Abstract:
:1. The hypothesis that adrenocorticotrophin (ACTH)-induced hypertension is a consequence of steroid-induced hyperinsulinaemia was tested using the somatostatin analogue (sandostatin, octreotide) to inhibit insulin release in Sprague-Dawley (SD) rats (n = 41). 2. Octreotide (20 micrograms, twice daily) did not modify blood pressure, plasma glucose, bodyweight, water and electrolyte balance, or organ weights but inhibited insulin secretion in the SD rat. 3. Compared with sham injection, ACTH-treated (0.5 mg/kg per day) SD rats showed an increase in blood pressure (sham 111 +/- 4 mmHg; ACTH 140 +/- 5 mmHg on treatment day 10 (P < 0.01), organ weights, water intake, urine volume, plasma glucose, insulin and sodium concentrations, and decrease of bodyweight and plasma potassium concentration. 4. Systolic blood pressure in rats treated with combined octreotide and ACTH was similar to that in rats on ACTH alone. Plasma insulin concentration was lower in octreotide + ACTH treated rats than with ACTH treatment alone. There were no differences in body or organ weights, plasma glucose, water or electrolyte balance. 5. Octreotide lowered plasma insulin concentration to the normal range but did not modify ACTH-induced hypertension in SD rats. These data do not support the notion that insulin-mediated alterations in blood pressure are a major mechanism for ACTH-induced hypertension in the rat.
journal_name
Clin Exp Pharmacol Physioljournal_title
Clinical and experimental pharmacology & physiologyauthors
Li M,Wong KS,Whitworth JAdoi
10.1111/j.1440-1681.1993.tb01647.xsubject
Has Abstractpub_date
1993-10-01 00:00:00pages
647-53issue
10eissn
0305-1870issn
1440-1681journal_volume
20pub_type
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