Marks E S, Ohman K P, Keiser H R
Hypertension-Endocrine Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD.
Acta Physiol Scand. 1990 Feb;138(2):161-5. doi: 10.1111/j.1748-1716.1990.tb08828.x.
The reduction in blood pressure due to ANF(103-126) fails to elicit reflex cardioacceleration in the conscious rat. To examine baroreflex sensitivity, the effect of ANF(103-126) on the heart period (HP) response to rapid central volume expansion and to alterations in mean arterial pressure (MAP) induced by bolus injections of phenylephrine and sodium nitroprusside was assessed. ANF(103-126) significantly augmented the bradycardic response induced by acute volume expansion from 426 +/- 21 to 391 +/- 23 beats min-1 versus 421 +/- 23 to 405 +/- 24 without ANF(103-126). Baroreflex sensitivity was defined by the ratio of the change in heart period to the maximal change in mean arterial pressure. The dose of ANF(103-126) utilized did not affect basal heart rate or the magnitude of the mean arterial pressure response to phenylephrine but did significantly enhance the nitroprusside-induced decrease in mean arterial pressure. Baroreceptor sensitivity to phenylephrine was significantly increased by ANF(103-126): 0.997 +/- 0.07 (ms mmHg-1) during ANF(103-126) vs 0.613 +/- 0.08 during vehicle. The total duration of the heart rate response to phenylephrine was also prolonged. In contrast, ANF(103-126) did not alter the baroreceptor sensitivity (1.45 +/- 0.3 vs 1.43 +/- 0.2 ms mmHg-1) or duration of heart rate response to nitroprusside. In the conscious rat, ANF(103-126) modifies the heart rate response to changes in mean arterial pressure and acute central volume expansion. This action appears to be dependent on stimulation of cardiac vagal afferents.