title: Deoxycorticosterone prevents the blood pressure-lowering effect of calcium in spontaneously hypertensive rats.
abstract: To study the effects of prolonged oral calcium loading on the development of hypertension in spontaneously hypertensive rats (SHR), 48 male animals (age 9 weeks) were divided into four groups according to the treatment: control, calcium, deoxycorticosterone (DOC) and calcium/DOC. Both calcium groups received 1.5% calcium chloride solution ad libitum as their drinking fluid. The animals in the DOC groups were treated with a mineralocorticoid, deoxycorticosterone trimethylacetate 25 mg kg-1 s.c. once a week. Systolic blood pressure (BP) was measured twice a week during the 4-week study period. Calcium loading alone lowered BP (p less than 0.01) after four weeks. Combined with DOC treatment, calcium administration had no significant effect on BP. Calcium loading increased the total plasma calcium concentration in the calcium group (p less than 0.05). Urinary excretions of sodium and potassium were augmented in both groups receiving calcium compared to DOC group. DOC treatment alone increased the excretion of calcium (P less than 0.05). Calcium supplementation decreased the plasma phosphate concentration in both groups (calcium p less than 0.05; calcium/DOC p less than 0.01) as well as the excretion phosphate (p less than 0.005) compared to control. The urinary excretion of cAMP remained unaffected by the calcium treatment. The present results indicate that mineralocorticoid treatment can prevent the BP-lowering effect of calcium in SHR. The mechanism of this action remains unclear, but it does not seem to depend on electrolyte or phosphate balance. The investigation of this action of DOC may provide a means for further exploration of the mechanisms by which increased calcium intake lowers BP in SHR.
authors.affiliation: Department of Biomedical Sciences, University of Tampere, Finland.
authors.forename: H
authors.initials: H
authors.lastname: Wuorela
authors.forename: I
authors.initials: I
authors.lastname: Pörsti
authors.forename: E
authors.initials: E
authors.lastname: Siltaloppi
authors.forename: P
authors.initials: P
authors.lastname: Arvola
authors.forename: A K
authors.initials: AK
authors.lastname: Nurmi
authors.forename: P
authors.initials: P
authors.lastname: Säynävälammi
authors.forename: H
authors.initials: H
authors.lastname: Vapaatalo
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D002118:Calcium / Q000037:antagonists & inhibitors* / Q000494:pharmacology / Q000652:urine; D000252:Calcium-Transporting ATPases / Q000037:antagonists & inhibitors; D000242:Cyclic AMP / Q000652:urine; D003900:Desoxycorticosterone / Q000494:pharmacology*; D004912:Erythrocytes / Q000187:drug effects / Q000378:metabolism; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology; D008297:Male; D010710:Phosphates / Q000652:urine; D011188:Potassium / Q000652:urine; D051381:Rats; D011918:Rats, Inbred SHR; D012964:Sodium / Q000652:urine; D014563:Urodynamics / Q000187:drug effects; D014882:Water-Electrolyte Balance / Q000187:drug effects
chemical_list: D010710:Phosphates; D003900:Desoxycorticosterone; D012964:Sodium; D000242:Cyclic AMP; D000252:Calcium-Transporting ATPases; D011188:Potassium; D002118:Calcium