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Autonomic imbalance in hypertension induces excessive blood pressure (BP) elevation during exercise, thereby increasing left ventricular mass (LVM). Although muscle weakness enhances autonomic imbalance by stimulating muscle sympathetic activity during exercise, it is unclear whether muscle weakness is associated with an increase of LVM in patients with hypertension. This study aimed to investigate the relationships between muscle weakness, BP elevation during exercise, and LVM in these patients. Eighty-six hypertensive patients aged 69 ± 8 years with controlled resting BP (ie, < 140/90 mmHg) were recruited. Plasma brain natriuretic peptide (BNP), left ventricular mass index (LVMI), and knee extension muscle strength were measured. Changes in plasma noradrenaline (NORA) and brachial-ankle pulse wave velocity (ba-PWV) were assessed before and after an ergometer exercise test performed at moderate intensity (ΔNORA and ΔPWV, respectively). A difference between baseline and peak systolic BP during the exercise test was defined as BP elevation during exercise (ΔSBP). Relationships between muscle strength, ΔNORA, ΔPWV, ΔSBP, BNP, and LVMI were analyzed, and significant factors increasing LVM were identified using univariate and multivariate regression analyses. Muscle strength was negatively correlated with ΔNORA (r = -0.202, P = 0.048), ΔPWV (r = -0.328, P = 0.002), ΔSBP (r = -0.230, P = 0.033), BNP (r = -0.265, P = 0.014), and LVMI (r = -0.233, P = 0.031). LVMI was positively correlated with ΔPWV (r = 0.246, P = 0.023) and ΔSBP (r = 0.307, P = 0.004). Muscle strength was a significant independent factor associated with LVMI (β = -0.331, P = 0.010). Our findings suggest that muscle weakness is associated with an increase of LVM through excessive BP elevation during exercise in patients with hypertension.

Background: Early diagnosis and optimal timing of surgical repair for chronic aortic regurgitation (AR) are topics of interest, because left ventricular compensation delays the clinical signs of the early stages of left ventricular dysfunction. Various physical signs have been described as indicators of chronic AR, but AR screening can be difficult depending on the proficiency of primary care providers. The recent use of the cardio-ankle vascular index (CAVI) measurement to assess peripheral atherosclerosis may detect AR objectively and simply because its arterial pulse wave configuration is closely related to the physical signs of AR., Methods: CAVI measurements include pulse pressure (PP), the difference in blood pressures between upper and lower limbs (ABD), ankle-brachial index (ABI), ejection time (ET), and upstroke time (UT). We evaluated the differences in CAVI parameters between AR group and age-matched control group, the relationships between CAVI parameters and the echocardiographic semi-quantitative measurements of AR severity such as left ventricular dimensions (Dd, Ds) and vena contracta (VC), and between the changes in CAVI parameters before and after aortic valve replacement., Results: ABD, PP, ET, ankle systolic pressure and ABI in the AR group were significantly higher than that in the control group. Brachial diastolic pressure and CAVI in the AR group were significantly lower than that in the control group. UT was lower than that in the control group (p=0.05). PP did not correlate with the semi-quantitative AR severity, but ABD was correlated with Dd, Ds, and VC and was negatively correlated with UT. The exaggerated ABD, PP, ET, and ABI were moderated after surgery., Conclusions: CAVI parameters could be useful in the screening and serial follow-up of AR patients., (Copyright © 2016 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.)

A J-shaped or U-shaped curve phenomenon might exist between systolic blood pressure (SBP) or pulse pressure (PP) at admission and in-hospital mortality in Japanese patients with acute myocardial infarction (AMI) undergoing primary percutaneous coronary intervention (PCI). However, data regarding a relationship between mean blood pressure (MBP) at admission and in-hospital outcome in AMI patients undergoing primary PCI are still lacking in Japan.A total of 1,413 primary PCI-treated AMI patients were classified into quintiles based on admission MBP (< 79 n = 283, 79-91 n = 285, 92-103 n = 285, 104-115 n = 279, and ≥ 116 mmHg n = 281). Patients with MBP < 79 mmHg had a significantly higher in-hospital mortality, while mortality was not significantly different among the other quintiles: 16.6% (< 79), 4.9% (79-91), 3.9% (92-103), 3.2% (104-115), and 5.0% (≥ 116 mmHg). On multivariate analysis, Killip class ≥ 3 at admission, LMT or multivessels as culprit lesions, admission MBP < 79 mmHg, and age were independent positive predictors of in-hospital mortality, whereas hypercholesterolemia and TIMI 3 flow before/after PCI were negative predictors, while the other MBP categories were not.These results suggest that admission MBP < 79 mmHg might be associated with in-hospital death, and the in-hospital prognostic effects of MBP, the steady component of blood pressure, at admission might be different from those of SBP or PP, the pulsatile component of blood pressure, at admission in Japanese AMI patients undergoing primary PCI.

Data regarding relationship between pulse pressure (PP) at admission and in-hospital outcome in patients with acute myocardial infarction (AMI) undergoing primary percutaneous coronary intervention (PCI) are still lacking. A total of 1413 primary PCI-treated AMI patients were classified into quintiles based on admission PP (<40, n = 280; 40-48, n = 276; 49-57, n = 288; 58-70, n = 288; and ≥71 mmHg, n = 281). The patients with PP < 40 mmHg tended to have higher prevalence of male, smoking, and Killip class ≥3 at admission; right coronary artery, left main trunk (LMT), or multivessels as culprit lesions; larger number of diseased vessels; lower Thrombolysis in Myocardial Infarction (TIMI) grade in the infarct-related artery before/after primary PCI; and higher value of peak creatine phosphokinase concentration. Patients with PP < 40 mmHg had highest mortality, while patients with PP 49-57 mmHg had the lowest: 11.8 % (<40), 7.2 % (40-48), 2.8 % (49-57), 5.9 % (58-70), and 6.0 % (≥71 mmHg). On multivariate analysis, Killip class ≥3 at admission, LMT or multivessels as culprit lesions, chronic kidney disease, and age were the independent positive predictors of the in-hospital mortality, whereas admission PP 49-57 mmHg, hypercholesterolemia, and TIMI 3 flow before/after PCI were the negative ones, but admission PP < 40 mmHg was not. These results suggest that admission PP 49-57 mmHg might be correlated with better in-hospital prognosis in Japanese AMI patients undergoing primary PCI.

Background: Data regarding the relationship between systolic blood pressure (SBP) at admission and in-hospital outcome in patients with acute myocardial infarction (AMI) undergoing primary percutaneous coronary intervention (PCI) are still lacking in Japan., Methods and Results: A total of 1475 primary PCI-treated AMI patients were classified into quintiles based on admission SBP (<105 mmHg, n=300; 105-125 mmHg, n=294; 126-140 mmHg, n=306; 141-158 mmHg, n=286; and ≥159 mmHg n=289). The patients with SBP<105 mmHg tended to have higher age, previous myocardial infarction, chronic kidney disease (CKD), Killip class≥3 at admission, right coronary artery, left main trunk (LMT), or multivessels as culprit lesions, larger number of diseased vessels, lower Thrombolysis In Myocardial Infarction (TIMI) grade in the infarct-related artery before primary PCI, and higher value of peak creatine phosphokinase concentration. Patients with SBP<105 mmHg had a significantly higher mortality, while mortality was not significantly different among the other quintiles: 24.3% (<105 mmHg), 4.8% (105-125 mmHg), 4.9% (126-140 mmHg), 2.8% (141-158 mmHg), and 5.2% (≥159 mmHg) (p<0.001). On multivariate analysis, Killip class≥3 at admission, LMT or multivessels as culprit lesions, admission SBP<105 mmHg, CKD, and age were the independent positive predictors of in-hospital mortality, whereas admission SBP 141-158 mmHg and TIMI 3 flow after PCI were the negative ones, but admission SBP 105-125 mmHg, admission SBP 126-140 mmHg, and admission SBP≥159 mmHg were not., Conclusions: These results suggest that admission SBP 141-158 mmHg might be correlated with better in-hospital prognosis, whereas admission SBP<105 mmHg was associated with in-hospital death in Japanese AMI patients undergoing primary PCI., (Copyright © 2012 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.)

Background: Several clinical studies have demonstrated an inverse relationship between systolic blood pressure (SBP) at admission and in-hospital mortality in patients hospitalized for acute myocardial infarction (AMI). However, data on the relation between admission SBP and in-hospital prognosis in AMI patients are still lacking in Japan., Methods and Results: A total of 1211 AMI patients were classified into quintiles based on SBP at hospital admission (<106 mmHg, n = 241; 106-125 mmHg, n = 239; 126-140 mmHg, n = 244; 141-159 mmHg, n = 238; and ≥ 160 mmHg, n = 249). The patients with SBP < 106 mmHg tended to have higher age, Killip class ≥ 3 at admission, right coronary artery, left main trunk, or multivessels as culprit lesions, larger number of diseased vessels, lower Thrombolysis In Myocardial Infarction grade in the infarct-related artery before primary percutaneous coronary intervention (PCI), and higher value of peak creatine phosphokinase concentration. Patients with SBP <106 mmHg had a significantly higher mortality, while mortality was not significantly different among the other quintiles: 25.7% (<106 mmHg), 5.4% (106-125 mmHg), 5.7% (126-140 mmHg), 2.5% (141-159 mmHg), and 5.6% (≥ 160 mmHg) (p<0.001). On multivariate analysis, Killip class ≥ 3 at admission, admission SBP <106 mmHg, and age were the independent positive predictors of in-hospital mortality, whereas admission SBP 141-159 mmHg and primary PCI were the negative ones, but admission SBP 106-125 mmHg, admission SBP 126-140 mmHg, and admission SBP ≥ 160 mmHg were not., Conclusions: These results suggest that admission SBP 141-159 mmHg might be correlated with better in-hospital prognosis, whereas admission SBP <106 mmHg was associated with in-hospital death in Japanese patients hospitalized for AMI., (Copyright © 2011 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.)

Chronotherapy has the potential to improve blood pressure (BP) variability and to decrease stroke and cardiovascular events. The present study examined the efficacy and safety of the bedtime administration in amlodipine-olmesartan combination therapy, as compared with the morning administration. The present study was an open-label, randomized crossover study of the effects of the morning vs. bedtime administration of amlodipine-olmesartan combination. The subject was 31 essential hypertensive patients. Morning BP surge (MBPS) and nocturnal BP pattern were analyzed from ambulatory BP data. Glucose and lipid profiles and cardiovascular-renal data were also collected. The bedtime administration reduced MBPS significantly (24.2 ± 13.5 mmHg vs. 32.3 ± 14.2 mmHg, p < 0.001) with no excessive nocturnal BP fall. In nondipper, the bedtime administration significantly improved nocturnal BP. On the other hand, it did not reduce nocturnal BP in dipper. Urinary albumin/creatinine ratio was lower in the bedtime administration than in the morning administration (42.5 ± 59.9 mg/g vs. 75.3 ± 26.4 mg/g, p = 0.044). In amlodipine-olmesartan combination therapy, the bedtime administration reduced better MBPS with correcting nocturnal BP fall and improved urinary albumin excretion. The bedtime dosing of amlodipine and olmesartan seems more apt than the morning dose to obtain the therapeutic goal.

Experiments were carried out in urethane-anesthetized, artificially ventilated, adult male Wistar rats. Microinjections (50 nL) of N-methyl-d-aspartic acid (1, 5, and 10 mmol/L), but not artificial cerebrospinal fluid, into the hypothalamic arcuate nucleus (ARCN) elicited increases in mean arterial pressure (5.7+/-0.5, 13.2+/-1.4, and 17.3+/-1.1 mm Hg, respectively) and heart rate (24.3+/-4.3, 49.3+/-5.2, and 75.2+/-8.0 bpm, respectively). ARCN stimulation was accomplished by microinjections of a maximally effective concentration of N-methyl-d-aspartic acid (10 mmol/L). The tachycardic responses to the ARCN stimulation were significantly attenuated after bilateral vagotomy. Intrathecal injections of ionotropic glutamate receptor (iGLUR) antagonists completely blocked pressor responses to the ARCN stimulation, whereas the tachycardic responses were significantly attenuated but not abolished. Intrathecal injections of iGLUR antagonists at T9 to T10, combined with bilateral vagotomy, completely blocked the tachycardic responses to ARCN stimulation. ARCN stimulation with N-methyl-d-aspartic acid elicited increased activities of the greater splanchnic nerve (91.7+/-14.8%) and the renal nerve (109.3+/-13%). Intrathecal injections of iGLURs at T9 to T10 blocked the increase in the greater splanchnic nerve activity in response to ARCN stimulation. These results indicate the following: (1) the chemical stimulation of the ARCN elicits increases in mean arterial pressure, greater splanchnic nerve and renal nerve activity, and heart rate; (2) the increases in mean arterial pressure and sympathetic nerve activity are mediated via the activation of spinal cord iGLURs; and (3) the increases in heart rate are mediated via the activation of spinal cord iGLURs and decreases in vagal input to the heart.

Urocortin 3 (Ucn3) is a new member of the corticotropin-releasing factor (CRF) peptide family and is considered to be a specific and endogenous ligand for CRF type 2 receptors (CRF2Rs). The presence of CRF(2)Rs has been reported in the nucleus tractus solitarius (NTS) of the rat. It was hypothesized that the activation of CRF2Rs in the medial NTS (mNTS) may play a role in cardiovascular regulation. This hypothesis was tested in urethane-anesthetized, artificially ventilated, adult male Wistar rats. Microinjections (100 nl) of Ucn3 (0.03, 0.06, 0.12, and 0.25 mM) into the mNTS of anesthetized rats elicited decreases in mean arterial pressure (MAP: 5.0 +/- 1.0, 21.6 +/- 2.6, 20.0 +/- 2.8, and 12.7 +/- 3.4 mmHg, respectively) and heart rate (HR: 7.8 +/- 2.6, 46.2 +/- 9.3, 34.5 +/- 8.4, and 16.6 +/- 4.9 beats/min, respectively). Microinjections of artificial cerebrospinal fluid (100 nl) into the mNTS did not elicit cardiovascular responses. Maximum decreases in MAP and HR were elicited by 0.06 mM concentration of Ucn3. Cardiovascular responses to Ucn3 were similar in unanesthetized midcollicular decerebrate rats. A bilateral vagotomy completely abolished Ucn3-induced bradycardia. The decreases in MAP and HR elicited by Ucn3 (0.06 mM) were completely blocked by astressin (1 mM; nonselective CRFR antagonist) and K41498 (5 mM; selective CRF2R antagonist). Microinjections of Ucn3 (0.06 mM) into the mNTS decreased the efferent greater splanchnic nerve activity. After the blockade of CRF2Rs in the mNTS, a Ucn3-induced decrease in the efferent sympathetic nerve discharge was abolished. These results indicate that Ucn3 microinjections into the mNTS exerted excitatory effects on the mNTS neurons via CRF2Rs, leading to depressor and bradycardic responses.

Adrenomedullin 2 (AM2), a novel member of the calcitonin gene-related peptide family, has emerged as a multifunctional peptide controlling endocrine and cardiovascular functions and physiological behaviors. Both central and peripheral administration of AM2 can have profound effects on systemic and/or pulmonary circulation in mammals. However, the target nuclei of AM2 and the role of central AM2 in cardiovascular regulation remain unknown. In the present study, we microinjected AM2 into the rat nucleus tractus solitarius (NTS), the central termination site of baroreceptor afferents. Consistent with previous reports showing the hypertensive effect of intracerebroventricular administration of AM2, the direct microinjection of the peptide into the NTS increased arterial pressure as well as heart rate in rats. Importantly, this effect of AM2 on cardiovascular regulation was significantly attenuated by an antagonist of receptor components for AM2 that were abundant in the rat NTS. Our results indicate that AM2 may play an important role in the regulation of the cardiovascular system at the NTS level.

Systemic administration of urocortin I (Ucn I), a member of the corticotrophin-releasing factor (CRF) peptide family, modulates cardiovascular system. In the central nervous system, Ucn I is found in the nucleus tractus solitarii (NTS), which plays an important role in regulating arterial blood pressure (ABP) and heart rate (HR) in response to activation of the baroreceptor afferents. In this study, we examined the effects of Ucn I, which has a high affinity for both type 1 and type 2 CRF receptors (i.e. CRF-R1 and -R2), on cardiovascular functions at the level of the NTS. A specific agonist of CRF-R1 (i.e. CRF) and a specific agonist of CRF-R2 (i.e. Urocortin II) were also tested to identify the specific cardiovascular effects induced by individual activation of either CRF-R1 or -R2. We found that Ucn I microinjected into the rat NTS produced a significant reduction in both ABP and HR. Both agonists for CRF-R1 and -R2 microinjected into the NTS also reduced ABP and HR. Our results suggest that Ucn I in the NTS may play an important role in cardiovascular regulation and the cardiovascular effects of Ucn I may be mediated by activation of both CRF-R1 and -R2, which are known to be present in the NTS.

This study was designed to delineate the medullary and spinal pathways mediating the cardiovascular responses to cold pressor test (CPT) and to identify neurotransmitters in these pathways. Experiments were done in barodenervated, urethane-anesthetized, male Wistar rats. The CPT was performed by immersing the limbs and ventral half of the body of the rat in ice-cold water (0.5 degrees C) for 2 min. CPT elicited an immediate increase in mean arterial pressure (MAP), heart rate (HR), and greater splanchnic nerve activity (GSNA). Bilateral blockade of ionotropic glutamate receptors (iGLURs) in the rostral ventrolateral medullary pressor area (RVLM) significantly attenuated the CPT-induced responses. Bilateral blockade of gamma-aminobutyric acid (GABA) receptors, but not iGLURs, in the nucleus ambiguus (nAmb) significantly reduced the CPT-induced increases in HR, but not MAP. Blockade of spinal iGLURs caused a significant reduction in CPT-induced increases in MAP and GSNA, whereas the increases in HR were reduced to a lesser extent. Combination of the blockade of spinal iGLURs and bilateral vagotomy or intravenous atropine almost completely blocked CPT-induced tachycardia. Midcollicular decerebration significantly reduced CPT-induced increases in MAP and HR. These results indicated that: 1) CPT-induced increases in MAP, HR, and GSNA were mediated by activation of iGLURs in the RVLM and spinal cord, 2) activation of GABA receptors in the nAmb also contributed to the CPT-induced tachycardic responses, and 3) brain areas rostral to the brain stem also participated in the CPT-induced pressor and tachycardic responses.

Purpose: The purpose of this study was to determine the effect of aerobic training under noninvasive positive pressure ventilation (NPPV) on maximal oxygen uptake (). Methods: Ten healthy young male volunteers participated in the study. Before the training, stroke volume (SV) and cardiac output (CO) were measured in all subjects under 0, 4, 8, and 12 cmH2O NPPV at rest. Then, the subjects exercised on a cycle ergometer at 60% of pre-training for 30 min daily for 5 consecutive days with/without NPPV. The 5-day exercise protocol was repeated after a three-week washout period without/with NPPV. The primary endpoint was changes in . The secondary endpoints were changes in SV, CO, maximum heart rate (HRmax), maximum respiratory rate (RRmax), maximum expiratory minute volume (VEmax) and the percent change in plasma volume (PV). Results: NPPV at 12 cmH2O significantly reduced SV and CO at rest. significantly increased after 5 days training with and without NPPV, but the magnitude of increase in after training under 12 cmH2O NPPV was significantly higher than after training without NPPV. VEmax significantly increased after training under NPPV, but not after training without NPPV. HRmax and RRmax did not change during training irrespective of NPPV. The percent change in PV was similar between training with and without NPPV. The 5-day training program with NPPV resulted in greater improvement in than without NPPV. Conclusions: Aerobic training under NPPV has add-on effects on and exercise-related health benefits in healthy young men. [ABSTRACT FROM AUTHOR]

Purpose: While non-noxious local cooling is widely used in physical medicine, its effect on muscle sympathetic nerve activity (MSNA) and cardiovascular regulation are not clear. The purpose of the present study was to assess the responses of MSNA, blood pressure (BP), heart rate (HR) and local blood flow during non-noxious local cooling.Methods: The study included two protocols. Both protocols consisted of 10-min rest in supine position, followed by 15-min local cooling (15 °C) of the shin and anterior foot, and 20-min recovery. MSNA of the right common peroneal nerve, BP, HR, and shin skin temperature (TSK) were recorded in eight men in the first protocol, while leg blood flow (LBF) was measured in the same subjects by strain-gauge plethysmography in the second protocol.Results: TSK gradually decreased from 31.5 ± 0.02 to 16.0 ± 1.01 °C (mean ± SEM) during local cooling, and gradually increased after the end of local cooling. No subject complained of pain, and BP and HR remained constant. The MSNA burst rate increased significantly (p < 0.05) to 141.1 ± 12.5 % during local cooling, but decreased significantly (p < 0.05) to 73.6 ± 5.9 % during the recovery period. Total MSNA also increased to 148.0 ± 14.2 % (p < 0.05) during local cooling, and decreased to 74.0 ± 13.9 % (p < 0.05) at recovery. LBF remained constant through the experiment.Conclusions: The results suggest that MSNA is activated by non-noxious local cooling, and attenuated after the end of local cooling without any changes in HR and BP. [ABSTRACT FROM AUTHOR]

Isometric muscle contraction (static exercise) induces circulatory response. Static exercise in individuals with thoracic spinal cord injury (TSCI) induces cardiovascular response and blood redistribution to the non-exercising muscles. The aim of our study was to determine the circulatory response during arm static exercise in individuals with TSCI and able-bodied (AB) controls. Mean blood pressure (MBP), heart rate (HR), cardiac output (CO), leg skin blood flow (SBF), and leg muscle blood flow (MBF) were recorded noninvasively, total peripheral resistance (TPR) was estimated by dividing MBP by CO, and hormonal changes were measured before, during and after static 35% maximal voluntary contraction (MVC) of the arm flexor muscles in seven male individuals with TSCI (T7-T11) and seven age-comparable AB control (32.2 ± 7.6 and 31.0 ± 4.7 years, respectively). The 35% MVC was similar in TSCI and AB individuals (107.3 ± 28.2 and 101.0 ± 22.5 N, respectively). HR, CO, MBP, TPR, SBF and MBF increased in both groups during arm static exercise. Plasma epinephrine concentration increased during arm static exercise in AB controls only ( P < 0.05). Circulation to leg muscles was similar in TSCI and AB individuals and the lack of sympathetic vasoconstriction in the paralyzed leg area did not alter the cardiovascular responses during 35% MVC of arm static exercise. We conclude that sympathetic vasoconstriction in the resting leg area did not contribute to the pressor reflex during 35% MVC of arm static exercise. [ABSTRACT FROM AUTHOR]

The study was designed to assess the effects of local heat (LH) application on postganglionic muscle sympathetic nerve activity (MSNA) measured by microneurography in healthy men. In the first protocol, MSNA of the left peroneal nerve, blood pressure (BP), heart rate (HR), and skin temperature of the shin (TSK) were recorded in nine men. In the second protocol, leg blood flow (LBF) was measured in the same subjects by strain-gauge plethysmography. In both protocols, after 10 min of rest in the supine position, a heated hydrocollator pack was applied to the shin and anterior foot for 15 min and recovery was monitored over a period of 20 min. TSK gradually increased from 31.7 ± 0.1 to 41.9 ± 0.5°C (mean ± SEM) during LH. No subject complained of pain, and BP and HR remained constant. The MSNA burst rate (16.1 ± 2.1 beats/min) during the control period decreased significantly (P < 0.05) to 72.0 ± 2.3% during LH. Total MSNA also decreased to 59.2 ± 2.6% (P < 0.05) during LH, but both immediately returned to baseline at recovery. In contrast, LBF in the left leg significantly and immediately increased (P < 0.05) after LH application and remained significantly elevated until the end of the recovery period. These results suggest that: (1) LH application significantly attenuates MSNA without any changes in HR and BP. (2) Other factors in addition to MSNA seem to control regional blood flow in the lower extremity during LH. [ABSTRACT FROM AUTHOR]