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Titolo:
Altered effects of potassium channel modulation in the coronary circulation in experimental hypercholesterolemia
Autore:
Mathew, V; Lerman, A;
Indirizzi:
Mayo Clin, Div Cardiovasc Dis & Internal Med, Rochester, MN 55905 USA MayoClin Rochester MN USA 55905 & Internal Med, Rochester, MN 55905 USA
Titolo Testata:
ATHEROSCLEROSIS
fascicolo: 2, volume: 154, anno: 2001,
pagine: 329 - 335
SICI:
0021-9150(20010201)154:2<329:AEOPCM>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
SENSITIVE K+ CHANNELS; SMOOTH-MUSCLE CELLS; FLOW VELOCITY; IN-VIVO; ENDOTHELIN; ARTERY; PINACIDIL; PORCINE;
Keywords:
potassium channels; coronary circulation; hypercholesterolemia;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
26
Recensione:
Indirizzi per estratti:
Indirizzo: Mathew, V Mayo Clin, Div Cardiovasc Dis & Internal Med, 200 1st St SW, Rochester, MN55905 USA Mayo Clin 200 1st St SW Rochester MN USA 55905 ster, MN55905 USA
Citazione:
V. Mathew e A. Lerman, "Altered effects of potassium channel modulation in the coronary circulation in experimental hypercholesterolemia", ATHEROSCLER, 154(2), 2001, pp. 329-335

Abstract

Objective: To evaluate the role of potassium channels in the regulation ofcoronary hemodynamics in experimental hypercholesterolemia. Background: Potassium (Ki) channels play an important role in coronary vasoregulation. Ithas previously been demonstrated that experimental hypercholesterolemia isassociated with altered coronary vasomotion: however, the role of K+ channels in modulating coronary blood flow in this pathophysiologic state has not been evaluated. Methods and results: Pinacidil (group 1, n = 5) at 2 mug/kg per min, glibenclamide (group 2, n = 5), or N-monomethyl-L-arginine (LNMMA) (group 3, n = 4) at 50 mug/kg per min were infused into the left anterior descending artery of pigs prior to and following 10 weeks of 2% cholesterol diet. After 10 weeks of cholesterol feeding, intracoronary pinacidil resulted in a significant increase in coronary blood flow (CBF) and coronary artery diameter (CAD) compared to the normolipidemic state (111 +/- 10 versus 59 +/- 12%. and 6 +/- 1.1 versus 2.7 +/- 1.0%, respectively. P < 0.05 for both comparisons), whereas intracoronary glibenclamide resulted in a significant decrease in CBF and CAD compared to the normolipidemic state (-17 +/- 5 versus 5 +/- 6%, and -0.8 +/- 1.4 Versus 3.6 +/- 1.6%. respectively, P< 0.05 for both comparisons). The effect of intracoronary LNMMA on CBF andCAD was significantly attenuated after 10 weeks of cholesterol feeding as compared to the normolipidemic state (-47 +/- 5.4 versus -0.8 +/- 6.8%, and-19.4 +/- 5.7 versus -2.3 +/- 3.3%, respectively. P < 0.05 for both comparisons). Furthermore, pretreatment with intracoronary LNMMA did not alter the CBF response to pinacidil in normal pigs (group 4, n = 4) (57.4 +/- 19 versus 59 +/- 12%, P = NS). Conclusions: The current study demonstrates an enhanced effect of coronary K+ channel modulation and confirms the attenuatedbasal NO activity previously reported in experimental hypercholesterolemia. Acute withdrawal of basal NO activity alone, however. does not explain the enhanced effect of coronary K+ channel modulation. These findings underscore the importance of the K+ channel pathway in the regulation of coronary vasomotor tone in pathophysiologic states. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/07/20 alle ore 10:56:34