by Kwok Fai (Simon) Leung. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1990. / Bibliography: leaves 72-99. / ACKNOWLEDGEMENTS --- p.i / ABSTRACT --- p.ii / Chapter SECTION 1: --- Literature Review / Chapter 1.1 --- Historical perspectives of ANP --- p.1 / Chapter 1.2 --- Nature of ANP --- p.5 / Chapter 1.3 --- Release of ANP --- p.13 / Chapter 1.4 --- Biological effects of ANP --- p.17 / Chapter 1.5 --- Clinical implications --- p.24 / Chapter SECTION 2: --- Effect of ANP on Left Atrium / Chapter 2.1 --- Introduction --- p.29 / Chapter 2.2 --- Methods --- p.32 / Chapter 2.3 --- Results --- p.37 / Chapter 2.4 --- Discussion --- p.44 / Chapter SECTION 3: --- Effect of ANP on Mesenteric Artery / Chapter 3.1 --- Introduction --- p.47 / Chapter 3.2 --- Methods --- p.51 / Chapter 3.3 --- Results --- p.62 / Chapter 3.4 --- Discussion --- p.66 / Chapter SECTION 4: --- General Discussion --- p.67 / Chapter SECTION 5: --- References --- p.72

Plasma natriuretic peptide concentrations rise in response to either atrial or ventricular wall stretch and have been found to be useful in the diagnosis and assessment of patients with congestive cardiac failure. Although previous studies have suggested that plasma natriuretic peptides may offer some prognostic information in patients with valvular heart disease, it is unclear whether concentrations reflect disease severity and how plasma concentrations vary across different valve lesions. The aim of this research was to identify the factors that affect natriuretic peptide releases in valvular heart disease (VHD) and to investigate whether natriuretic peptides can be used in clinical practice to identify those patients who may benefit from early intervention. Plasma brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) concentrations were measured in patients with normal left ventricular (LV) systolic function and isolated VHD (mitral regurgitation, MR, n=33; aortic regurgitation, AR, n=39; aortic stenosis, AS, n=34; mitral stenosis, MS, n=30), and age and sex matched controls (n=39) immediately prior to exercise stress echocardiography. Peptide levels were compared against age and sex matched controls and against markers of severity for each valve lesions and across different valve lesions. Compared to controls, patients with all types of VHD had elevated plasma BNP concentrations [(MR median 35(inter quartile range 23-52), AR 34(22-45), AS 31(22-60), MS 58(34-90); controls 24(16-33) pg/mL; p < 0.01 for all]. LV end diastolic volume index varied by valve lesion; [MR (mean ± standard deviation 77±14), AR (91±28), AS (50±17), MS (43±11), controls (52±13) mL/m2; p < 0.0001]. There were no associations between LV volume and BNP. Left atrial (LA) area index varied [MR (18±4cm2/m2), AR (12±2), AS (11±3), MS (19±6), controls (11±2); p < 0.0001], but correlated with plasma BNP concentrations: MR (r=0.42,p=0.02), MS (r=0.86,p < 0.0001), AR (r=0.53,p=0.001), AS (r=0.52, p=0.002). Higher plasma BNP concentrations were associated with increased pulmonary artery pressure and reduced exercise capacity. Despite adverse cardiac remodelling, 81(60%) patients had a BNP concentration within the normal range. In patients with MS BNP was strongly associated with left atrial area index (r=0.86; p < 0.0001) and a BNP level of greater than 2 times the upper limit of normal identified patients who fulfilled guideline criteria for intervention (Area under the curve (AUC) 0.87 [0.74,0.99], p =0.006) and lower exercise capacity (AUC 0.82 [0.67,0.97]; p=0.004). In AR patients significant remodelling could occur whilst BNP remained within the normal range and in general BNP appeared less useful in assessing disease severity. However raised levels of BNP was associated with more severe AR as assessed by left ventricular outflow tract:AR Jet area ratio (r=0.43 p=0.0007). AR patients with an abnormal BNP had signs of early LV dysfunction on exercise with a lower LV longitudinal strain rate post exercise compared to AR patients with a normal BNP (0.68±0.31 vs. 1.06±0.45 1/sec; p=0.02). In MR patients, higher plasma BNP concentrations were associated with larger left atrial area index (r=0.42, p=0.02), higher pulmonary artery pressure (r=0.53, p=0.002) and a lower exercise time (r=-0.60, p=0.0002). BNP was not associated with any marker of left ventricular size or function in MR. These findings suggest that despite significant LV remodelling, plasma BNP concentrations are often normal in patients with VHD. Consequently, plasma BNP concentrations should be interpreted with caution when assessing patients with VHD. However natriuretic peptide levels offer complementary information to the standard assessment of patients with VHD and an unexplained finding of an elevated BNP in an otherwise asymptomatic patient should prompt further investigation.

Thesis (M. Med. Sc.)--University of Queensland, 2003. / Date on spine is 2002. Includes bibliographical references.

Thesis (M. Med. Sc.)--University of Hong Kong, 2005.

The mechanisms which cause post exercise hypotension (a phenomenon of prolonged, decreased resting blood pressure following physical exertion) are unknown. Atrial natriuretic peptide (ANP) is known to exert potent natriuretic and vasodilatory properties which play an integral role in fluid regulation and blood pressure control. Elevations in plasma ANP concentration have been shown to occur during dynamic endurance exercise, and to a lesser extent during heavy resistance exercise. The purposes of this investigation were to 1) examine the effects of resistance and endurance exercise on the release of ANP, 2) examine the effects of resistance and endurance exercise on post exercise blood pressure and 3) evaluate the potential correlations of ANP release with any observed changes. Thirteen males (24.3±2.4yrs.) performed 15 min of unilateral leg press (65% 1 RM) and, one week later ~15 min (based on summed cardiac cycles of the resistance trial) of cycle ergometry (65% V0₂ ₚₑₐₖ). Blood pressure was measured using an intra-arterial catheter during exercise and for 1 h post exercise. Arterial blood was drawn at rest, 5, 10 and 15 min of exercise and 1 1/2, 3, 5, 10, 15, 30, 45 and 60 min post exercise for subsequent analysis of hematocrit and αANP. No differences occurred in blood pressure responses between trials, but significant decrements in blood pressure occurred post exercise compared to pre exercise. Systolic pressure was ~20mmHg lower from 10 min post exercise until measurements terminated at 60 min post exercise. Mean pressure was also significantly attenuated by ~7 mmHg from 30 min post exercise onwards. Only slight (non significant) elevations in αANP concentration were detected immediately following exercise with no elevation present by 5 min post exercise. It was concluded that post exercise hypotension occurs with acute bouts of either resistance or endurance exercise and that αANP does not appear to be directly related to this hypotensive effect. This study was supported by the Natural Sciences and Engineering Research Council of Canada / Thesis / Master of Science (MSc)

No description available.

No description available.

by Ngai Wing Keung Clement. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1992. / Includes bibliographical references (leaves 172-206). / Chapter 1. --- Acknowledgment --- p.iv / Chapter 2. --- Abstract --- p.v / Chapter 3. --- Lists of Tables and Figures --- p.vii / Chapter 4. --- General Introduction --- p.1 / Chapter 5. --- Review of Literature --- p.5 / Chapter 5.1. --- Historical Background of Natriuretic Peptides --- p.5 / Chapter 5.2. --- Secretion of Natriuretic Peptides --- p.8 / Chapter 5.3. --- Structure and Function Relationships --- p.12 / Chapter 5.4. --- Physiological Actions --- p.17 / Chapter 5.5. --- Natriuretic Peptide Receptors and Second Messengers --- p.22 / Chapter 5.6. --- Clinical Implications --- p.28 / Chapter 5.7. --- Review on Astrocytes --- p.31 / Chapter 6. --- General Materials and Methods --- p.43 / Chapter 6.1. --- Sources of Chemicals --- p.43 / Chapter 6.2. --- Culture of Mouse Astrocytes --- p.43 / Chapter 6.3. --- Culture of human astrocytoma cells --- p.57 / Chapter 6.4. --- Protein Determination --- p.57 / Chapter 6.5. --- Gamma Counting --- p.58 / Chapter 6.6. --- Beta Counting --- p.58 / Chapter 7. --- Receptor Identification and Characterization --- p.59 / Chapter 7.2 --- Materials and Methods --- p.60 / Chapter 7.3 --- Results --- p.66 / Chapter 7.4 --- Discussion --- p.81 / Chapter 8. --- Second Messenger Systems --- p.83 / Chapter 8.1 --- Introduction --- p.83 / Chapter 8.2 --- Materials and Methods --- p.85 / Chapter 8.3 --- Results --- p.97 / Chapter 8.4 --- Discussion --- p.109 / Chapter 9. --- Biological Actions of Natriuretic Peptides --- p.113 / Chapter 9.1. --- Potassium Transport --- p.113 / Chapter 9.1.1. --- Introduction --- p.113 / Chapter 9.1.2. --- Materials and Methods --- p.116 / Chapter 9.1.3. --- Results --- p.121 / Chapter 9.1.4. --- Discussion --- p.131 / Chapter 9.2 --- Taurine Release --- p.135 / Chapter 9.2.1. --- Introduction --- p.135 / Chapter 9.2.2. --- Materials and Methods --- p.137 / Chapter 9.2.3. --- Results --- p.139 / Chapter 9.2.4. --- Discussion --- p.143 / Chapter 9.3 --- Thymidine Incorporation --- p.144 / Chapter 9.3.1. --- Introduction --- p.144 / Chapter 9.3.2. --- Materials and Methods --- p.146 / Chapter 9.3.3. --- Results --- p.148 / Chapter 9.3.4. --- Discussion --- p.156 / Chapter 10. --- Interaction with Other Hormonal Systems --- p.160 / Chapter 10.1 --- Introduction --- p.160 / Chapter 10.2 --- Materials and Methods --- p.162 / Chapter 10.3 --- Result --- p.163 / Chapter 10.4 --- Discussion --- p.167 / Chapter 11. --- Conclusion --- p.169 / Chapter 12. --- References --- p.172 / Chapter 13. --- Appendix --- p.208

by Lee Suk Kuen Zoe. / Thesis (Ph.D.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (p. 271-314). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstract in Chinese.

In this study, both physiological and cellular effects are elicited by natriuretic peptides (NPs), a novel type of plant hormone. It was found that rat ANP (rANP) influenced stomatal opening movement in Tradescantia sp., where a significant increase in stomatal opening was observed in the presence of 1 µM rANP. Furthermore, this effect is mediated by cGMP, a (putative) second messenger of NPs. Two inhibitors of guanylyl cyclase, LY 83583 and methylene blue, inhibited rANP-induced stomatal opening. In contrast, stomatal opening is induced in a concentration dependent manner by the cell permeant cGMP analogue 8-Br-cGMP. In addition it was found, that like in animals, the secondary structure of rANP is essential for rANP responses. Linearised rANP is biologically inactive. Since ANP elicit plant responses, an attempt was made to isolate NP analogues from plants. A protocol for partially purifying NP from plants was developed. It was found that two fractions eluted from an immunoaffinity chromatography column (0.5 M KCI eluted fraction and 0.75 M KCI eluted fraction) were biologically active. The level of cGMP in response to NPs was also tested. It is suggested that the receptor of NP is specific since only 0.75 M KCI eluted fractions increased cGMP levels in Zea mays root stele tissue. rANP did not elicit an effect on cGMP levels in this tissue and LY 83583 did not affect this response. It is therefore argued that a plant specific biologically active NP system is present in the stele and it is predicted that NPs modulate solute movement in this tissue. NPs also influence K⁺, Na⁺ and H⁺ fluxes in Zea mays root stele. Increase in both K⁺ and Na+ uptake were observed after 30 min., while H⁺ flux shifted immediately toward influx in the presence of both 0.5 and 0.75 KCI eluted fractions. Finally, a model is proposed for the effect of NPs on solute movement and its signalling system in plants.