No abstract

The effect of atrial natriuretic factor (ANF; 1, 10, 100, 1000 pmol/l) on insulin release from the isolated perfused rat pancreas was studied. ANF weakly augmented the glucose (10 mmol/l)-stimulated insulin release during the second (controls: 100%; 1 pmol/l: 99%; 10 pmol/l: 149%, P less than 0.05; 100 pmol/l: 111%; 1000 pmol/l 135%), but not the first phase of the secretory response. In contrast, the first, but not the second phase of arginine (10 mmol/l)-stimulated insulin release was significantly enhanced by ANF (1000 pmol/l; controls: 100%; 1000 pmol/l: 235%, P less than 0.05). The hormone did not influence basal insulin secretion. Our data indicate an insulinotropic effect of ANF on the rat pancreas, which is dependent on the utilized background secretagogues.

The effect of acute modifications of pacing mode and rate on plasma ANP levels was evaluated. ANP was determined in ten resting patients with DDD pacemakers due to binodal disease or intermittent second-and third-degree AV block. At 82/minute pacing rate the ANP plasma levels (normal range 2 to 30 fmol/mL) corresponded to those under AAI (4.05 +/- 2.10 fmol/mL) and DDD (4.18 +/- 2.02 fmol/mL) pacing, but increased significantly (P 0.05) during VVI pacing (6.96 +/- 3.70 fmol/mL). Acceleration of DDD stimulation frequency from 82 to 113/minutes led to significant increase of ANP levels by the factor of three in all chosen AV delays. The lowest ANP plasma levels were measured at 175 msec AV delay under 82/minute pacing rate in DDD mode. Under 113/minutes the differences of ANP concentration after variations of AV delays were less pronounced. The influences of altered atrial pressure and tension on ANP release are discussed to account for changes in ANP plasma levels following different modes and rates of pacemaker stimulation.

Recent reports suggest a role for serotonin in the pathogenesis of primary hypertension and left ventricular (LV) hypertrophy. In this study, we have induced LV hypertrophy by oral feeding of thyroxine at increasing dosages (150-450 micrograms/kg b.wt.) over a 5-week period. The effects of hyperthyroidism on cardiovascular parameters, blood and myocardial serotonin concentrations were assessed. Water-fed rats and formerly hyperthyroid recovered animals served as controls. Thyroxine caused a significant LV hypertrophy: hyperthyroid rats 2.19 +/- 0.16*; controls 1.65 +/- 0.13 g/kg b.wt. (mean +/- SD; *P less than 0.05). An almost complete regression of LV hypertrophy occurred in the recovery group (1.66 +/- 0.20 g/kg b.wt.) 3 weeks after cessation of thyroid hormone application. Thyroxine-treated animals showed a significant increase of serotonin blood levels (thyroxine rats: 2108 +/- 781*, recovery: 1132 +/- 726, controls: 705 +/- 480 ng/ml; *P less than 0.05). The concentrations of serotonin in left ventricular myocardium were increased after thyroid hormone application, whereas the highest levels were found in the recovery group (thyroxine rats: 139.1 +/- 30.4, recovery: 167.2 +/- 43.1, controls: 68.9 +/- 27.9 mg/ml homogenate). Serotonin-containing cells in the left ventricular myocardium were stained immunohistochemically. They were localized perivascularly and were assumed to represent tissue mast cells. In experimental hyperthyroidism the serotonin levels in blood and heart are increased possibly indicating an interaction of both hormones in thyroxine-induced cardiomyopathy.