(ATP))- opener pinacidil in rabbit pulmonary artery

Dániel Rácz, Stefán Zillkens, Péter Forstreuter, Zsolt Nagykáldi, K. Magyar, Tamás Torök

Research output: Contribution to journalArticle

Abstract

Low frequency (2 Hz) of electrical depolarisation induced [3H]noradrenaline ([3H]NA) release has been measured from the isolated main pulmonary artery of the rabbit in the presence of uptake blockers (cocaine, 3x10-5M and corticosterone, 5x10-5M), with parallel measurements of post- junctional contractile responses. The K+(ATP)-channel opener pinacidil (10- 6-10-4M), slightly potentiated the nerve-evoked release of [3H]NA which failed to show close concentration-dependency. Large concentration of pinacidil (10-4M) increased the ratio of [3H]NA release from 0.99±0.02 to 1.28±0.05 (P-4M caused nearly 70% inhibition of contractile response. The pre- and post-junctional effects of pinacidil were studied under the following experimental conditions: 1) exogenously applied 1-NA; 2) excess K+; 3) 'L-type' Ca2±- channel activation (BAY K 8644); K+-channel inhibition (4-AP); and 5) Na+- pump inhibition/reactivation. Pinacidil (10-4M) retained its marginal NA- release stimulatory effect in all cases. However, pinacidil inhibited the contraction of smooth muscle, although to a different extent, in all of the experimental conditions used in our study.

Original languageHungarian
Pages (from-to)159-170
Number of pages12
JournalActa Pharmaceutica Hungarica
Volume69
Issue number3
Publication statusPublished - Jun 1999

Fingerprint

Pinacidil
Pulmonary Artery
Adenosine Triphosphate
Rabbits
Corticosterone
Cocaine
Smooth Muscle
Norepinephrine

ASJC Scopus subject areas

  • Pharmaceutical Science

Cite this

Az ATP-fuggo K+-csatorna-(K+(ATP))-aktivalo pinacidil pre- es poszt- szinaptikus hatasa nyul pulmonaris arterian. / Rácz, Dániel; Zillkens, Stefán; Forstreuter, Péter; Nagykáldi, Zsolt; Magyar, K.; Torök, Tamás.

In: Acta Pharmaceutica Hungarica, Vol. 69, No. 3, 06.1999, p. 159-170.

Research output: Contribution to journalArticle

Rácz, D, Zillkens, S, Forstreuter, P, Nagykáldi, Z, Magyar, K & Torök, T 1999, 'Az ATP-fuggo K+-csatorna-(K+(ATP))-aktivalo pinacidil pre- es poszt- szinaptikus hatasa nyul pulmonaris arterian', Acta Pharmaceutica Hungarica, vol. 69, no. 3, pp. 159-170.
Rácz, Dániel ; Zillkens, Stefán ; Forstreuter, Péter ; Nagykáldi, Zsolt ; Magyar, K. ; Torök, Tamás. / Az ATP-fuggo K+-csatorna-(K+(ATP))-aktivalo pinacidil pre- es poszt- szinaptikus hatasa nyul pulmonaris arterian. In: Acta Pharmaceutica Hungarica. 1999 ; Vol. 69, No. 3. pp. 159-170.
@article{602e82ce78eb4ff8ae8cd9dfe1c97933,
title = "Az ATP-fuggo K+-csatorna-(K+(ATP))-aktivalo pinacidil pre- es poszt- szinaptikus hatasa nyul pulmonaris arterian",
abstract = "Low frequency (2 Hz) of electrical depolarisation induced [3H]noradrenaline ([3H]NA) release has been measured from the isolated main pulmonary artery of the rabbit in the presence of uptake blockers (cocaine, 3x10-5M and corticosterone, 5x10-5M), with parallel measurements of post- junctional contractile responses. The K+(ATP)-channel opener pinacidil (10- 6-10-4M), slightly potentiated the nerve-evoked release of [3H]NA which failed to show close concentration-dependency. Large concentration of pinacidil (10-4M) increased the ratio of [3H]NA release from 0.99±0.02 to 1.28±0.05 (P-4M caused nearly 70{\%} inhibition of contractile response. The pre- and post-junctional effects of pinacidil were studied under the following experimental conditions: 1) exogenously applied 1-NA; 2) excess K+; 3) 'L-type' Ca2±- channel activation (BAY K 8644); K+-channel inhibition (4-AP); and 5) Na+- pump inhibition/reactivation. Pinacidil (10-4M) retained its marginal NA- release stimulatory effect in all cases. However, pinacidil inhibited the contraction of smooth muscle, although to a different extent, in all of the experimental conditions used in our study.",
author = "D{\'a}niel R{\'a}cz and Stef{\'a}n Zillkens and P{\'e}ter Forstreuter and Zsolt Nagyk{\'a}ldi and K. Magyar and Tam{\'a}s Tor{\"o}k",
year = "1999",
month = "6",
language = "Hungarian",
volume = "69",
pages = "159--170",
journal = "Acta Pharmaceutica Hungarica",
issn = "0001-6659",
publisher = "Magyar Gyogyszereszeti Tarsasag",
number = "3",

}

TY - JOUR

T1 - Az ATP-fuggo K+-csatorna-(K+(ATP))-aktivalo pinacidil pre- es poszt- szinaptikus hatasa nyul pulmonaris arterian

AU - Rácz, Dániel

AU - Zillkens, Stefán

AU - Forstreuter, Péter

AU - Nagykáldi, Zsolt

AU - Magyar, K.

AU - Torök, Tamás

PY - 1999/6

Y1 - 1999/6

N2 - Low frequency (2 Hz) of electrical depolarisation induced [3H]noradrenaline ([3H]NA) release has been measured from the isolated main pulmonary artery of the rabbit in the presence of uptake blockers (cocaine, 3x10-5M and corticosterone, 5x10-5M), with parallel measurements of post- junctional contractile responses. The K+(ATP)-channel opener pinacidil (10- 6-10-4M), slightly potentiated the nerve-evoked release of [3H]NA which failed to show close concentration-dependency. Large concentration of pinacidil (10-4M) increased the ratio of [3H]NA release from 0.99±0.02 to 1.28±0.05 (P-4M caused nearly 70% inhibition of contractile response. The pre- and post-junctional effects of pinacidil were studied under the following experimental conditions: 1) exogenously applied 1-NA; 2) excess K+; 3) 'L-type' Ca2±- channel activation (BAY K 8644); K+-channel inhibition (4-AP); and 5) Na+- pump inhibition/reactivation. Pinacidil (10-4M) retained its marginal NA- release stimulatory effect in all cases. However, pinacidil inhibited the contraction of smooth muscle, although to a different extent, in all of the experimental conditions used in our study.

AB - Low frequency (2 Hz) of electrical depolarisation induced [3H]noradrenaline ([3H]NA) release has been measured from the isolated main pulmonary artery of the rabbit in the presence of uptake blockers (cocaine, 3x10-5M and corticosterone, 5x10-5M), with parallel measurements of post- junctional contractile responses. The K+(ATP)-channel opener pinacidil (10- 6-10-4M), slightly potentiated the nerve-evoked release of [3H]NA which failed to show close concentration-dependency. Large concentration of pinacidil (10-4M) increased the ratio of [3H]NA release from 0.99±0.02 to 1.28±0.05 (P-4M caused nearly 70% inhibition of contractile response. The pre- and post-junctional effects of pinacidil were studied under the following experimental conditions: 1) exogenously applied 1-NA; 2) excess K+; 3) 'L-type' Ca2±- channel activation (BAY K 8644); K+-channel inhibition (4-AP); and 5) Na+- pump inhibition/reactivation. Pinacidil (10-4M) retained its marginal NA- release stimulatory effect in all cases. However, pinacidil inhibited the contraction of smooth muscle, although to a different extent, in all of the experimental conditions used in our study.

UR - http://www.scopus.com/inward/record.url?scp=0033146190&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0033146190&partnerID=8YFLogxK

M3 - Article

C2 - 10401160

AN - SCOPUS:0033146190

VL - 69

SP - 159

EP - 170

JO - Acta Pharmaceutica Hungarica

JF - Acta Pharmaceutica Hungarica

SN - 0001-6659

IS - 3

ER -