Comparison of K+ channel properties in freshly isolated myocytes from thoracic aorta of WKY and SHR

被引:31
作者
Cox, RH
机构
[1] Bockus Research Institute, Department of Physiology, University of Pennsylvania, Philadelphia, PA
[2] Bockus Research Institute, Graduate Hospital, Philadelphia, PA 19146, One Graduate Plaza
关键词
thoracic aorta; hypertension; K+ channel components; smooth muscle tone; patch clamp currents; electrophysiology;
D O I
10.1016/S0895-7061(96)00179-3
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
Altered function of smooth muscle cell K+ channels have been reported in hypertension, but the contribution of various K+ channel types to these changes has not been completely determined. The purpose of this study was to compare the contribution of K+ channel types to whole cell K+ currents recorded from isolated thoracic aorta myocytes of 13 to 15 week old Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Cells were isolated by collagenase and elastase digestion, and K+ currents recorded using whole cell voltage clamp methods at room temperature. Cells were superfused with a solution containing (in mmol/L) 140 NaCl, 5 KCl, 2 CaCl2, 1 MgCl2, 10 HEPES, and 10 glucose. Pipettes were filled with a solution containing (in mmol/L) 120 KCl, 5 NaCl, 5 MgATP, 20 HEPES, and 10 BAPTA. The K+ currents (I-K) recorded from a holding potential (HP) of -80 mV were smaller in the SHR compared to those in WKY (for example, at 20 mV: WKY = 6.1 +/- 0.6 pA/pF and SHR = 3.7 +/- 0.2 pA/pF). Values of cell capacitance were not different between the two groups (WKY = 25.2 +/- 3.2 pF and SHR = 26.6 +/- 1.9 pF). A component of I-K inhibited by voltage (K,) over the range from -80 to -20 mV was smaller in SHR. The voltage dependence of K-v availability and activation were not significantly different between the two groups. I-K recorded from a HP = -20 mV (K-Ca) was not different between the two groups. Difference currents calculated from I-K measured at HP of -80 and -20 mV (that is, K-v) were smaller in SHR as was the fraction of I-K inhibited by 4-aminopyridine. These results suggest that under conditions of low intracellular [Ca2+] there are no differences in K-Ca currents, but the K-v currents are smaller in SHR. Inhibition of K-v by 4-aminopyridine (0.1 to 10 mmol/L) caused larger increases in basal tone in WKY aorta. These results suggest that K-v channels contribute to resting K+ conductance in both WKY and SHR aorta, but with a relatively larger contribution in the WKY.
引用
收藏
页码:884 / 894
页数:11
相关论文
共 35 条
[1]   CHARYBDOTOXIN-SENSITIVE K+ CHANNELS REGULATE THE MYOGENIC TONE IN THE RESTING STATE OF ARTERIES FROM SPONTANEOUSLY HYPERTENSIVE RATS [J].
ASANO, M ;
MASUZAWAITO, K ;
MATSUDA, T .
BRITISH JOURNAL OF PHARMACOLOGY, 1993, 108 (01) :214-222
[2]   2 COMPONENTS OF POTASSIUM CURRENT ACTIVATED BY DEPOLARIZATION OF SINGLE SMOOTH-MUSCLE CELLS FROM THE RABBIT PORTAL-VEIN [J].
BEECH, DJ ;
BOLTON, TB .
JOURNAL OF PHYSIOLOGY-LONDON, 1989, 418 :293-309
[3]  
BHALLA RC, 1978, MOL PHARMACOL, V14, P468
[4]   DELAYED RECTIFIER POTASSIUM CHANNELS IN CANINE AND PORCINE AIRWAY SMOOTH-MUSCLE CELLS [J].
BOYLE, JP ;
TOMASIC, M ;
KOTLIKOFF, MI .
JOURNAL OF PHYSIOLOGY-LONDON, 1992, 447 :329-350
[5]  
BUKOSKI RD, 1994, J HYPERTENS, V12, P15
[6]   EFFECTS OF AGING ON AGONIST-ACTIVATED RB-86 EFFLUX IN ARTERIES OF FISCHER-344 RATS [J].
COX, RH ;
TULENKO, TN .
AMERICAN JOURNAL OF PHYSIOLOGY, 1989, 257 (02) :H494-H501
[7]   AN EXAMINATION OF THE SOURCES OF CALCIUM FOR CONTRACTIONS MEDIATED BY POSTJUNCTIONAL ALPHA-1-ADRENOCEPTORS AND ALPHA-2-ADRENOCEPTORS IN SEVERAL BLOOD-VESSELS ISOLATED FROM THE RABBIT [J].
DALY, CJ ;
DUNN, WR ;
MCGRATH, JC ;
MILLER, DJ ;
WILSON, VG .
BRITISH JOURNAL OF PHARMACOLOGY, 1990, 99 (02) :253-260
[8]   HYPOXIC DILATION OF CORONARY-ARTERIES IS MEDIATED BY ATP-SENSITIVE POTASSIUM CHANNELS [J].
DAUT, J ;
MAIERRUDOLPH, W ;
VONBECKERATH, N ;
MEHRKE, G ;
GUNTHER, K ;
GOEDELMEINEN, L .
SCIENCE, 1990, 247 (4948) :1341-1344
[9]   ENHANCED SINGLE-CHANNEL K+ CURRENT IN ARTERIAL MEMBRANES FROM GENETICALLY HYPERTENSIVE RATS [J].
ENGLAND, SK ;
WOOLDRIDGE, TA ;
STEKIEL, WJ ;
RUSCH, NJ .
AMERICAN JOURNAL OF PHYSIOLOGY, 1993, 264 (05) :H1337-H1345
[10]   INTRACELLULAR VASCULAR MUSCLE CA-2+ MODULATION IN GENETIC-HYPERTENSION [J].
ERNE, P ;
HERMSMEYER, K .
HYPERTENSION, 1989, 14 (02) :145-151