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Quantifying Acute Changes in Renal Sympathetic Nerve Activity in Response to Central Nervous System Manipulations in Anesthetized Rats
Published on: September 11, 2018
Smoking is associated with chronic sympathetic activation in hypertension
Dagmara Hering1, Wieslawa Kucharska, Tomas Kara
1Department of Hypertension and Diabetology, Medical University of Gdansk, Gdansk, Poland.
Objective:
Previous studies have shown that smoking contributes importantly to short-term modulation of sympathetic nerve traffic. However, effect of smoking status on resting muscle sympathetic nerve activity (MSNA) in hypertension is unknown. Therefore, we tested the hypothesis that smoking is associated with chronic sympathetic activation in patients with essential hypertension.
Methods:
We measured MSNA, heart rate (HR) and blood pressure during undisturbed supine rest and in 30 hypertensive smokers (22 males, age 38+/-4 years, body mass index, BMI 27+/-1 kg/m(2), mean+/-SEM). These measurements were compared with those obtained 38 non-smoking hypertensive patients matched for gender, age and BMI. All hypertensives underwent 24-h ambulatory blood pressure monitoring. Patients were newly diagnosed, never treated for hypertension and were free of any other known diseases.
Results:
In comparison with non-smokers, smokers had smaller office-daytime systolic blood pressure difference (6+/-2 vs 15+/-3 mmHg, respectively; p<0.01). Despite similar resting values, HR in smokers was greater than in non-smokers during both daytime (86+/-3 vs 77+/-2 beats/min, respectively; p< 0.001) and night-time (73+/-3 vs 66+/-2 beats/min, respectively; p<0.01). MSNA was elevated in smokers (36+/-3 bursts/min) compared with non-smokers (28+/-3 bursts/min; p<0.01). Similar results were obtained when MSNA was expressed as bursts/100 heart beats. Multiple linear regression analysis revealed that only age and smoking status were linked independently to MSNA (R(2)=0.42, p< 0.001).
Conclusions:
In patients with essential hypertension, smoking is independently associated with chronic increase in MSNA. These findings may have implications for our understanding of the mechanisms linking smoking to cardiovascular events.
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