Journal of hypertension · 1995
Role of the adrenal medulla in control of blood pressure and renal function during frusemide-induced volume depletion.
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Hasbak P, Petersen J S, Shalmi M, Lam H R, Christensen N J, Christensen S
Аннотация
OBJECTIVE: To examine the role of the adrenal medulla in reflex control of mean arterial pressure (MAP), heart rate and renal function parameters during frusemide-induced volume depletion.
DESIGN: Frusemide (6 mg/kg per h) was administered intravenously to two groups of chronically instrumented rats with either sham adrenal medullectomy (n = 15) or adrenal medullectomy (n = 11).
RESULTS: Adrenal medullectomy reduced adrenal adrenaline concentration by 99% and plasma adrenaline concentration by 97%. Plasma corticosterone levels were similar in the two groups, which suggests that adrenal cortical function was not affected by adrenal medullectomy. Although frusemide did not affect arterial pressure in the sham-operated rats, MAP fell by 21 +/- 3 mmHg (mean +/- SEM) during frusemide diuresis in the rats with adrenal medullectomy. Heart rate was lower in the rats with adrenal medullectomy than in the sham-operated rats throughout the study. There were no major differences in renal haemodynamics or overall renal water and sodium handling between the two groups but, at the time of maximal activation of compensatory sodium reabsorption, fractional sodium excretion in the distal nephron segment was significantly higher in the rats with adrenal medullectomy than in the sham-operated rats.
CONCLUSIONS: Adrenal medullary adrenaline release is essential in the control of MAP during frusemide-induced volume depletion. Circulating adrenaline might contribute, by modifying distal tubular sodium reabsorption, to compensatory sodium reabsorption during frusemide-induced volume depletion.
DESIGN: Frusemide (6 mg/kg per h) was administered intravenously to two groups of chronically instrumented rats with either sham adrenal medullectomy (n = 15) or adrenal medullectomy (n = 11).
RESULTS: Adrenal medullectomy reduced adrenal adrenaline concentration by 99% and plasma adrenaline concentration by 97%. Plasma corticosterone levels were similar in the two groups, which suggests that adrenal cortical function was not affected by adrenal medullectomy. Although frusemide did not affect arterial pressure in the sham-operated rats, MAP fell by 21 +/- 3 mmHg (mean +/- SEM) during frusemide diuresis in the rats with adrenal medullectomy. Heart rate was lower in the rats with adrenal medullectomy than in the sham-operated rats throughout the study. There were no major differences in renal haemodynamics or overall renal water and sodium handling between the two groups but, at the time of maximal activation of compensatory sodium reabsorption, fractional sodium excretion in the distal nephron segment was significantly higher in the rats with adrenal medullectomy than in the sham-operated rats.
CONCLUSIONS: Adrenal medullary adrenaline release is essential in the control of MAP during frusemide-induced volume depletion. Circulating adrenaline might contribute, by modifying distal tubular sodium reabsorption, to compensatory sodium reabsorption during frusemide-induced volume depletion.