Central hypercapnic chemoreflex modulation of renal sympathetic nerve activity in experimental heart failure.

Activation of the sympathetic nervous system plays an important role in the pathophysiology and progression of congestive heart failure (CHF). The precise mechanisms responsible for sympathetic activation in CHF are not yet clearly established. An altered central hypercapnic chemoreflex modulation of sympathetic nerve activity (SNA) might be an explanation. Therefore, the response of postganglionic renal SNA to elevation of CO2 concentration in the inspiratory air to 2, 4, and 6% was determined in anesthetized, artificially ventilated rats after denervation of peripheral baro- and chemoreceptors 2 weeks (group A; n=8) or 6 weeks (group B; n=11) after induction of an aorto-caval shunt, or 4 weeks after aortic banding (group C; n=7). In all CHF models, left ventricular enddiastolic pressure was increased (A 8 +/- 1, B 8 +/- 1, C 10 +/- 2 mmHg) as compared to sham operated controls (A 3 +/- 1, B 4 +/- 1, C 5 +/- 1 mmHg). Indicative of left ventricular hypertrophy and pulmonary congestion, wet weight of heart (A + 60%, B + 93%, C + 49%) and lungs (A + 15%, B + 36%, C + 12%) were also enhanced as compared to controls. Elevation of inspiratory CO2 concentration to 2,4, and 6% increased renal SNA by approximately 10, 20, and 30% from resting activity in all groups. The maximum SNA responses at 6% CO2 in the groups with CHF (A + 390 +/- 95, B + 425 +/- 133, C + 368 +/- 158 microVs) did not differ from those in the respective controls (A + 510 +/- 130, B + 570 +/- 180, C + 275 +/- 25 microVs). It is concluded that under these experimental conditions the central hypercapnic chemoreflex sensitivity is not altered in either of the employed models of CHF and therefore may not play a major role for the well-known elevation of SNA in CHF.