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Responses of Cremasteric Arterioles of Spontaneously Hypertensive Rats to Changes in Extracellular K + Concentration
Author(s) -
Lombard Julian H.,
Stekiel William J.
Publication year - 1995
Publication title -
microcirculation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.793
H-Index - 83
eISSN - 1549-8719
pISSN - 1073-9688
DOI - 10.3109/10739689509148279
Subject(s) - dilator , cremaster muscle , medicine , chemistry , endocrinology , arteriole , ouabain , microcirculation , extracellular , spontaneously hypertensive rat , contraction (grammar) , sodium , blood pressure , biochemistry , organic chemistry
ABSTRACT Objective : The goal of this study was to determine the effect of changes in extracellular K + concentration ([K + ] 0 ) on active tone in cremasteric arterioles of spontaneously hypertensive rats (SHR) and their normotensive Wistar‐Kyoto (WKY) and Wistar controls. Methods : Diameters of third‐ and fourth‐order arterioles were measured in the cremaster muscle of hypertensive and normotensive rats during abrupt changes in superfusate K + concentration from 4.7 mM to 0 mM to 15 mM K + . Results : Arterioles constricted in response to superfusion with 0 mM K + and exhibited a large, transient dilation in response to an abrupt change from 0 mM to 15 mM [K + ] o . Arteriolar dilation in response to 15 mM K + was significantly larger in 12–15‐week‐old SHR than in WKY or Wistar controls. Arteriolar responses to 15 mM K + were not significantly different in 4–6‐week‐old SHR and WKY. Dilator responses to 15 mM K + were generally inhibited by 1 mM ouabain, although ouabain was less effective in inhibiting 15 mM K + ‐induced dilation in arterioles of SHR and WKY than in Wistar rats. Conclusions : Dilation of cremasteric arterioles in response to 15 mM [K + ] 0 , is mediated, at least in part, via stimulation of the electrogenic Na + /K + pump, although Na + /K + ‐pump‐independent components may also contribute to the response. Arterioles of SHR with established hypertension exhibit an altered response to elevated [K + ] 0 which is not present in SHR in the early stage of hypertension.