The effect of chronic ACTH treatment on blood pressure and urinary excretion of steroids in the rat

Haack, D.; Engel, R.P.; Vecsei, P.

doi:10.1007/bf01477471

Cited by 32 publications

(22 citation statements)

References 13 publications

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“…Thus there is evidence for a neurally mediated mechanism in the maintainance of hypertension in this model. ACTH has been shown to raise blood pressure in the rat (Haack et al 1978) and in our own studies (Whitworth et al 1990) we have shown that this rise is adrenally dependent. In previous studies we showed that the increase in blood pressure that can be attributed to ACTH is about 12 mmHg by direct cannulation and 27 mmHg by the tail cuff method.…”

Section: Discussionmentioning

confidence: 87%

Role of the Sympathetic Nervous System in the Onset of Hypertension in the Rat: The Effect of 6‐oh‐dopamine

Whitworth

1991

Clin Exp Pharma Physio

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1. The effect of chemical sympathectomy with 6-OH-dopamine (6-OHDA) on the onset of adrenocorticotrophin (ACTH)-induced hypertension was examined in Sprague-Dawley rats (n = 23). 2. 6-OHDA injection produced a fall in systolic blood pressure (SBP) from 100 +/- 5 mmHg control to 74 +/- 4 mmHg post-6-OHDA Treatment Day 1 (P less than 0.001), but did not alter food or water intake, urine volume or electrolyte excretion. 3. Compared with sham injection, ACTH-treated rats showed an increase in blood pressure (sham: 98 +/- 7 mmHg; ACTH: 123 +/- 9 mmHg on Treatment Day 10; P less than 0.01), loss of bodyweight, and increases in water intake and urine volume. 4. The magnitude of the blood pressure rise on ACTH was greater in 6-OHDA-treated rats than in intact control rats. Metabolic changes were similar. 5. Chemical sympathectomy with 6-OHDA did not delay or block the onset of ACTH hypertension in the rat.

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Section: Discussionmentioning

confidence: 87%

Role of the Sympathetic Nervous System in the Onset of Hypertension in the Rat: The Effect of 6‐oh‐dopamine

Whitworth

1991

Clin Exp Pharma Physio

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“…In addition, the usual increase in aldoste¬ rone secretion by dispersed cell preparations in response to stimulation with ACTH or potassium ions was absent in the ACTH treated adrenals (Fig. 5) (Tucci et al 1967;Newton & Laragh 1968;Biglieri et al 1969Biglieri et al , 1979Scoggins et al 1974;Haack et al 1978;Henderson & McCaa 1979;Komor & Müller 1979). A decrease in the number of angiotensin II receptors in the rat adrenal following 6 days ACTH-treatment has been described recently, together with a decreased responsiveness of dispersed cell preparations to stimulation by various agents including angiotensin II, potassium, ACTH and 8-Br-cyclic AMP (Rao & Lehoux 1979;Aguilera & Fujita 1980).…”

Section: Synthesis Of Aldosteronementioning

confidence: 92%

“…This paper therefore re-examines some of the functional aspects of adrenocortical zonation after prolonged ACTH treatment. Furthermore, since this is known to induce hypertension in several species (Scoggins et al 1974;Haack et al 1978;McCaa 1978;Henderson & McCaa 1979;Freeman et al 1980), changes in blood pressure in ACTH-treated rats were monitored in an at¬ tempt to relate them to changes in adrenal func¬ tion.…”

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confidence: 99%

Effects of prolonged ACTH treatment on adrenal steroidogenesis and blood pressure in rats

Vazir

Whitehouse

Vinson

et al. 1981

Acta Endocrinologica

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The effects of long-term (8\p=n-\16 days) treatment of rats with synthetic 1\p=n-\24 ACTH (100 \g=m\g/day) on adrenocortical function and blood pressure have been investigated. After 16 days, treated animals had considerably enlarged adrenals, a reduced body weight and systolic blood pressures of 169 \m=+-\3 mmHg compared with 117 \m=+-\4 mmHg in untreated controls. Corticosterone and 18-hydroxydeoxycorticosterone (18-OH-DOC) production in vitro from endogenous precursors was increased 3\p=n-\4-foldin capsules and 1.5-fold in inner zones, whereas production of aldosterone and 18-hydroxycorticosterone was reduced. Similar increases in corticosterone and 18-OH-DOC production by capsules and inner zones were found with 12 days' treatment, during which blood pressure increased to a constant level after 8 days. Secretion of 18-OH-DOC and corticosterone by the left adrenal gland in anaesthetised rats was significantly higher in the ACTH treated group while the secretion of aldosterone was more than 80% lower. The aldosterone response of dispersed capsule cells to stimulation by potassium (8.4 mmol/l) and ACTH (10\m=-\8mol/l) was lost following ACTH treatment. The responses of inner zone and capsule dispersed cell preparations to ACTH (10\m=-\8mol/l) were reduced compared with controls. Restriction of the rats' sodium intake (to less than 20 \g=m\mol/day)during ACTH treatment did not prevent the decrease in aldosterone production in vitro, nor the increase in blood pressure. Overall chronic ACTH treatment resulted in a marked inhibition of aldosterone production and response to stimulation coupled with an increase in corticosterone and 18-OH-DOC production. The results are consistent with the hypothesis that ACTH induces functional transformation of the glomerulosa cell to a fasciculata-like cell. It appears that the hypertension in ACTH treated rats should be related to the increased secretion of corticosterone and 18-OH-DOC, and that aldosterone and 18-hydroxycorticosterone are not involved.Address reprint requests to :

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“…6 Several lines of evidence indicate the existence of digitalis-like immunoreactive endogenous inhibitors of Na,K-ATPase in mammalian tissues.…”

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confidence: 99%

Plasma Marinobufagenin-Like and Ouabain-Like Immunoreactivity in Adrenocorticotropin-Treated Rats

Федорова

Anderson

Bagrov

1998

American Journal of Hypertension

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Recently, an endogenous digitalis-like factor (EDLF) was shown to be stimulated in corticotropin (ACTH) hypertension in the rat. We have shown that mammalian plasma contains a vasoconstrictor Na,K-ATPase inhibitor, which cross-reacts with an antibody to amphibian EDLF, marinobufagenin. In the present experiment, the effect of 8 days of intramuscular ACTH treatment (0.5 mg/kg/day) of male Fisher 344؋ ؋NB rats on blood pressure, plasma ouabain-like and marinobufagenin-like immunoreactivity, and on the activity of Na,KATPase in aortic sarcolemma were studied.The C hronic administration of ACTH has been reported to raise the blood pressure of various mammalian species, including humans and rats.1,2 The hypertensinogenic effects of ACTH administration are dependent on the adrenal cortex and could be prevented by adrenalectomy.1,3 ACTH-induced hypertension has been attributed to the action of various adrenocorticosteroids, including aldosterone and progesterone derivatives in sheep, 4 cortisol in humans, 5 and corticosterone in the rat. 6 Several lines of evidence indicate the existence of digitalis-like immunoreactive endogenous inhibitors of Na,K-ATPase in mammalian tissues.7,8 Endogenous digitalis-like factors (EDLF) are believed to play an important role in sodium homeostasis and to contribute to several forms of human and animal hypertension.9,10 The adrenal cortex has been shown to be one of the major sources of EDLF in mammals.11,12 Endogenous ouabain was the first EDLF to be purified from human plasma, 13 and recent evidence indicates that Recently, we showed that a bufodienolide Na,KATPase inhibitor, marinobufagenin, elicits vasoconstrictor and Na,K-pump inhibitory effects in rat aorta. 19 Subsequently, it was established that mammalian plasma contains marinobufagenin-like immunoreactive material, which is responsive to saline volume expansion and is chromatographically indistinguishable from amphibian marinobufagenin. 15,20,21 When effects of marinobufagenin and ouabain were compared in membrane fractions prepared from rat aortae, marinobufagenin preferentially inhibited Na,KATPase in vascular smooth muscle membranes (␣-1 isoform), whereas ouabain demonstrated higher affinity toward Na,K-ATPase from vascular nerve endings (␣-3 isoform). 22In 1994, Li et al 23 showed that hypertension in rats occurring after 8 days of ACTH administration was associated with an increase in plasma digoxin-like immunoreactivity. Subsequently, Yamada et al 24 showed that ACTH treatment of rats for 15 days increased blood pressure and plasma levels and urinary release of an ouabain-like immunoreactive material.Recent observations suggest that mammalian plasma contains several substances with the ability to inhibit the sodium pump and to interact with digitalis antibodies, 8,25 and that different digoxin antibodies demonstrate wide variability in their capacity to detect EDLF. 7,26 The purpose of the present study was to investigate whether ACTH hypertension in the rat is associated with increased plasma levels of marinobufagenin-l...

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The effect of chronic ACTH treatment on blood pressure and urinary excretion of steroids in the rat

Cited by 32 publications

References 13 publications

Role of the Sympathetic Nervous System in the Onset of Hypertension in the Rat: The Effect of 6‐oh‐dopamine

Role of the Sympathetic Nervous System in the Onset of Hypertension in the Rat: The Effect of 6‐oh‐dopamine

Effects of prolonged ACTH treatment on adrenal steroidogenesis and blood pressure in rats

Plasma Marinobufagenin-Like and Ouabain-Like Immunoreactivity in Adrenocorticotropin-Treated Rats

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