Effects of the Restraint on Body Temperature in Spontaneously Hypertensive Rats (SHR) and Stroke-Prone SHR(SHRSP)

Body temperature (BT) was significantly greater in spontaneously hypertensive rats (SHR) than in Wistar-Kyoto (WKY) rats regardless of the time of day, length of rectal probe, sex, age, or commercial vendor. Bath temperature (theta) for excised aortic rings was controlled by a thermoelectric Peltier module with an accuracy of 0.1 degree C. At peak force in individual contractions of norepinephrine (NE) dose-response experiments, theta was changed from 37 to 39 degrees C. Active and resting wall tension (Tw) were increased, and the mean effective dose (ED50) was decreased in the SHR aorta with and without endothelium. For the WKY aorta, active and resting Tw were increased, but ED50 was the same with and without endothelium. These results were supported by experiments where theta was decreased from 39 to 37 degrees C and by experiments on Sprague-Dawley rats. Potassium dose-response experiments with aorta from SHR and WKY rats show an increase in sensitivity at 39 degrees C, but active Tw is the same at 39 and 37 degrees C. When compared at the BT of each rat, the NE ED50 was lower and resting Tw was higher in the SHR aorta than in the WKY aorta, but active Tw was the same.(ABSTRACT TRUNCATED AT 250 WORDS)

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Membrane ATPase mechanism of K+-return relaxation in arterial muscles of stroke-prone SHR and WKY

AJP Cell Physiology ◽

10.1152/ajpcell.1986.250.4.c557 ◽

1986 ◽

Vol 250 (4) ◽

pp. C557-C562 ◽

Cited By ~ 31

Author(s):

K. Hermsmeyer ◽

D. Harder

Keyword(s):

Membrane Potential ◽

Body Temperature ◽

Low Temperature ◽

Spontaneously Hypertensive Rats ◽

Hypertensive Rats ◽

Extracellular Solution ◽

Spontaneously Hypertensive ◽

Level Of Activity ◽

Membrane Atpase ◽

Wistar Kyoto

These studies compared the importance of electrogenic Na+-K+ active (ATP driven) transport, changes in K+ conductance, and passive Ca2+-Na+ countertransport in the large relaxation that occurs in the rat caudal and basilar artery on return to K+ from K+-free solutions. Furthermore, we compared the importance of these three membrane electrical mechanisms in stroke-prone spontaneously hypertensive rats (SP-SHR) versus their normotensive Wistar-Kyoto control rats (WKY) in basilar (cerebral) and caudal arteries. We found that in both basilar and caudal arteries the hyperpolarization and relaxation that occurred on return to K+ after exposure to a 0 K+ (extracellular) solution was consistently greater in SP-SHR than in WKY. The change in membrane potential occurring on transition to 0 K+ in arteries maintained at low temperature (16 degrees C), used as an estimate of the change in K+ conductance during the K+ transition, was not different in either basilar or caudal arteries between SP-SHR and WKY. Thus the hyperpolarization on return to K+ at body temperature would depend primarily on the level of activity of the membrane ATPase, referred to as the Na+ pump. We also sought to compare the passive (but electrogenic) Ca2+-Na+ countertransport mechanism between strains for both arteries, but we were unable to detect any evidence of the predicted hyperpolarization-contraction on transition from 145 to 10 mM extracellular Na+. Furthermore, the return to extracellular Na+ solution failed to show the depolarization-relaxation predicted by the Ca2+-Na+ countertransport mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

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