Influence of somatostatin analogue (SMS 201-995, octreotide) on blood pressure in adrenocorticotrophin (ACTH) treated rats: role of hyperinsulinaemia in ACTH hypertension

• Published in: Clinical and experimental pharmacology & physiology Vol. 20; no. 10; p. 647
• Main Authors: Li, M, Wong, K S, Whitworth, J A
• Format: Journal Article
• Language: English
• Published: Australia 01-10-1993
• Subjects: Adrenocorticotropic Hormone - pharmacology; Animals; Blood Pressure - drug effects; Hyperinsulinism - physiopathology; Hypertension - chemically induced; Hypertension - drug therapy; Hypertension - physiopathology; Insulin - blood; Male; Octreotide - pharmacology; Radioimmunoassay; Rats; Rats, Sprague-Dawley
• ISSN: 0305-1870
• DOI: 10.1111/j.1440-1681.1993.tb01647.x

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.