Effect of β-Receptor-Blocking Agents on Cardiovascular Structural Changes in Spontaneous and Noradrenaline-Induced Hypertension in Rats

1980 ◽  
Vol 59 (s6) ◽  
pp. 457s-460s ◽  
Author(s):  
Yukio Yamori ◽  
R. C. Tarazi ◽  
Akira Ooshima
Keyword(s):  
Blood Pressure ◽  
Protein Synthesis ◽  
Structural Changes ◽  
Cardiovascular Response ◽  
Left Ventricular ◽  
Spontaneously Hypertensive ◽  
Receptor Blocking ◽  
Blocking Agents ◽  
Collagen Protein ◽  
Β Receptor

1. Continuous intravenous noradrenaline infusion for 1 week into rats by osmotic minipumps significantly increased blood pressure and left ventricular weight. 2. Concomitant α-receptor-blockade infusion significantly lowered blood pressure and the aortic weight without significant reduction in left ventricular weight. 3. Two β-receptor-blocking agents in noradrenaline-infused rats normalized left ventricular weight and significantly reduced the aortic weight, although blood pressure was still higher than control non-infused rats. 4. In 7-week-old spontaneously hypertensive rats, propranolol (perorally for 2 weeks) did not lower blood pressure but reduced significantly cardiovascular protein synthesis ([14C]lysine and [3H]uridine incorporation into non-collagen protein and RNA respectively) in both left ventricle and aorta. This effect was in contrast to hydrallazine, which normalized blood pressure but did not reduce cardiovascular protein synthesis. 5. Results suggest that β-receptors play a modulating role in the structural cardiovascular response to blood pressure.

A Comparison of the Acute Haemodynamic Effects of Propranolol and Pindolol at Rest and during Supine Exercise in Man

1980 ◽  
Vol 59 (s6) ◽  
pp. 465s-468s ◽  
Author(s):  
T. L. Svendsen ◽  
J. E. Carlsen ◽  
O. Hartling ◽  
A. McNair ◽  
J. Trap-Jensen
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Response Curves ◽  
Receptor Blocking ◽  
Artery Pressure ◽  
Arterial Blood ◽  
Β Receptor

1. Dose-response curves for heart rate, cardiac output, arterial blood pressure and pulmonary artery pressure were obtained in 16 male patients after intravenous administration of three increasing doses of pindolol, propranolol or placebo. All patients had an uncomplicated acute myocardial infarction 6–8 months earlier. 2. The dose-response curves were obtained at rest and during repeated bouts of supine bicycle exercise. The cumulative dose amounted to 0.024 mg/kg body weight for pindolol and to 0.192 mg/kg body weight for propranolol. 3. At rest propranolol significantly reduced heart rate and cardiac output by 12% and 15% respectively. Arterial mean blood pressure was reduced by 9.2 mmHg. Mean pulmonary artery pressure increased significantly by 2 mmHg. Statistically significant changes in these variables were not seen after pindolol or placebo. 4. During exercise pindolol and propranolol both reduced cardiac output, heart rate and arterial blood pressure to the same extent. After propranolol mean pulmonary artery pressure was increased significantly by 3.6 mmHg. Pindolol and placebo did not change pulmonary artery pressure significantly. 5. The study suggests that pindolol may offer haemodynamic advantages over β-receptor-blocking agents without intrinsic sympathomimetic activity during low activity of the sympathetic nervous system, and may be preferable in situations where the β-receptor-blocking effect is required only during physical or psychic stress.

scholarly journals Effects of Transgenic Expression of Dopamine Beta Hydroxylase (Dbh) Gene on Blood Pressure in Spontaneously Hypertensive Rats

2016 ◽  
pp. 1039-1044
Author(s):  
M. PRAVENEC ◽  
V. LANDA ◽  
V. ZÍDEK ◽  
P. MLEJNEK ◽  
J. ŠILHAVÝ ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Spontaneously Hypertensive Rat ◽  
Reduce Blood Pressure ◽  
Left Ventricular ◽  
Brown Norway ◽  
Catecholamine Metabolism ◽  
Mrna Levels ◽  
Spontaneously Hypertensive ◽  
Dopamine Beta Hydroxylase

The spontaneously hypertensive rat (SHR) is the most widely used animal model of essential hypertension and left ventricular hypertrophy. Catecholamines play an important role in the pathogenesis of both essential hypertension in humans and in the SHR. Recently, we obtained evidence that the SHR harbors a variant in the gene for dopamine beta hydroxylase (Dbh) that is associated with reduced adrenal expression of Dbh mRNA and reduced DBH enzymatic activity which correlated negatively with blood pressure. In the current study, we used a transgenic experiment to test the hypothesis that reduced Dbh expression predisposes the SHR to hypertension and that augmentation of Dbh expression would reduce blood pressure. We derived 2 new transgenic SHR-Dbh lines expressing Dbh cDNA under control of the Brown Norway (BN) wild type promoter. We found modestly increased adrenal expression of Dbh in transgenic rats versus SHR non-transgenic controls that was associated with reduced adrenal levels of dopamine and increased plasma levels of norepinephrine and epinephrine. The observed changes in catecholamine metabolism were associated with increased blood pressure and left ventricular mass in both transgenic lines. We did not observe any consistent changes in brainstem levels of catecholamines or of mRNA levels of Dbh in the transgenic strains. Contrary to our initial expections, these findings are consistent with the possibility that genetically determined decreases in adrenal expression and activity of DBH do not represent primary determinants of increased blood pressure in the SHR model.

Abstract 1378: NFkb Blockade Attenuate Cytokines And Oxidative Stress In The Paraventricular Nucleus And Decreases Neurohumoral Excitation In Spontaneously Hypertensive Rats

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Nithya Mariappan ◽  
Carrie Elks ◽  
Masudul Haque ◽  
Philip J Ebnezer ◽  
Elizabeth McIIwain ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Paraventricular Nucleus ◽  
Spontaneously Hypertensive Rats ◽  
Left Ventricular ◽  
Oxidative Stress Markers ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Stress Markers ◽  
And Oxidative Stress

The transcriptional factor, nuclear factor kappa B (NFkB) plays an important role in the regulation of cytokines. Among the cytokines, tumor necrosis factor-alpha (TNF) plays an important role in cardiovascular pathophysiology. This study was done to determine whether TNF-α blockade with etanercept (ETN) or NFkB blockade with dithiol pyrolidine thiocarbamate (PDTC) attenuate oxidative stress in the paraventricular nucleus (PVN) and contribute to neurohumoral excitation in spontaneously hypertensive rats. Method: Male 20 week old SHR rats were treated with ETN (1 mg/kg BW, sc) or PDTC (100mg/kg BW, ip) for 5 week period. Left ventricular function was measured at baseline (20 weeks) and at 25 weeks using echocardiography. Blood pressure was measured at weekly intervals throughout the study. At the end of the protocol rats were sacrificed the PVN was microdissected for the measurement of cytokines, oxidative stress markers using real time PCR (fold increase compared to WKY controls) and by immunohistochemistry. Superoxide, total reactive oxygen species and peroxynitrite were measured in the PVN and LV using electron paramagnetic resonance. Plasma norepinephrine and epinephrine an indicator of neurohumoral excitation was measured using HPLC-EC. Results: PVN data are tabulated. SHR animals had increased expression of protein and mRNA for cytokines and oxidative stress markers in the PVN and LV with increased MAP and cardiac hypertrophy when compared to WKY rats. Treatment with ETN and PDTC attenuated these increases with PDTC showing marked effect than ETN on hypertrophy and blood pressure responses. Conclusion: These findings suggest that cytokine activation in the PVN contributes to increased oxidative stress and neurohumoral excitation in hypertension.

Abstract P043: Correlation Between Blood Pressure And Left Ventricular Metabolism In HIV Individuals With And Without Cocaine Use As Assessed By FDG-PET/CT

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Abhijit Bhattaru ◽  
Rina Ghorpade ◽  
Chaitanya Rojulpote ◽  
Paco E Bravo ◽  
Shivaraj Patil ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Metabolic Activity ◽  
Fdg Pet ◽  
Structural Changes ◽  
Left Ventricular ◽  
Myocardial Uptake ◽  
Hiv Patients ◽  
Cocaine Use ◽  
Pet Ct ◽  
Fdg Pet Ct

Objectives: Elevated blood pressure from cocaine can increase left ventricular (LV) metabolic activity, leading to structural changes such as hypertrophy. We aimed to assess the association between blood pressure and LV myocardial uptake of FDG, hypothesizing that HIV individuals with raised blood pressure will have higher FDG uptake. Methods: University of Pennsylvania enrolled patients with HIV on antiretroviral therapy with viral load <200 copy/ml. Cocaine usage in moderate to high amounts (cocaine disease score≥5) was subsequently documented. Full body PET scans were acquired 120 minutes post-injection of 18F-FDG(15 mCi) with low-dose CT scans for attenuation correction. Patients with imaging artifacts were excluded from the analysis. Regions of interest were drawn on axial slices using computer software (OsirixMD, v9.0.02) around LV myocardium. Average standard uptake value means (aSUVmean) were calculated for each patient. Systolic blood pressure (SBP) and diastolic blood pressure (DBP) were obtained prior to imaging; mean arterial pressure (MAP) was subsequently calculated. Linear regressions and Mann-Whitney U tests were employed for statistical analysis. Results: aSUVmean was higher in HIV patients with cocaine use (U(Ncocaine = 11, Nno cocaine=11) = 93, p=0.0336). In patients with cocaine use, there was a positive correlation between blood pressure and aSUVmean (SBP: r=0.70, p=0.0164; DBP: r=0.69, p=0.0185; MAP: r=0.72, p=0.0120). No significant correlations were found in HIV patients without cocaine use (SBP: r=0.03, p=0.9239; DBP: r=-0.50, p=0.1153; MAP: r=-0.32, p=0.3345). Conclusions: LV myocardial metabolism was more strongly positively correlated with blood pressure in HIV patients using cocaine compared to HIV patients without cocaine. These data suggest FDG-PET/CT can be used to monitor LV metabolic activity and allow for timely assessment of structural changes caused by cocaine use and hypertension.

Modulation of cardiovascular response to dynamic exercise by fastigial nucleus

1984 ◽  
Vol 56 (5) ◽  
pp. 1369-1377 ◽  
Author(s):  
K. J. Dormer
Keyword(s):  
Blood Pressure ◽  
Repeated Measures ◽  
Cardiovascular Response ◽  
Systolic Pressure ◽  
Cardiovascular Responses ◽  
Left Ventricular ◽  
Dynamic Exercise ◽  
Fastigial Nucleus ◽  
Ventricular Systolic Pressure ◽  
Arterial Blood

Mongrel dogs (n = 34) were used to record the cardiovascular responses during submaximal exercise-tolerance tests (ETT) before and after the placement of lesions in rostral portions of the cerebellar fastigial nucleus (FN). Sterile surgical procedures were used to implant solid-state pressure transducers into the left ventricle or descending aorta (anesthesia 1% halothane in O2) and multipolar stainless steel electrodes into FN (anesthesia alpha-chloralose 115 mg/kg iv). Heart rate (HR), maximal left ventricular systolic pressure ( LVPmax ) and its first derivative ( dLVP /dt), and mean arterial blood pressure (MAP) were recorded during a motorized treadmill ETT. Electrolytic direct-current or radio-frequency lesions were made through the indwelling FN electrodes, and the ETT was repeated following 10–14 days recovery. Two-way analysis of variance (ANOVA), with repeated measures on one, and one-way ANOVA for simple effects indicated a significant reduction in HR and MAP (P less than 0.01) but not LVPmax and dLVP /dt occurred during exercise as a result of rostral FN lesions. Although the trend for reduced LVPmax and dLVP /dt was also evident, a relatively greater decrease in blood pressure occurred in the peripheral vasculature during exercise. It was concluded that FN acts as a modulator of HR and MAP during dynamic exercise because of the observed deficits, and because FN is known to both send efferent projections to medullary vasomotor areas and receive projections from motor cortex and muscle and joint afferents.

Exercise training modifies myocardial mitochondria and myofibril growth in spontaneously hypertensive rats

1985 ◽  
Vol 248 (1) ◽  
pp. H8-H14
Author(s):  
R. P. Crisman ◽  
R. J. Tomanek
Keyword(s):  
Blood Pressure ◽  
Exercise Training ◽  
Spontaneously Hypertensive Rats ◽  
Pressure Overload ◽  
Volume Ratio ◽  
Volume Density ◽  
Left Ventricular ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

We tested the hypothesis that exercise training provides a stimulus that could modify the decrement in mitochondria-to-myofibril volume ratio characteristic of myocardial cells hypertrophied in response to a pressure overload. Spontaneously hypertensive rats (SHR) were trained 5 days/wk on a treadmill at 70-90% maximal VO2 between the ages of 6 and 16 wk corresponding to the development of hypertension and cardiac hypertrophy. The training program increased maximal VO2 and effected a resting bradycardia but did not alter blood pressure, left ventricular hypertrophy, or peak cardiac output. Our stereological data from electron micrographs shows that the decrement in mitochondrial volume density and the increase in myofibril volume density characteristic of SHR compared with their normotensive controls (WKY, Wistar-Kyoto rats) were reversed. Thus the relative volumes of mitochondria and myofibrils and their ratio in trained SHR were similar to those of the WKY group. The similarity was noted in myocytes from both the subepicardium and subendocardium. These data suggest that exercise training facilitates a proportional growth of energy-producing and energy-consuming organelles in SHR and that this effect is not secondary to modification of blood pressure or left ventricular mass.

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