Mechanosensitive cardiac C-fiber response to changes in left ventricular filling, coronary perfusion pressure, hemorrhage, and volume expansion in rats

Left ventricular (LV) end-diastolic pressure (LVEDP) increase due to volume expansion (VExp) enhances mechanosensitive vagal cardiac afferent C-fiber activity (CNFA), thus decreasing renal sympathetic nerve activity (RSNA). Hypotensive hemorrhage (hHem) attenuates RSNA despite decreased LVEDP. We hypothesized that CNFA increases with any change in LVEDP. Coronary perfusion pressure (CPP), supposedly affected in both conditions, might also be a stimulus of CNFA. VExp and hHem were performed in anesthetized male Sprague-Dawley rats while blood pressure, heart rate, and RSNA were measured. Cervical vagotomy abolished RSNA response in both reflex responses. Single-unit CNFA was recorded while LVEDP was changed. Rapid changes ( +/- 4, +/- 6, +/- 8 mmHg) were obtained by graded occlusion of the caval vein and descending aorta. Prolonged changes were obtained by VExp and hHem. Furthermore, CNFA was recorded in a modified Langendorff heart while CPP was changed ( 70, 100, 40 mmHg). Rapid LVEDP changes increased CNFA [ caval vein occlusion: + 16 +/- 3 Hz ( approximately + 602%); aortic occlusion: + 15 +/- 3 Hz ( approximately + 553%); 70 units; P < 0.05]. VExp and hHem ( n = 6) increased CNFA [ VExp: + 10 +/- 4 Hz ( approximately + 1,033%); hHem: + 10 +/- 2 Hz ( approximately + 1,225%); P < 0.05]. An increase in CPP increased CNFA [ + 2 +/- 1 Hz ( approximately + 225%); P < 0.05], whereas a decrease in CPP decreased CNFA [- 0.8 +/- 0.4 Hz ( approximately - 50%); P < 0.05]. All C fibers recorded originated from the LV. CNFA increased with any LVEDP change but changed equidirectionally with CPP. Thus neither LVEDP nor CPP fully accounts directly for afferent C-fiber and reflex sympathetic responses. The intrinsic afferent stimuli and receptive fields accounting for reflex sympathoinhibition still remain cryptic.