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1.
Summary— To investigate if the functional alterations observed in resistance arteries of spontaneously hypertensive rats (SHRs) were also present at the coronary level, in vitro experiments were performed in mesenteric resistance arteries (MRA) and in right (RIC) and left interventricular coronary (LIC) arteries taken from 15–25-week-old SHR and age-matched Wistar Kyoto rats WKYs. Using a passive extension protocol, internal diameters corresponding to 100 mmHg intraluminal pressure (D100) were determined and vessels were set up to a normalized internal diameter (0.9 D100). SHR mesenteric resistance arteries had a significantly smaller diameter compared to WKY arteries, whereas both types of SHR coronary arteries had a greater diameter compared to those of WKY rats. In arteries in the absence of contracting agonist, nitro-L-arginine (NOLA, 100 μM) induced a progressive rise in basal tone, which could be reversed by subsequent addition of L-arginine (100 μM) but not D-arginine (100 μM). When expressed as percent of maximal contractions induced by agonists (noradrenaline, NA [10 μM] in MRA; serotonin, 5-HT [10 μM], in RIC and LIC), these contractions were significantly stronger in WKY compared to SHR coronary and mesenteric resistance arteries. In NA-precontracted MRA and 5HT-precontracted coronary arteries in the presence of indomethacin (10 μM), the magnitude of acetylcholine-induced maximal relaxations (expressed as percent of maximal contractions induced by agonists) was greater in WKY compared to SHR arteries. After a 30-min incubation period, NOLA (100 μM) completely inhibited relaxations induced by acetylcholine (0.01–10 μM) in all types of precontracted arteries. Subsequent additions of sodium nitroprusside, (SNP, 10 μM) induced complete relaxations in all preparations. These results show that a basal release of NO or NO-like compound by endothelial cells is present in isolated mesenteric resistance and coronary arteries of WKY rats and SHRs. The contribution of endothelium-derived relaxing factor-nitric oxide (EDRF-NO) to arterial tone was lower in MRA compared to coronary arteries in both strains and in SHR compared to WKY arteries. In the SHR preparations, the impaired relaxation induced by acetylcholine appeared to be due to a functional alteration of the endothelium in the presence of normal reactivity of the smooth muscle cells. 相似文献
2.
M. R. Wang C. Y. Chai J. S. Kuof 《Clinical and experimental pharmacology & physiology》1994,21(1):21-29
1. In chloralose-urethane anaesthetized cats, the dorsal cardiovascular reactive area (DCRA) in the parvocellular reticular nucleus dorsomedial to the facial nucleus, and the ventral cardiovascular reactive area (VCRA) ventromedial to the facial nucleus, were stimulated by microinjections of sodium glutamate (100–200 nmol) or electric current. 2. Stimulation of DCRA, with a long latency of 15–20 s, elicited a marked increase of blood flow in the contralateral femoral artery with little change to moderate increase in systemic arterial blood pressure (ABP). In the relatively dorsal portion of DCRA, however, a smaller increase of blood flow in the ipsilateral femoral artery was elicited. 3. On the other hand, stimulation of VCRA with a short latency (3–5 s) evoked an increase of blood flow in both femoral arteries which was more prominent on the contralateral side. The responses were accompanied with decreases in the blood flow of other vascular beds with only a slight increase or minimal change in ABP. 4. The data suggest that DCRA and VCRA are both viscerotopically organized to alter the resistance of individual vascular beds for redistribution of blood flow. 相似文献
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4.
肺血管扩张在肝肺综合征发病机制中作用的研究进展 总被引:3,自引:0,他引:3
肺血管扩张是肝肺综合征的主要发病机制,然而导致HPS肺血管扩张的机制相当复杂,至今仍不清楚.目前认为肺血管内巨噬细胞聚积和雌激素升高导致的血管活性因子增多和活性增强可能与此有关,近年来这方面的研究很多,本文对此作一综述. 相似文献
5.
The peak effects of 10 mg nisoldipine p.o. with or without 80mg propranolol p.o. on systemic and regional haemodynamics inconscious pigs were investigated. Nisoldipine increased heartrate (70%), cardiac output (67%) and maxLVdP/dt (75%), but decreasedmean arterial pressure (21%) as systemic vascular conductanceincreased by 120%. Left ventricular systolic and end-diastolicpressures were not affected. Vasodilatation occurred in mostorgans. The increase in left ventricular blood flow (150%) favouredthe epicardial (195%) over the endocardial (110%) layers. Asa result the endoepi blood flow ratio decreased by 30% When nisoldipine was administered simultaneously with propranolol,heart rate (29%), cardiac output (35%) and systemic vascularconductance (65%) increased, but maxL VdP/dt did not change.Mean arterial (18%) and left ventricular systolic (10%) pressuredecreased; left ventricular end-diastolic pressure was againunaffected. In most organs vasodilatation was attenuated, butstill present, compared to the changes after nisoldipine alone.The increase in epicardial blood flow (70%) again exceeded thatin endocardial blood flow (35%), however, the endoepiratio decreased by only 15%. In the presence of propranolol,nisoldipine did not exert a negative inotropic action whilethe reflex-tachycardia was attenuated. In addition, no detrimentaleffects on perfusion of regional vascular beds were observed. 相似文献
6.
- Adrenomedullin (ADM) is a recently characterized circulating hormone which affects haemodynamic, renal and pituitary function in mammals. We have shown previously that in sheep, ADM produces vasodilatation together with increases in cardiac output and contractility. However, whether these effects are direct or mediated by autonomic reflexes is unclear. The present study examined the cardiovascular actions of an intravenous infusion of ADM in conscious, chronically instrumented sheep with either sympathetic, parasympathetic or autonomic ganglion blockade, to determine the role of the autonomic nervous system in mediating these cardiovascular changes.
- Human ADM (1–52) was infused for 60 min at 2 μg kg−1 h−1 following: (1) saline control, (2) combined α/β-adrenoceptor (sympathetic) blockade (proporanolol 0.4 mg kg−1 h−1+phentolamine 0.15 mg kg−1 h−1 for 20 h), (3) muscarinic (parasympathetic) blockade (methscopolamine 0.05 mg kg−1 h−1 for 20 h) or (4) ganglion blockade (hexamethonium 3 mg kg−1 h−1 for 4 h). Measurements were made of mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), stroke volume (SV), total peripheral conductance (TPC), maximal aortic flow (Fmax) and maximal rate of change of aortic flow (dF/dt).
- ADM reduced MAP by 3±1 mmHg, and increased CO (1.2±0.2 l min−1), HR (14±2 beats min−1), TPC (21±3 ml min−1 mmHg−1), Fmax (2.3±0.8 l min−1) and dF/dt (86±21 l min−1 s−1) in normal sheep. In animals with α/β blockade, similar changes were observed with ADM. However, during muscarinic blockade, the increases in HR (32±4 beats min−1), CO (2.1±0.4 l min−1), TPC (31±4 ml min−1 mmHg−1), Fmax (4.0±0.6 l min−1), and dF/dt (150±12 l min−1 s−1) produced by ADM were enhanced. During ganglion blockade, ADM produced a greater reduction in MAP (−10±2 mmHg) compared to controls (−3±1 mmHg). However, there was no increase in HR. The changes in CO, TPC and contractility were similar to those observed in control animals.
- These results suggest that the vasodilator effects of ADM on the periphery and its ability to increase CO and cardiac contractility are not mediated by the autonomic nervous system, but are probably the result of direct actions of ADM on the heart and vasculature.
7.
Tomohiro Komatsu Makoto Ayaori Harumi Uto-Kondo Katsumi Hayashi Katsumi Tamura Hiroki Sato Makoto Sasaki Takafumi Nishida Shunichi Takiguchi Emi Yakushiji Kazuhiro Nakaya Katsunori Ikewaki 《Journal of atherosclerosis and thrombosis》2022,29(5):775
Aims: Inflammation is involved in various processes of atherosclerosis development. Serum C-reactive protein (CRP) levels, a predictor for cardiovascular risk, are reportedly reduced by statins. However, several studies have demonstrated that CRP is a bystander during atherogenesis. While S100A12 has been focused on as an inflammatory molecule, it remains unclear whether statins affect circulating S100A12 levels. Here, we investigated whether atorvastatin treatment affected S100A12 and which biomarkers were correlated with changes in arterial inflammation. Methods: We performed a prospective, randomized open-labeled trial on whether atorvastatin affected arterial (carotid and thoracic aorta) inflammation using18fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG-PET/CT) and inflammatory markers. Thirty-one statin-naïve patients with carotid atherosclerotic plaques were randomized to either a group receiving dietary management (n=15) or one receiving atorvastatin (10mg/day,n=16) for 12weeks.18F-FDG-PET/CT and flow-mediated vasodilation (FMD) were performed, the latter to evaluate endothelial function. Results: Atorvastatin, but not the diet-only treatment, significantly reduced LDL-cholesterol (LDL-C, -43%), serum CRP (-37%) and S100A12 levels (-28%) and improved FMD (+38%).18F-FDG-PET/CT demonstrated that atorvastatin, but not the diet-only treatment, significantly reduced accumulation of18F-FDG in the carotid artery and thoracic aorta. A multivariate analysis revealed that reduction in CRP, S100A12, LDL-C, oxidized-LDL, and increase in FMD were significantly associated with reduced arterial inflammation in the thoracic aorta, but not in the carotid artery. Conclusions: Atorvastatin treatment reduced S100A12/CRP levels, and the changes in these circulating markers mirrored the improvement in arterial inflammation. Our observations suggest that S100A12 may be an emerging therapeutic target for atherosclerosis. 相似文献
8.
Guang‐Yuan Mar Ming‐Ting Chou Hsien‐Hui Chung Nien‐Hua Chiu Mei‐Fen Chen Juei‐Tang Cheng 《International journal of experimental pathology》2013,94(1):17-24
The role of imidazoline receptors in the regulation of vascular function remains unclear. In this study, we evaluated the effect of agmatine, an imidazoline receptor agonist, on systolic blood pressure (SBP) in spontaneously hypertensive rats (SHRs) and investigated the expressions of imidazoline receptors by Western blot. The isometric tension of aortic rings isolated from male SHRs was also estimated. Agmatine decreased SBP in a dose‐dependent manner in SHRs but not in the normal group [Wistar–Kyoto (WKY) rats]. This reduction in SBP in SHRs was abolished by BU224, a selective antagonist of imidazoline I2‐receptors. Higher expression of imidazoline receptors in SHR was observed. Moreover, agmatine‐induced relaxation in isolated aortic rings precontracted with phenylephrine or KCl. This relaxation was also abolished by BU224 but was not modified by efaroxan, an imidazoline I1‐receptor antagonist. Agmatine‐induced relaxation was also attenuated by PNU 37883, a selective blocker of vascular ATP‐sensitive potassium (KATP) channels. Additionally, vasodilatation by agmatine was reduced by an inhibitor of protein kinase A (PKA). We suggest that agmatine can lower blood pressure in SHRs through activation of the peripheral imidazoline I2‐receptor, which is expressed more highly in SHRs. 相似文献
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10.
Breno José Acauan Filho Bartira Ercilia Pinheiro da Costa Patrícia Barcelos Ogando Matias Costa Vieira Ivan Carlos Antonello Carlos Eduardo Poli-de-Figueiredo 《Hypertension in pregnancy》2016,35(2):226-233
Objectives: To compare nitric oxide (NO) serum levels in women with and without preeclampsia. Methods: 106 women were classified into preeclampsia group (n = 40) and normotensive group (n = 66). NO content was measured in the serum. Clinical and laboratorial data were recorded for comparison. Results: Preeclampsia presented a significant increase in nitrate and NOx levels compared to the control group. Uric acid, gestational age, systolic and diastolic blood pressure, and creatinine showed correlation with nitrates and NOx. Conclusion: Increase of NO was observed in preeclampsia women. Failure in the mechanism of action, dependent on cyclic GMP, may justify this finding. 相似文献