Effects of octreotide on cardiovascular hormones and haemodynamics in conscious dogs

Octreotide inhibits the secretion of several hormones and exerts vasopressor effects. To clarify the mechanism of atrial natriuretic factor (ANF) secretion and to assess the cardiovascular effects of octreotide in relation to changes in vasoactive peptide secretion, four groups of conscious dogs were studied: group I (n=11) received saline infusion after placebo, group II (n=10), the same infusion after octreotide, group III (n=10), placebo only and group IV (n=10) octreotide injection only. Saline (10% body wt) was infused over 40 min after subcutaneous injection of placebo or octreotide (1 mu g/kg), Saline produced a rise (p<0.001) of plasma ANF from 32.4+/-4.1 to 59.0+/-8.5 pM after placebo and from 35.6+/-5.5 to 77.0+/-12.6 pM after octreotide. This rise, not significantly different between groups I and II paralleled a 4-5-fold increase (p<0.005) of right and left atrial pressures, With a higher dose of octreotide (4 mu g/kg) injected in 4 dogs, plasma ANF increased by 27.5+/-5 pM. During hypervolemia, plasma endothelin-1 remained unchanged but plasma angiotensin II and epinephrine decreased (p<0.05) approximately by 80% without being affected by octreotide. Octreotide did not influence the basal secretion of ANF, endothelin-1, angiotensin II and catecholamines. However, in basal conditions, octreotide injection resulted in a 9% increase (p<0.005) of left ventricular systolic pressure, unobserved after placebo, Plasma glucose decreased (p<0.005) in groups receiving octreotide. Thus, octreotide does not impair the stretch-mediated release of ANF which implies a release mechanism independent from somatostatin receptors and consequent changes in intracellular c-AMP. Octreotide has also a presser effect, unrelated to changes in vasoactive peptide production.