Diurnal and seasonal variations of plasma adrenal steroid hormone in the white-throated sparrow, Zonotrichia albicollis

Intramuscular injections of long-acting synthetic ACTH (45 U twice daily for 5 days) caused a large increase in the intake of 0.5 M NaCl in sheep. Mean Na intake of the sheep on the last 3 days of treatment approximated 50% of their total extracellular fluid Na. The mineral appetite was specific for NaCl. Intakes of 0.5 M KCl or 0.25 M CaCl2 were not significantly altered. The enhanced appetite for Na induced by ACTH appeared to precede any increase in urinary Na excretion. ACTH treatment was ineffective in adrenalectomized sheep. However, an infusion into adrenalectomized sheep of a combination of adrenal steroid hormones (including aldosterone, deoxycorticosterone, 11-deoxycortisol, cortisol, and corticosterone) that contrived blood levels similar to those, obtained with ACTH treatment in normal sheep did induce Na appetite. Thus, ACTH induces a specific, adrenal-steroid hormone-dependent Na appetite in sheep.

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TeBG- and CBG-bound steroid hormones in rabbits are available for influx into uterus in vivo

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1988.254.1.e79 ◽

1988 ◽

Vol 254 (1) ◽

pp. E79-E83

Author(s):

G. Chaudhuri ◽

K. A. Steingold ◽

W. M. Pardridge ◽

H. L. Judd

Keyword(s):

Steroid Hormones ◽

Plasma Proteins ◽

Steroid Hormone ◽

Rabbit Serum ◽

Injection Technique ◽

Metabolic Clearance ◽

Adrenal Steroid ◽

Corticosteroid Binding Globulin

The metabolic clearance rate (MCR) of gonadal or adrenal steroid hormones in rabbits often does not bear the expected inverse relationship with hormone binding to testosterone-binding globulin (TeBG) or corticosteroid-binding globulin (CBG). This suggests TeBG or CBG may not impede steroid hormone delivery to tissues. The effects of rabbit plasma proteins on the influxes of 3H-labeled steroids from the circulation into the rabbit uterus were measured in vivo using a tissue sampling single-injection technique. In the absence of plasma proteins, estradiol (E2) and testosterone (T) were freely diffusible through the uterine microvasculature (i.e., extraction greater than 80%). The extractions of dihydrotestosterone (DHT) and corticosterone (B) ranged from 60 to 72%, while that of cortisol (F) was reduced at 40%. Rabbit serum exerted no inhibition of the influxes of the steroids tested. The influxes of T and B greatly exceeded the rates that would be expected if only the free and albumin-bound fractions estimated in vitro were diffusible in vivo. However, the extraction of [3H]corticosteroid-binding globulin or bovine [3H]albumin were low, consistent with little, if any, extravascular uptake of the plasma proteins. The results indicate both albumin-bound and globulin-bound steroid hormone are available for transport into the uterus in the rabbit in vivo without significant exodus of the plasma protein, per se.

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Adrenal steroid hormone imbalance predicts survival in chronic heart failure

Journal of Cardiac Failure ◽

10.1016/j.cardfail.2004.06.312 ◽

2004 ◽

Vol 10 (4) ◽

pp. S102

Author(s):

Darlington O. Okonko ◽

Martino Crosato ◽

Stephan von Haehling ◽

Paul R. Kalra ◽

Gerhard Diller ◽

...

Keyword(s):

Heart Failure ◽

Chronic Heart Failure ◽

Steroid Hormone ◽

Adrenal Steroid ◽

Hormone Imbalance

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Dehydroepiandrosterone inhibits ICa,L and its window current in voltage-dependent and -independent mechanisms in arterial smooth muscle cells

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00291.2018 ◽

2018 ◽

Vol 315 (6) ◽

pp. H1602-H1613

Author(s):

Rikuo Ochi ◽

Sukrutha Chettimada ◽

Igor Kizub ◽

Sachin A. Gupte

Keyword(s):

Smooth Muscle ◽

Smooth Muscle Cells ◽

Steroid Hormone ◽

Muscle Cells ◽

Channel Blockers ◽

Adrenal Steroid ◽

Voltage Dependent ◽

Window Current ◽

Arterial Smooth Muscle Cells ◽

Glucose 6 Phosphate Dehydrogenase

Dehydroepiandrosterone (DHEA) is an adrenal steroid hormone, which has the highest serum concentration among steroid hormones with DHEA sulfate (DHEAS). DHEA possesses an inhibitory action on glucose-6-phosphate dehydrogenase (G6PD), the first pentose-phosphate pathway enzyme that reduces NADP+ to NADPH. DHEA induced relaxation of high K+-induced contraction in rat arterial strips, whereas DHEAS barely induced it. We studied the effects of DHEA on L-type Ca2+ current ( ICa,L) of A7r5 arterial smooth muscle cells and compared the mechanism of inhibition with that produced by the 6-aminonicotinamide (6-AN) competitive inhibitor of G6PD. DHEA moderately inhibited ICa,L that was elicited from a holding potential (HP) of −80 mV [voltage-independent inhibition (VIDI)] and accelerated decay of ICa,L during the depolarization pulse [voltage-dependent inhibition (VDI)]. DHEA-induced VDI decreased peak ICa,L at depolarized HPs. By applying repetitive depolarization pulses from multiple HPs, novel HP-dependent steady-state inactivation curves ( f∞-HP) were constructed. DHEA shifted f∞-HP to the left and inhibited the window current, which was recorded at depolarized HPs and obtained as a product of current-voltage relationship and f∞-HP. The IC50 value of ICa,L inhibition was much higher than serum concentration. DHEA-induced VDI was downregulated by the dialysis of guanosine 5′- O-(2-thiodiphosphate), which shifted f∞-voltage to the right before the application of DHEA. 6-AN gradually and irreversibly inhibited ICa,L by VIDI, suggesting that the inhibition of G6PD is involved in DHEA-induced VIDI. In 6-AN-pretreated cells, DHEA induced additional inhibition by increasing VIDI and generating VDI. The inhibition of G6PD underlies DHEA-induced VIDI, and DHEA additionally induces VDI as described for Ca2+ channel blockers. NEW & NOTEWORTHY Dehydroepiandrosterone, the most abundantly released adrenal steroid hormone with dehydroepiandrosterone sulfate, inhibited L-type Ca2+ current and its window current in aortic smooth muscle cells. The IC50 value of inhibition decreased with the depolarization of holding potential to 15 µM at −20 mV. The inhibition occurred in a voltage-dependent manner as described for Ca2+ channel blockers and in a voltage-independent manner because of the inhibition of glucose-6-phosphate dehydrogenase.

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