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An association between a decreased responsiveness to varying painful stimuli and arterial hypertension both in animals and in humans has been documented. The relationship between essential hypertension and silent myocardial ischemia in coronary artery disease (CAD) populations is not well understood. The aims of this study in CAD patients with and without essential hypertension were (1) to determine dental pain threshold and reaction to tooth pulp stimulation and (2) to ascertain whether hypertensive CAD patients differ from normotensive ones in reactivity to pain. This study involved 182 patients who were affected by mild and moderate hypertension (G1) and 174 normotensive patients (G2). The inclusion criteria were reproducible exercise-induced myocardial ischemia, CAD documented at angiography, and dental formula suitable for pulp test. All patients underwent an ergometric stress test, coronary angiography, and pulp test. Our CAD hypertensive patients showed a lower prevalence of angina during daily life (64.8% in G1 versus 81.6% in G2, P<.05) and a higher incidence of exercise-induced silent myocardial ischemia (60.4% in G1 versus 48.8% in G2, P<.05) than the normotensive group. The mean anginal pain intensity, which was suffered both during spontaneous transitory episodes of ischemia and/or during acute myocardial infarction, was significantly lower in G1 than in G2 patients (P<.05). During pulp test, 31.8% of G1 and 13.7% of G2 referred no symptoms, even at the highest current intensity of 500 mA. The hypertensive patients with symptoms during pulp test had a higher mean dental pain threshold and lower mean threshold reaction and maximal reaction than did the normotensive symptomatic ones. In patients of both groups, a positive correlation between the mean maximal reaction during pulp test and the prevalence of angina during daily life was also found. In conclusion, patients with CAD and essential hypertension differ from normotensive CAD patients in reactivity to pain. Significantly higher pain thresholds and lower reactions to tooth pulp stimulation characterized patients with increased blood pressure values.

Background and objectives The plasma concentration of the endogenous inhibitor of nitric oxide synthase asymmetric dimethylarginine (ADMA) associates with sympathetic activity in patients with CKD, but the driver of this association is unknown.Design, setting, participants, & measurements In this longitudinal study (follow-up: 2 weeks-6 months), repeated measurements over time of muscle sympathetic nerve activity corrected (MSNAC), plasma levels of ADMA and symmetric dimethylarginine (SDMA), and BP and heart rate were performed in 14 patients with drug-resistant hypertension who underwent bilateral renal denervation (enrolled in 2013 and followed-up until February 2014). Stability of ADMA, SDMA, BP, and MSNAC over time (6 months) was assessed in two historical control groups of patients maintained on stable antihypertensive treatment.Results Time-integrated changes in MSNAC after renal denervation ranged from -40.6% to 10% (average, -15.1%), and these changes were strongly associated with the corresponding changes in plasma ADMA (r= 0.62, P=0.02) and SDMA (r=0.72, P=0.004). Changes in MSNAC went along with simultaneous changes in standardized systolic (r=0.65, P=0.01) and diastolic BP (r=0.61, P=0.02). In the historical control groups, no change in ADMA, SDMA, BP, and MSNAC levels was recorded during a 6-month follow-up. ConclusionsIn patients with resistant hypertension, changes in sympathetic activity after renal denervation associate with simultaneous changes in plasma levels of the two major endogenous methylarginines, ADMA and SDMA. These observations are compatible with the hypothesis that the sympathetic nervous system exerts an important role in modulating circulating levels of ADMA and SDMA in this condition.