32 research outputs found
Gender difference in cardiopulmonary reflex inhibition of sympathetic nerve activity
No full text We tested the hypothesis that reflex responses to mechanical [increase in left atrial pressure (LAP) 0-25 mmHg] and chemical stimulation [left atrial injection of phenylbiguanide (PBG), 0.5-10 mg/kg] of cardiopulmonary receptors are greater in female (n = 9; 335 +/- 9 g) than in male (n = 10; 558 +/- 23 g) age-matched rats. Anesthetized (500 mg/kg urethan and 80 mg/kg alpha-chloralose), tracheotomized, and artificially ventilated (100% oxygen), sinoaortic-denervated animals were instrumented with left atrial, femoral venous, and arterial catheters and a Tygon occluder around the ascending aorta. Reflex inhibition of lumbar sympathetic nerve activity (LSNA) vs. LAP and dose PBG was higher in female rats. A two-way analysis of variance revealed a significant gender effect, males vs. females (P = 0.023), and a significant gender x dose interaction (P < 0.001) for LSNA vs. LAP. There was also a significant gender x dose interaction (P < 0.001) for LSNA vs. PBG. However, there was no influence of gender on the reflex inhibition of mean arterial pressure (P = 0.751) or heart rate (P = 0.561). These responses were associated with a higher left ventricular weight-to-body weight ratio in females (2.14 +/- 0.06 vs. 1.95 +/- 0.07 g/kg, P = 0.039). </jats:p
Differential role of ionotropic glutamatergic mechanisms in responses to NTS P<sub>2x</sub> and A<sub>2a</sub> receptor stimulation
No full text Activation of ATP P2x receptors in the subpostremal nucleus tractus solitarii (NTS) via microinjection of α,β-methylene ATP (α,β-MeATP) elicits fast initial depressor and sympathoinhibitory responses that are followed by slow, long-lasting inhibitory effects. Activation of NTS adenosine A2a receptors via microinjection of CGS-21680 elicits slow, long-lasting decreases in arterial pressure and renal sympathetic nerve activity (RSNA) and an increase in preganglionic adrenal sympathetic nerve activity (pre-ASNA). Both P2x and A2a receptors may operate via modulation of glutamate release from central neurons. We investigated whether intact glutamatergic transmission is necessary to mediate the responses to NTS P2x and A2areceptor stimulation. The hemodynamic and neural (RSNA and pre-ASNA) responses to microinjections of α,β-MeATP (25 pmol/50 nl) and CGS-21680 (20 pmol/50 nl) were compared before and after pretreatment with kynurenate sodium (KYN; 4.4 nmol/100 nl) in chloralose-urethan-anesthetized male Sprague-Dawley rats. KYN virtually abolished the fast responses to α,β-MeATP and tended to enhance the slow component of the neural responses. The depressor responses to CGS-21680 were mostly preserved after pretreatment with KYN, although the increase in pre-ASNA was reduced by one-half following the glutamatergic blockade. We conclude that the fast responses to stimulation of NTS P2x receptors are mediated via glutamatergic ionotropic mechanisms, whereas the slow responses to stimulation of NTS P2x and A2a receptors are mediated mostly via other neuromodulatory mechanisms. </jats:p
Differential control of renal vs. adrenal sympathetic nerve activity by NTS A<sub>2a</sub> and P<sub>2x</sub> purinoceptors
No full text Activation of adenosine A2a and ATP P2x purinoceptors in the subpostremal nucleus tractus solitarii (NTS) via microinjection of the selective agonists CGS-21680 and α,β-methylene ATP (α,β-MeATP), respectively, elicits large dose-dependent decreases in arterial pressure and heart rate, differential regional vasodilation, and differential inhibition of regional sympathetic outputs. With marked hypotensive hemorrhage, preganglionic adrenal sympathetic nerve activity (pre-ASNA) increases, whereas renal (RSNA) and postganglionic adrenal sympathetic nerve activity (post-ASNA) decrease. In this setting, adenosine levels in the brain stem increase. Therefore, we investigated whether stimulation of specific purinoceptors in the NTS may evoke differential sympathetic responses. RSNA was recorded simultaneously with pre-ASNA or post-ASNA in chloralose-urethan-anesthetized male Sprague-Dawley rats. CGS-21680 (2 and 20 pmol in 50 nl) inhibited RSNA and post-ASNA, whereas pre-ASNA increased markedly. α,β-MeATP (25 and 100 pmol in 50 nl) inhibited all sympathetic outputs. Sinoaortic denervation plus vagotomy markedly prolonged the responses to P2x-purinoceptor stimulation. Glutamate (100 pmol in 50 nl) caused differential inhibition of all sympathetic outputs similar to that evoked by α,β-MeATP. We conclude that NTS A2a-purinoceptor activation evokes differential sympathetic responses similar to those observed during hemorrhage, whereas P2x-purinoceptor and glutamate-receptor activation evokes differential inhibition of sympathetic outputs similar to arterial baroreflex responses. </jats:p
Daily exercise improved blood pressure homeostasis of rats subjected to surgical stress
No full text The effect of daily spontaneous running on blood pressure homeostasis (BPH) was evaluated in 19 male and 13 female control rats and 7 male and 13 female daily spontaneous running rats subjected to surgery and subsequent repetitive hemodynamic disturbances. BPH was operationally defined as the ability to maintain mean arterial pressure above 60 mmHg during the experimental protocol. The length of time the rats maintained BPH was compared across males and females and trained and control groups. Significant sex (P = 0.01) and training (P = 0.05) effects were found. Females maintained homeostasis longer than males and trained longer than controls. Sex effects were not due to differences in the body mass. The mechanisms responsible for the higher resistance to deterioration of homeostasis merit further investigation. </jats:p
Daily spontaneous running attenuated the central gain of the arterial baroreflex
No full text Exercise training attenuates arterial baroreflex function. Mechanisms responsible may include an attenuated aortic baroreceptor reactivity (afferent mechanisms) and/or an attenuated central baroreflex gain. We tested the hypothesis that the aortic baroreceptor reactivity and/or central gain is attenuated by daily spontaneous running (DSR). Eighteen anesthetized Sprague-Dawley rats (11 control and 7 DSR) were tracheotomized and instrumented with femoral venous and right carotid arterial catheters. Electrodes were placed around the left aortic depressor nerve and the lumbar sympathetic trunk. Eight to thirteen weeks of DSR were associated with a 20% increase in heart weight-to-body weight ratio (2.83 +/- 0.04 vs. 3.39 +/- 0.10 g/kg; P < 0.001) and resting bradycardia (413 +/- 6 vs. 384 +/- 10 beats/min; P = 0.01). DSR reduced the central gain of the baroreflex regulation of heart rate (0.210 +/- 0.046 vs. 0.005 +/- 0.021 beats.min-1.%-1; P = 0.004) during decreases in arterial pressure. However, the reactivity of aortic baroreceptor afferents and the central gain of the baroreflex control of lumbar sympathetic nerve activity were not different in control and DSR rats. Thus DSR reduced the central gain of the arterial baroreflex regulation of heart rate without changing the reactivity of aortic baroreceptor afferents. We conclude that afferent mechanisms are not responsible for the training-induced reduction in arterial baroreflex function. </jats:p
Daily spontaneous running did not alter vagal afferent reactivity
No full text Exercise training alters the cardiopulmonary baroreflex regulation of the circulation; however, the mechanisms responsible are unknown. One possibility is an enhanced afferent response to cardiopulmonary stimulation. We therefore tested the hypothesis that daily spontaneous running (DSR) would enhance cardiopulmonary vagal afferent responses to mechanical (increase in left atrial pressure, LAP) and chemical (phenyl biguanide, PBG) stimulation. Reactivity of single-fiber cardiopulmonary vagal afferents was evaluated in 16 control and 12 DSR anesthetized Sprague-Dawley rats. Rats were weaned at 3 wk of age and randomly assigned to a control or DSR group. Eight to twelve weeks of DSR was associated with a 27% increase in heart weight-to-body weight ratio (3.27 +/- 0.08 vs. 2.56 +/- 0.05 g/kg, P < 0.001) and resting bradycardia (394 +/- 10 vs. 421 +/- 8 beats/min, P = 0.036). However, DSR did not alter the stimulus-response curves to increases in LAP (frequency of discharge vs. LAP) for either the high-frequency (maximum response, sedentary 59.6 +/- 3.2, DSR 60.1 +/- 5.0 spikes/s) or low-frequency (maximum response, sedentary 20.0 +/- 2.9 DSR 20.6 +/- 3.9 spikes/s) receptors. Dose-response curves to chemical stimulation (spikes/s vs. PBG dose) were also not altered by DSR. Thus DSR did not change vagal afferent reactivity to mechanical or chemical stimulation. </jats:p
Mechanisms mediating NTS P<sub>2x</sub> receptor-evoked hypotension: cardiac output vs. total peripheral resistance
No full text We have previously shown that P2x purinoceptor activation in the subpostremal nucleus tractus solitarius (NTS) produces dose-dependent decreases in mean arterial pressure (MAP), heart rate, efferent sympathetic nerve activity, and significant peripheral vasodilation. However, the relative roles of cardiac output (CO) and total peripheral resistance (TPR) in mediating this depressor response are unknown. Bradycardia does not necessarily result in decreased CO, because, with the greater filling time, stroke volume may increase such that CO may be unchanged. We measured changes in CO (via a chronically implanted flow probe on the ascending aorta) and MAP in α-chloralose- and urethane-anesthetized male Sprague-Dawley rats in response to microinjection of the selective P2x purinoceptor agonist α,β-methylene ATP (25 and 100 pmol/50 nl) into the subpostremal NTS. TPR was calculated as MAP/CO. At the low dose of NTS P2x purinoceptor agonist, the reduction in MAP was primarily mediated by reductions in TPR (−31.3 ± 3.3%), not CO (−8.7 ± 1.7%). At the high dose, both CO (−34.4 ± 6.6%) and TPR (−40.2 ± 2.5%) contribute to the reduction in MAP. We conclude that the relative contribution of CO and TPR to the reduction in MAP evoked by NTS P2x purinoceptor activation is dependent on the extent of P2x purinoceptor activation. </jats:p
575 New irrigated bipolar radiofrequency device in curative surgical treatment of nonmitral atrial fibrillation - early clinical experience and mid-term results
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532 Is the false tendon of the left ventricle thrombi risk factor after myocardial infarction?
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