1. The renal response to aldosterone, measured by urinary sodium and potassium excretion, was determined in adrenalectomized rats that had been previously fed either a high potassium diet or a control diet. High K+ rats showed an enhanced response to aldosterone at all doses tested. 2. The induction of this enhanced response to aldosterone could be suppressed by a high sodium intake. It may also require the presence of the adrenal glands during the induction period, although interpretation of adrenalectomy experiments in the present study was made difficult by the effect of maintenance DOC therapy on the renal response to aldosterone. 3. The enhanced response could not be induced by a low sodium diet alone or by the administration of high doses of exogenous aldosterone. 4. No difference between high K+ and control rats could be detected in rat kidney mineralocorticoid receptors, assessed by both in vivo and in vitro binding of tritiated aldosterone. 5. The method of the induction, and the mechanism of the enhanced response remains to be defined.

Adrenalectomy↗

PubMedDate not supplied

Enhancement by L-dopa of the renal action of aldosterone in the rat.

1. The administration of aldosterone to adrenalectomized rats produces an increase in K+ and decrease in Na+ excretion in the urine. The relationship of the post-aldosterone to the pre-aldosterone urinary sodium and potassium excretion is termed the renal response to aldosterone. 2. The administration of L-dopa enhances the renal response to aldosterone. This enhanced renal response does not appear to be due to the enhanced urinary creatinine and sodium excretion also seen with L-dopa. 3. The enhanced response to aldosterone seen in the L-dopa loaded rat is inhibited by spironolactone (an aldosterone antagonist), carbidopa (an inhibitor of the enzyme producing dopamine from L-dopa in the periphery), and haloperidol (a putative dopamine receptor blocker). The action of L-dopa in enhancing the renal response to aldosterone would thus appear to be mediated by dopamine within the kidney. 4. Modification of the renal response to aldosterone may be one role of the high levels of dopamine produced within the kidney.

Aldosterone↗

PubMedDate not supplied

Dopamine and the enhanced renal response to aldosterone in the rat on a high potassium diet.

1. The enhanced renal response to aldosterone observed in rats on a high potassium diet is reduced by the administration of either haloperidol, a dopamine receptor blocker, or carbidopa, a peripheral blocker of dopa decarboxylase. This suggests that one peripheral action of dopamine is to modulate the action of aldosterone on the kidney. 2. No difference in urinary dopamine excretion after an 18 h fast was found in rats that had been either on a control diet or a high potassium diet. Both groups of rats responded by a similar elevation after an acute potassium load. This suggests that dopaminergic mediation of the enhanced response to aldosterone in rats on a chronic high potassium diet is not detectable by changes in urinary dopamine excretion.

Aldosterone↗

PubMedDate not supplied

Opiates inhibit the dopaminergic enhancement of the renal response to aldosterone in the rat.

1. Both naloxone, an opiate antagonist, and levorphanol, an opiate agonist, inhibit the enhanced renal response to aldosterone produced by both l-dopa pretreatment and a high K+ diet. 2. This supports the evidence for a common mechanism of action for the enhancement of the renal response to aldosterone produced by l-dopa and a high K+ diet. Whether this mechanism is dopaminergic or opiate is uncertain. 3. The inhibition of the enhanced response, produced by l-dopa, by opiates is consistent with previous findings of displacement of 3H-dopamine from renal homogenates by opiates and supports the hypothesis that the binding sites relate to the renal response to aldosterone.

Aldosterone↗

PubMedDate not supplied

The relationship between urinary kallikrein excretion and mineralocorticoids in the rat.

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Aldosterone↗

PubMedDate not supplied

Inhibition of guinea-pig renal [Na + K]-ATPase by normotensive human plasma: effects of a high sodium diet.

The effect of plasma taken from normotensive humans, while on a low and high sodium diet, on [Na + K]-ATPase and 3H-ouabain binding was measured in tubules from guinea-pig kidneys. Plasma from the high sodium, compared to the low sodium, diet period: (a) inhibited [Na + K]-ATPase activity; (b) decreased 3H-ouabain affinity for binding sites; (c) increased the number of available 3H-ouabain binding sites; (d) decreased [Na + K]-ATPase turnover (activity/3H-ouabain binding sites). The inhibition of [Na + K]-ATPase suggests an increase in a (possible) natriuretic factor. The decreased affinity of 3H-ouabain binding suggests an endogenous ouabainoid, which may be the natriuretic factor.

Adult↗

PubMedDate not supplied

Plasma aldosterone levels after KCl loading in rats adapted to a high potassium diet.

Plasma levels of aldosterone, corticosterone, potassium and renin activity, and urinary potassium excretion, were measured in control (CK) rats, and in rats adapted to a high potassium diet (HK), before and after an acute intragastric KCl load. Prior to the KCl load there was no difference in plasma potassium (K) or plasma aldosterone. Following the KCl load, HK rats maintained a lower plasma K, and, except at 30 min after the load, a lower plasma aldosterone than CK rats. At a low plasma K there was no difference in plasma aldosterone between CK and HK rats. At a high plasma K (greater than 8 mmol/l) the HK rats had a higher plasma aldosterone for the same plasma K than CK rats. The enhanced ability to excrete an acute K load seen in HK rats seems unlikely to be due to higher levels of plasma aldosterone.

Aldosterone↗