AJP - Heart and Circulatory Physiology, Vol 256, Issue 3 707-H712, Copyright © 1989 by American Physiological Society
Potassium-induced relaxation of arteries in hypertension: modulation by extracellular calcium
G. Rinaldi and D. F. Bohr
Department of Physiology, University of Michigan, Ann Arbor 48109.
Smooth muscle relaxation due to activation of
Na+-K+-adenosinetriphosphatase (ATPase) (K+ relaxation) was studied in
isolated tail arteries from stroke-prone spontaneously hypertensive (SHRSP)
and Wistar-Kyoto (WKY) rats. Exposure to K+ (7 mM) relaxed a norepinephrine
(1 microM) contraction induced in K+-free physiological salt solution (PSS)
by 46 +/- 3% in WKY and by 81 +/- 3% in SHRSP. Incubation with monensin (10
microM) augmented the K+-relaxation in WKY to 61 +/- 5%. Incubation with
amiloride (10 microM) or with low-Na+ (10 mM) PSS attenuated the K+
relaxation in SHRSP to 34 +/- 3 and 5 +/- 2%, respectively. Incubation with
high-Ca2+ (6.6 mM) PSS attenuated the K+ relaxation in WKY to 25 +/- 3% but
resulted in only a slight decrease in the relaxation in SHRSP (to 73 +/-
2%). We conclude 1) that a greater Na+ leakiness of the plasma membrane in
SHRSP than in WKY while the Na+ pump is inactive in K+-free PSS can explain
the greater relaxation observed when the Na+ pump is reactivated and 2)
that the Na+ leakiness of the membrane is more attenuated by Ca2+ in the
WKY than in the SHRSP. We hypothesize that this Ca2+ effect reflects a
normally large amount of this ion that can be bound to and thereby
stabilize the membrane of the WKY, decreasing its permeability to Na+. The
membrane of the SHRSP is deficient in its Ca2+-binding sites. Hence the
added Ca2+ does not further stabilize its membrane.(ABSTRACT TRUNCATED AT
250 WORDS)
