Evaluation of Cardiac Autonomic Balance and Sympathetic Vasomotor Activation to Different Targets in a Model of Hypertension Induced by Nitric Oxide Synthase Blockade

High blood pressure is a global public health problem. Several factors are involved in the generation and maintenance of hypertension, such as increased sympathetic nerve activity (SNA), although controversies have been reported. Our aims were to evaluate cardiac autonomic balance and sympathetic activation of the renal (rSNA) and the splanchnic nerve (sSNA), in animals with hypertension induced by nitric oxide synthase blockade (L‐NAME). Wistar rats were treated with L‐NAME (20mg/kg/day, once a day, for 8 days). L‐NAME treated group presented increased blood pressure (152 ± 02 mmHg, n=17), compared with control group (101±01 mmHg, n= 15).Plasma nitric oxide (NO) measurement presented a significantly reduction in L‐NAME (6.8 ±0.4 pg/L n=15), compared to CTL group (9.9 ± 1.2 pg/L n=06), both rSNA (147 ± 10spikes/s, n=16) and sSNA (137 ± 13 spike/s n=14) were higher in L‐NAME treated group, compared with control group (114 ± 5, n=10 and 74 ± 13spikes/s, n=09, respectively). The spectral analysis of the pulse interval (PI) demonstrated that the L‐NAME group presented increased low frequency component (LF) (19.75±1.75, n=07 vs CTL: 6.75±1,10, n=07), reduced high frequency component (HF) (81.29 ± 1.80 n=07 vs CTL: 92.50±1.20, n=07) leading to a sympatho‐vagal imbalance (LF/HF) (0.24 ± 0.02, n=07 vs CTL: 0.08 ± 0.01, n=07). Taken altogether, our data show that the hypertension induced by nitric oxide synthase blockade is characterized by cardiac autonomic imbalance and sympathoexcitation to more than one territory and that can be involved in the generation and/or maintenance of high blood pressure. Support or Funding Information CAPES, CNPq, UNAH.