Serum corticosteroids at the high and low points of the circadian rhythm in rats with regenerating adrenals

Gallant, Samuel; Brownie, Alexander C.

doi:10.1016/0024-3205(79)90043-2

Cited by 18 publications

(10 citation statements)

References 12 publications

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“…This rat strain was initially shown to be resistant to adrenalregeneration hypertension, 11 which is believed to be due to excess production of mineralocorticoids. 12 - 13 More recently it has been demonstrated that WF rats are also resistant to hypertension produced by administration of DOC and salt. 9 The resistance to hypertension in the WF strain may be specific to mineralocorticoid hypertension since two-kidney Goldblatt hypertension develops comparably in WF and Sprague-Dawley rats.…”

Section: Resultsmentioning

confidence: 99%

Vascular responsiveness in rats resistant to aldosterone-salt hypertension.

Bruner

1992

Hypertension

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Wistar-Furth rats have been shown to be resistant to mineralocortlcoid-salt hypertension, but the mechanism for this resistance is unknown. In the current experiments, adult male Wistar and Wistar-Furth rats were given a subcutaneous aldosterone infusion (0.15 /ig/hr) for 4 weeks, and changes in blood pressure and vascular reactivity were studied. Rats received a 1% NaCI, 0.2% KC1 solution to drink. After 4 weeks of aldosterone infusion, systolic blood pressure measured using a tail-cuff technique had increased by 60 mm Hg in Wistar rats but was unchanged in Wistar-Furth rats. Hypokalemia occurred in both strains in response to the aldosterone infusion. Isolated, helically cut strips of common carotid artery and aorta were prepared for isometric force recording. Cumulative concentration-response curves to norepinephrine, serotonin, KCI, calcium, nitroprusside, and acetylcholine were performed in carotid artery strips, and concentration-response curves to ouabain were performed in aortic strips. Increased vascular contractile sensitivity to KCI, ouabain, norepinephrine, and serotonin was observed in vessels from Wistar rats treated with aldosterone and salt The same treatment in Wistar-Furth rats produced only increased vascular sensitivity to ouabain and serotonin, and these changes were of smaller magnitude than those seen in Wistar rats. Aldosterone-salt treatment produced decreased vascular sensitivity to acetylcholine and nitroprusside in both Wistar and Wistar-Furth rats. These results support the hypothesis that resistance of Wistar-Furth rats to aldosterone-salt hypertension is due to resistance to the effects of aldosterone-salt treatment that normally result in increased vasoconstrictor sensitivity. espite long-standing recognition that hypertension can be produced by mineralocorticoid excess, the physiological mechanisms that contribute to the genesis and maintenance of such hypertension are still a matter of debate. One factor that has been suggested to contribute to mineralocorticoid-salt hypertension in experimental animals is changes in the sensitivity of vascular smooth muscle to vasoactive stimuli. An increase in sensitivity to vasoconstrictors such as norepinephrine and serotonin has been demonstrated in vascular preparations from mineralocorticoid-salt-treated rats, 1 " 4 and in some cases these vascular changes have been shown to precede the development of elevated blood pressure.5 - 6 The changes in vascular reactivity do not seem to be secondary to hypertension per se because protection of vascular beds from high pressure by proximal arterial ligation or antihypertensive therapy does not prevent the appearance of such changes. It recently has been reported that hypertension does not develop in response to the administration of excess deoxycorticosterone (DOC) and salt in the WistarFurth (WF) rat strain. 9 The current experiments were designed to test the hypothesis that a lack of development of changes in vascular reactivity is a mechanism involved in the resistance of WF rats to this form o...

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Section: Resultsmentioning

confidence: 99%

Vascular responsiveness in rats resistant to aldosterone-salt hypertension.

Bruner

1992

Hypertension

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“…17 The serum samples were extracted and then chromatographed in a solvent system of cyclohexane:methanol:water (100:50:25 v/v) by a similar method previously described. 18 In this chromatography system, DOC had an Rf value of 0.29 and was well separated from MT, MAD, B, 18-hydroxy-DOC, and progesterone, which had Rf values of 0.46, 0.11, 0.01, 0.001 and 0.81 respectively. The cross-reactivities of these steroids with the DOC antibody were: MT (0.2%), MAD (0.1%), B (2%), 18-hydroxy-DOC (0.01%), and progesterone (95%).…”

Section: Collection Of Rat Serum and Serum Steroid Assaysmentioning

confidence: 99%

“…However, when the 1800-hour blood samples are analyzed, it is clear that the DOC/B ratio is much higher in the MAD-treated rats than in controls. The advantage of measuring corticosteroid concentrations on blood samples withdrawn at or near the high point of the circadian rhythm has been shown by us for adrenal regeneration hypertension 18 and now this is also applicable to androgen-induced hypertension.…”

Section: Four Weeks Treatmentmentioning

confidence: 99%

Peripheral serum corticosteroid concentrations in relation to the rat adrenal cortical circadian rhythm in androgen-induced hypertension.

Fink¹,

Gallant²,

Brownie³

1980

Hypertension

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SUMMARY Adrenal function was assessed in control rats and in rats treated for 2 and 4 weeks with 17a-methylandrosteriediol (MAD; 17a-methyl-5-androstene-30,170-diol), a synthetic androgen known.to produce hypertensive cardiovascular disease. In both groups and at both time periods, a circadian rhythm of blood corticosteroid concentrations was observed. The high point for serum corticosterone (B), 18-hydroxy-lldeoxycordcosterone (18-hydroxy-DOC), and 11-deoxycorticosterone (DOC) concentrations occurred at the beginning of the dark period (1800 hours), and the low point occurred at the onset of the light period (0600 hours). Serum concentrations of DOC were always found to be higher in MAD-treated rats as compared with controls. The serum concentrations of B and 18-hydroxy-DOC were lower than control values at 1800 hours but higher than control concentrations at 0600 hours. The in vitro 11/3-and 18-hydroxylation of DOC was markedly reduced with MAD treatment. In contrast, cholesterol side-chain cleavage activity was higher in animals treated with MAD. These in vitro findings correlated with spectral studies that showed a decreased binding of DOC to cytochrome P45O 1U and increased binding of cholesterol to cytochrome P450^x. These studies suggest that MAD treatment selectively decreases 11/9-and 18-hydroxylatlon in adrenal mitochondria, and this results in an increased serum concentration of DOC, a hypertensinogenic steroid. This effect of MAD on peripheral serum DOC concentration is most readily observed in quiescent animals at the high point of the circadian rhythm.

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“…The development of high BP is associated with regeneration of the adrenal cortex and raised plasma steroid levels of both mineralocorticoids (e.g. Gallant & Brownie, 1979) and glucocorticoids (e.g. Buckingham & Hodges, 1975 mg/kg/h).…”

Section: Mean Concentrations Of 0-and S-substituted Metabolites Inmentioning

confidence: 99%

Untitled

1982

British J Pharmacology

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Serum corticosteroids at the high and low points of the circadian rhythm in rats with regenerating adrenals

Cited by 18 publications

References 12 publications

Vascular responsiveness in rats resistant to aldosterone-salt hypertension.

Vascular responsiveness in rats resistant to aldosterone-salt hypertension.

Peripheral serum corticosteroid concentrations in relation to the rat adrenal cortical circadian rhythm in androgen-induced hypertension.

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