ROLE OF CAROTID BODY TO HYPERTENSION AND PULMONAR VENTILATION IN RENOVASCULAR HYPERTENSIVE RATS
Authors: Melo Mariana Rosso , Gasparini Silvia , Speretta Guilherme F.F. , da Silva Elaine Fernanda , Pedrino Gustavo Rodrigues , Menani Jose Vanderlei , Zoccal Daniel Breseghello , de Almeida Colombari Debora Simoes , Colombari Eduardo 
Published: November 2023

A previous study demonstrated that the commissural portion of the nucleus of the solitary tract (cNTS) is fundamental for the maintenance of the 2 kidneys, 1 clip (2K1C) renovascular hypertension. The cNTS is the first synaptic site in the central nervous system that receives the peripheral chemoreceptor inputs. Therefore, in the present study we sought to evaluate the effects of carotid body removal (CBR) on the development of hypertension and on respiratory changes in 2K1C rats. In addition, the respiratory responses to hypoxia in 2K1C rats were also tested. Male Holtzman rats (150–180g) had the left renal artery partially occluded with a silver clip (0.2 mm width) to produce the 2K1C hypertension (n = 21) or received sham surgery (normotensive rats, NT, n = 19). Three weeks later, rats were implanted with telemetry transducers into the abdominal aorta. After 4 days of recovery, baseline mean arterial pressure (MAP) was recorded for 3 days, followed by CBR or sham surgery. Four groups of rats were formed: sham‐NT, CBR‐NT, sham‐2K1C and CBR‐2K1C. MAP was recorded every other day by telemetry for the next two weeks and at the end of the 2nd week, tidal volume (VT), respiratory frequency (fR) and pulmonary ventilation (VE) were measured by whole‐body plethysmography during normoxia or hypoxia (7% O2). The results showed that 3 days after the CBR, MAP was significantly reduced in CBR‐2K1C rats in the light (141 ± 5, vs. sham‐2K1C: 165 ± 6 mmHg, p<0.05) and dark period (152 ± 8 vs. sham‐2K1C rats: 175 ± 7 mmHg, p<0.05). The reduction in MAP in CBR‐2K1C persisted until the end of the recording period in the light (161 ± 12, vs.sham‐2K1C: 189 ± 8 mmH, p < 0.05) and dark period (176 ± 10, vs.sham‐2K1C: 206 ± 6 mmHg). CBR did not change MAP in NT rats (93 ± 1.8 vs. sham‐NT: 93 ± 2.1 mmHg). The baseline VT (9.2 ± 0.6 ml.kg−1) and VE (897.6 ± 61.4 ml.kg−1.min−1) in normoxia, in sham‐2K1C rats were increased compared to sham‐NT (VT: 7.2 ± 0.3 ml.kg−1; VE: 628.6 ± 25.9 ml.kg−1.min−1, p<0.01). This increase in VT and VE was abolished in CBR‐2K1C rats (VT: 5.3 ± 0.5 ml.kg−1; VE: 630.4 ± 73.1 ml.kg−1.min−1). CBR‐2K1C showed increased fR (117.6 ± 6.3 resp.min−1) compared with all other groups (sham CBR‐NT: 87.8 ± 3.4; sham CBR‐2K1C: 98 ± 3; CBR‐NT: 93.8 ± 5 resp.min−1, p<0.05). During hypoxia, the increase of VT (Δ= 4.9 ± 0.8 ml.kg−1) and VE (Δ= 724.2 ± 90.9 ml.kg−1.min−1) was more intense in sham CBR‐2K1C, compared to sham CBR‐NT (ΔVT= 2.7 ± 0.6 ml.Kg−1, ΔVE: 380.4 ± 50.8 ml.Kg−1.min−1, p<0.05). Hypoxia produced reduced changes on VE, VT and fR in CBR‐2K1C (ΔVT= 1.8 ± 0.5 ml.kg−1; ΔfR= ‐4 ± 8.1 resp.min−1; ΔVE: 172.6 ± 60.4 ml.kg−1.min−1) or in CBR‐NT (ΔVT= 2.1 ± 0.4 ml.kg−1; ΔfR= −7.6 ± 6 resp.min−1; ΔVE: 133 ± 49.1 ml.kg−1.min−1). These results suggest that an increased activity of carotid body is present in normoxic or hypoxic conditions in 2K1C hypertensive rats as indicated by the increased respiratory responses. This increased activity of carotid body may contribute to the development and maintenance of hypertension in these rats.

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