Comparative study on development of corticosterone and DOCA hypertension in rats

Abstract

The administration of corticosterone for 5 consecutive days to normal rats on a standard sodium intake induced negative sodium and water balance. These effects were opposite those observed under DOCA treatment. However, not only under DOCA but also under corticosterone treatment extracellular fluid volume (ECFV) and plasma volume (PV) increased, and blood pressure (BP) rose in parallel. Plasma renin and angiotensin II concentrations declined under the influence of both steroids. Plasma arginine vasopressin concentrations increased under DOCA, whereas they transiently decreased under corticosterone administration. These data suggest that the common mediator for BP elevation due to steroid excess would be an increase in ECFV and PV. The pathways by which this increase is achieved seem to be different. Under DOCA treatment ECFV and PV increased subsequent to renal sodium and water retention. Under corticosterone, however, sodium and water were shifted from intra- to extracellular compartments, and a fraction of this shifted sodium and water was conserved in extracellular space, most likely because corticosterone also affected renal sodium handling.

Effects of Antenatal Corticosteroids on Blood Pressure in Very Low Birth Weight Infants During the First 24 Hours of Life

“…26 Considerable evidence implicates the pituitary-adrenal axis and glucocorticoids as regulators of systemic BP in the preterm infant. [27][28][29][30][31][32] Glucocorticoids influence BP through several mechanisms: (1) increasing plasma and extracellular fluid by shifting fluid from the intracellular compartment, 29,30 (2) inducing the synthesis of angiotensinogen in hepatic cells, 33 (3) inhibiting the synthesis of vasodilator prostaglandins, 34,35 (4) increasing vascular responsiveness to ␣ adrenergic amines, 36,37 and (5) inhibiting nitric oxide production. 38 Preterm infants with hypotension that is resistant to vasopressors and volume expanders respond to relatively small doses of hydrocortisone.…”

11β-Hydroxysteroid Dehydrogenase and Corticosteroid Action in Lyon Hypertensive Rats

“…Conventionally, mineralocorticoid hormones cause an antinatriuresis and kaliuresis, whereas glucocorticoids, as found in the present study, cause a natriuresis and kaliuresis. 17,18 A smaller natriuretic response was observed in LL rats at 24 hours, but there was no difference in potassium excretion. The relative natriuresis seen in LH rats may relate to inherent differences of blood pressure between strains rather than altered 11␤-HSD activity.…”

Pharmacological Studies on (4S)-1-Methyl-3-{(2S)-2-[N-((1S)-1-Ethoxycarbonyl-3-Phenylpropyl)amino] Propionyl}-2-Oxolmidazolidine-4-Carboxylic Acid Hydrochloride (TA-6366), a New ACE Inhibitor: I. ACE Inhibitory and Anti-Hypertensive Activities

“…On the other hand, it is known that PRA is suppressed in DOCA/s HRs (9). Considering that TA-6366 showed a remarkable antihypertensive effect in 2K, 1 C-RHRs, but exhibited little effect in DOCA/ s-HRs, the effect in 2K,1 C-RHRs seems to be mainly attributable to a decrease in circulating AT-II levels via ACE inhibition.…”