EFFECTS OF OCTREOTIDE ON CARDIOVASCULAR HORMONES AND HEMODYNAMICS IN CONSCIOUS DOGS

Octreotide inhibits the secretion of several hormones and exerts vasop ressor 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 o f conscious dogs were studied: group I (n=11) received saline infusion after placebo, group II (n=10), the same infusion after octreotide, g roup 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 ris e (p<0.001) of plasma ANF from 32.4+/-4.1 to 59.0+/-8.5 pM after place bo 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-f old increase (p<0.005) of right and left atrial pressures, With a high er dose of octreotide (4 mu g/kg) injected in 4 dogs, plasma ANF incre ased 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. Octreotid e did not influence the basal secretion of ANF, endothelin-1, angioten sin II and catecholamines. However, in basal conditions, octreotide in jection resulted in a 9% increase (p<0.005) of left ventricular systol ic pressure, unobserved after placebo, Plasma glucose decreased (p<0.0 05) in groups receiving octreotide. Thus, octreotide does not impair t he stretch-mediated release of ANF which implies a release mechanism i ndependent from somatostatin receptors and consequent changes in intra cellular c-AMP. Octreotide has also a presser effect, unrelated to cha nges in vasoactive peptide production.