Potassium channel antagonists and vascular reactivity in stroke-prone spontaneously hypertensive rats

Theodore J. Kolias, Siangshu Chai, R Clinton Webb

Research output: Contribution to journalArticle

26 Citations (Scopus)

Abstract

The goal of this study was to characterize differences in contractile responsiveness to several potassium channel antagonists in vascular smooth muscle from stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto normotensive rats (WKY). Helically-cut strips of carotid arteries (endothelium removed) from SHRSP and WKY were mounted in muscle baths for measurement of isometric force generation. Contractile responses to tetraethylammonium (10-4 to 3 X 10” 2 mol/L) and barium (3 X 10“5 mol/L), blockers of the voltage-dependent and large conductance, calcium activated potassium channels, were greater in carotid arteries from SHRSP than in those from WKY. In contrast, contractile responses to the voltage-dependent potassium channel blockers 3,4-diamino- pyridine (10-6 to 3 X 10“3 mol/L) and sparteine (10-6 to 3 X 10“ 2 mol/L) in arteries from SHRSP did not differ from WKY values. Carotid arteries from SHRSP and WKY did not contract to apamin (10—9 to 10“6 mol/L), an antagonist of the small conductance, calcium activated potassium channel. Furthermore, relaxation responses to diazoxide (3 X 10“ 4 mol/L), an activator of the ATP-sensitive potassium channel, and subsequent contractions to the ATP-sensitive potassium channel blocker gly- buride (10—8 to 3 X 10”6 mol/L) in arteries from SHRSP did not differ from WKY values. Carotid artery segments from SHRSP were more sensitive to the contractile effects of elevated potassium than those from WKY. We conclude that altered activity of the large conductance, calcium activated potassium channel may play a role in the increased responsiveness observed in arteries from SHRSP. Am J Hypertens 1993;6:528-533.

Original languageEnglish (US)
Pages (from-to)528-533
Number of pages6
JournalAmerican journal of hypertension
Volume6
Issue number6
DOIs
StatePublished - Jan 1 1993

Fingerprint

Potassium Channels
Inbred SHR Rats
Carotid Arteries
Blood Vessels
Stroke
Potassium Channel Blockers
Large-Conductance Calcium-Activated Potassium Channels
KATP Channels
Arteries
Small-Conductance Calcium-Activated Potassium Channels
Sparteine
Apamin
Diazoxide
Tetraethylammonium
Inbred WKY Rats
Glyburide
Barium
Baths
Vascular Smooth Muscle
Endothelium

Keywords

  • Barium
  • Carotid artery
  • Hypertension
  • Potassium channel
  • Stroke-prone spontaneously hypertensive rat
  • Tetraethylammonium
  • Wistar- Kyoto rat

ASJC Scopus subject areas

  • Internal Medicine
  • Cardiology and Cardiovascular Medicine

Cite this

Potassium channel antagonists and vascular reactivity in stroke-prone spontaneously hypertensive rats. / Kolias, Theodore J.; Chai, Siangshu; Webb, R Clinton.

In: American journal of hypertension, Vol. 6, No. 6, 01.01.1993, p. 528-533.

Research output: Contribution to journalArticle

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abstract = "The goal of this study was to characterize differences in contractile responsiveness to several potassium channel antagonists in vascular smooth muscle from stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto normotensive rats (WKY). Helically-cut strips of carotid arteries (endothelium removed) from SHRSP and WKY were mounted in muscle baths for measurement of isometric force generation. Contractile responses to tetraethylammonium (10-4 to 3 X 10” 2 mol/L) and barium (3 X 10“5 mol/L), blockers of the voltage-dependent and large conductance, calcium activated potassium channels, were greater in carotid arteries from SHRSP than in those from WKY. In contrast, contractile responses to the voltage-dependent potassium channel blockers 3,4-diamino- pyridine (10-6 to 3 X 10“3 mol/L) and sparteine (10-6 to 3 X 10“ 2 mol/L) in arteries from SHRSP did not differ from WKY values. Carotid arteries from SHRSP and WKY did not contract to apamin (10—9 to 10“6 mol/L), an antagonist of the small conductance, calcium activated potassium channel. Furthermore, relaxation responses to diazoxide (3 X 10“ 4 mol/L), an activator of the ATP-sensitive potassium channel, and subsequent contractions to the ATP-sensitive potassium channel blocker gly- buride (10—8 to 3 X 10”6 mol/L) in arteries from SHRSP did not differ from WKY values. Carotid artery segments from SHRSP were more sensitive to the contractile effects of elevated potassium than those from WKY. We conclude that altered activity of the large conductance, calcium activated potassium channel may play a role in the increased responsiveness observed in arteries from SHRSP. Am J Hypertens 1993;6:528-533.",
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