deoxycortone-pivalate and Cardiomegaly

The effects of increased dietary calcium intake on blood pressure and arterial function were investigated in one-kidney deoxycorticosterone-salt hypertensive Wistar rats. The calcium content of the control diet was 1.1%, and that of the high calcium diet, 2.5%. During the 10-week study calcium supplementation markedly attenuated the steroid-salt-induced rise in blood pressure and the associated cardiac hypertrophy. Responses of mesenteric arterial rings in vitro were examined at the end of the study. In deoxycorticosterone-salt-treated rats, the contractile sensitivity of endothelium-denuded preparations to norepinephrine, 5-hydroxytryptamine, and KCl, and the inhibitory effect of nifedipine on KCl-evoked responses were enhanced. It is interesting that the high calcium diet alleviated the steroid-salt-induced increase in sensitivity to KCl but did not significantly affect it to the receptor-mediated agonists norepinephrine and 5-hydroxytryptamine. Thus, sensitivity to membrane depolarization was reduced by calcium supplementation. Smooth muscle responses were also studied by challenging the preparations with KCl in a calcium-free solution, after which calcium was added to the organ bath in increasing concentrations. In steroid-salt-treated rats, these calcium contractions were attenuated, but concomitant calcium supplementation normalized the responses, suggesting improved cell membrane handling of calcium. In addition, the mineralocorticoid-salt treatment impaired relaxation responses of endothelium-intact arterial rings to acetylcholine, sodium nitroprusside, and isoproterenol.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Acetylcholine; Animals; Blood Pressure; Calcium; Calcium, Dietary; Cardiomegaly; Desoxycorticosterone; Endothelium, Vascular; Hypertension; In Vitro Techniques; Isoproterenol; Male; Mesenteric Arteries; Nitroprusside; Norepinephrine; Potassium Chloride; Rats; Rats, Wistar; Serotonin; Sodium Chloride; Vasoconstriction

Dietary sodium and the myocardial alpha 1-receptor have been implicated in the hypertrophic response of myocardial tissue. Alterations in sodium homeostasis have been demonstrated to influence sympathetic nervous function, centrally and peripherally. In this investigation, we have examined the effect of dietary sodium on the development of myocardial hypertrophy; and the role of sympathetic neuroeffector mechanisms in the hypertrophic response. Studies were performed in three groups of uninephrectomized rats: A-regular diet; B-1% saline/regular diet; C-1% Saline/doca/regular diet. Groups A and B did not develop systemic hypertension (SHT). Saline treatment increased heart weight and the density of surface alpha 1-receptors; myocardial norepinephrine (NE) was reduced. Group C developed SHT. Heart weight was greatest in Group C; and myocardial NE was severely depleted. Downregulation of myocardial alpha 1-receptors, a finding consistent with the hyperadrenergic state, was observed in Group C. Our results suggest dietary sodium may modulate hypertrophic response in myocardial tissue, by altering sympathetic neuroeffector mechanisms.

Topics: Animals; Blood Pressure; Cardiomegaly; Desoxycorticosterone; Hypertension; Iodine Radioisotopes; Male; Myocardium; Norepinephrine; Organ Size; Rats; Rats, Inbred Strains; Receptors, Adrenergic, alpha; Sodium, Dietary; Sympathetic Nervous System