Renal Na+-K+-ATPase in Okamoto and Dahl hypertensive rats.

Abstract

SUMMARY Plasma renin activity (PRA, ng Al/ml/hr), plasma aldosterone (PA, ng%) and renal Na + -K + -ATPase (pm PO</mg protein/hr) were measured in two groups of eight spontaneously hypertensive rats (SHR), two groups of eight Dahl salt hypertensive rats (SS), and their controls (16 normal Wistar and 16 saltresistant rats). Measurements were made in one group after 2 weeks on a normal (0.48% sodium) and in the other group after 2 weeks on a low (0.01% sodium) sodium diet. After a normal sodium diet, PRA and PA were lower in both groups of hypertensive rats than in control normotensive animals. Renal Na + -K + -ATPase was lower in SS than in controls: in SHR it was not different from control. On a sodium-free diet, SHR exhibited a rise in renal Na + -K + -ATPase but PRA and PA remained low. In contrast, under similar conditions PRA, PA, and renal Na + -K + -ATPase increased in SS rats, although to a lesser extent than in SR. These results suggest that under basal conditions and after low salt diet, renal Na + -K + -ATPtse activity in SHR behaves as it does in normal rats. However, the changes are independent of PA in SHR. The reduction in PRA and PA in SS suggests volume expansion hypertension. In SHR, volume expansion is not present, and renal Na + -K + -ATPase is not altered. Enzyme activity is lower in SS than in SHR and control. This suggests that some factor that results from volume expansion may be responsible for inhibition of renal Na + -K + -ATPase. 1 " 1 Most studies, however, indicate that during sustained hypertension plasma renin activity (PRA) is low in both strains. This hyporeninemic state could result from expanded extracellular fluid volume; however, plasma volume measurements in SS and SHR on a normal salt diet have not been different from normal. 4 Despite this, small but significant changes in extracellular fluid volume may be present which are undetectable by current methodology. This assumption is supported by the results of studies of acute intragastric saline loading studies which have demonstrated an exaggerated natriuretic response in these models of experimental hypertension."'"

Dahl salt-susceptible and salt-resistant rats. A review.

“…The S rats have unequivocally lower plasma renin activity, 4 *-M - 55 lower renal renin activity, 54 and lower juxtaglomerular granularity 4 ' than R rats. Plasma and renal renin activity in both strains respond appropriately to changes in NaCl intake, but a difference between S and R remains regardless of diet.…”

“…Plasma and renal renin activity in both strains respond appropriately to changes in NaCl intake, but a difference between S and R remains regardless of diet. 54 ' 55 The strain difference in plasma renin activity was present as early as 39 to 42 days of age; small differences in blood pressure were also present at this young age, S pressures being higher than R. 56 Perfused S kidneys also released less renin than perfused R kidneys. 4 " A possible inhibitory action of S-rat plasma on hog renin in vitro has been reported.…”

Kinetics of Na+ and K+ transport in red blood cells of Dahl rats. Effects of age and salt.

“…2 An acceleration of ouabain-sensitive and ouabainresistant Rb + uptake was reported in vascular smooth muscle of salt hypertensive DS and DS/Jr rats, 34 whereas normal or even decreased activity of microsomal sodium-potassium adenosine triphosphatase (Na + ,K + -ATPase) was found in heart and kidney of hypertensive DS and DS/Jr rats. 5 " 8 Normal Na + , K + , and Cl" contents as well as unaltered membrane potentials were observed in smooth muscle cells of tail arteries in adult hypertensive DS females. 9 The cellular K + pool, but not the steadystate K + turnover, was reported to be increased in the thoracic aorta of young hypertensive DS males.…”

Free cytosolic calcium in renal proximal tubules from the spontaneously hypertensive rat.

“…37 -42 In one study, Na + ,K + -ATPase activity measured in homogenates of kidney tissue was reduced in Dahl salt-sensitive rats but normal in SHR. 39 An earlier report by Postnov et al 37 claimed a reduction in the activity of Na + ,K + -ATPase in the outer medulla of kidneys from SHR and from rats with renovascular hypertension. Our renal preparation was obtained from renal cortex and contained mainly proximal tubules.…”

“…43 In contrast, there is reasonable evidence for reduced Na + ,K + -ATPase activity in various tissues (renal, cardiac, blood vessels) from animals with volumedependent hypertension and in volume-expanded animals. 39 - 44~46 The putative circulating ouabainlike factor may not circulate in sufficient amounts to inhibit renal Na + ,K + -ATPase activity in the SHR. If this is the case, an increase in [Ca 2+ ], in renal proximal tubules from the SHR should not be expected on the basis of reduced Na + ,K + -ATPase activity.…”