scholarly journals Significance of blood pressure levels achieved with felodipine anti-hypertensive treatment on cardiovascular structure and function changes

1998 ◽  
Vol 12 (7) ◽  
pp. 427-432 ◽  
Author(s):  
GP Vyssoulis ◽  
AG Trikas ◽  
AA Paleologos ◽  
MG Toutouza ◽  
PK Toutouzas
Keyword(s):  
Blood Pressure ◽  
Structure And Function ◽  
Cardiovascular Structure ◽  
And Function

scholarly journals α1D-adrenoceptors are responsible for maintenance of the cardiovascular structure and function independently of blood pressure

2018 ◽  
Vol WCP2018 (0) ◽  
pp. PO2-3-6
Author(s):  
Itzell A Gallardo-Ortiz ◽  
Cesar E Perez-Medina ◽  
Javier D Sanchez-Gonzalez ◽  
Juan J Lopez-Guerrero ◽  
Akito Tanoue ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Structure And Function ◽  
Cardiovascular Structure ◽  
And Function

Growth hormone receptor deficiency in mice results in reduced systolic blood pressure and plasma renin, increased aortic eNOS expression, and altered cardiovascular structure and function

2007 ◽  
Vol 292 (5) ◽  
pp. E1418-E1425 ◽  
Author(s):  
E. Egecioglu ◽  
I. J. Andersson ◽  
E. Bollano ◽  
V. Palsdottir ◽  
B. G. Gabrielsson ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Growth Hormone ◽  
Systolic Blood Pressure ◽  
Hormone Receptor ◽  
Growth Hormone Receptor ◽  
Plasma Renin ◽  
Structure And Function ◽  
Enos Expression ◽  
Cardiovascular Structure ◽  
And Function

To study the role of the growth hormone receptor (GHR) in the development of cardiovascular structure and function, female GHR gene-disrupted or knockout (KO) and wild-type (WT) mice at age 18 wk were used. GHR KO mice had lower plasma renin levels (12 ± 2 vs. 20 ± 4 mGU/ml, P < 0.05) and increased aortic endothelial NO synthase (eNOS) expression (146%, P < 0.05) accompanied by a 25% reduction in systolic blood pressure (BP, 110 ± 4 vs. 147 ± 3 mmHg, P < 0.001) compared with WT mice. Aldosterone levels were unchanged, whereas the plasma potassium concentration was elevated by 14% ( P < 0.05) in GHR KO. Relative left ventricular weight was 14% lower in GHR KO mice ( P < 0.05), and cardiac dimensions as analyzed by echocardiography were similarly reduced. Myograph studies revealed a reduced maximum contractile response in the aorta to norepinephrine (NE) and K+ ( P < 0.05), and aorta media thickness was decreased in GHR KO ( P < 0.05). However, contractile force was normal in mesenteric arteries, whereas sensitivity to NE was increased ( P < 0.05). Maximal acetylcholine-mediated dilatation was similar in WT and GHR KO mice, whereas the aorta of GHR KO mice showed an increased sensitivity to acetylcholine ( P < 0.05). In conclusion, loss of GHR leads to low BP and decreased levels of renin in plasma as well as increase in aortic eNOS expression. Furthermore, GHR deficiency causes functional and morphological changes in both heart and vasculature that are beyond the observed alterations in body size. These data suggest an important role for an intact GH/IGF-I axis in the maintenance of a normal cardiovascular system.

scholarly journals Blood pressure-induced physiological strain variability modulates wall structure and function in aorta rings

2018 ◽  
Vol 39 (10) ◽  
pp. 105014 ◽  
Author(s):  
Jasmin Imsirovic ◽  
Erzsébet Bartolák-Suki ◽  
Samer Bou Jawde ◽  
Harikrishnan Parameswaran ◽  
Béla Suki
Keyword(s):  
Blood Pressure ◽  
Structure And Function ◽  
Wall Structure ◽  
Physiological Strain ◽  
And Function ◽  
Strain Variability

scholarly journals Is the Wistar Rat a more Suitable Normotensive Control for SHR to Test Blood Pressure and Cardiac Structure and Function?

2021 ◽  
Author(s):  
Leonardo Mateus Teixeira de Rezende ◽  
Leôncio Lopes Soares ◽  
Filipe Rios Drummond ◽  
Pedro Zavagli Suarez ◽  
Luciano Leite ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Wistar Rat ◽  
Structure And Function ◽  
Cardiac Structure ◽  
Cardiac Structure And Function ◽  
And Function ◽  
Normotensive Control

Abstract 19478: Endothelial and Cardiomyocyte -derived C-type Natriuretic Peptide Coordinate Heart Structure and Function

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Amie J Moyes ◽  
Sandy M Chu ◽  
Reshma S Baliga ◽  
Adrian J Hobbs
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Function ◽  
Infarct Size ◽  
Natriuretic Peptide ◽  
Vascular Tone ◽  
Ex Vivo ◽  
Pressure Overload ◽  
Structure And Function ◽  
And Function

Background: Endothelium-derived C-type natriuretic peptide (CNP) plays a key vascular homeostatic role governing vascular tone, blood pressure, leukocyte flux, platelet reactivity and the integrity of the vessel wall. However, relatively little is known about physiological role(s) for endogenous CNP in regulating cardiac structure and function. Herein, we have utilised novel mouse strains with endothelium or cardiomyocyte -specific deletion of CNP to determine if the peptide modulates heart function under basal conditions and during cardiac stress. Methods: Blood pressure and ECG were assessed by radiotelemetry. A Langendorff heart model was used to study coronary vascular reactivity and ischemia-reperfusion (I/R) injury ex vivo. Echocardiography was performed to determine cardiac function at baseline and following pressure overload (trans-aortic constriction; 6 weeks) -induced left ventricular hypertrophy/heart failure. Results: Hearts from endothelium-specific CNP knockout (ecCNP KO) mice exhibited smaller reductions in coronary perfusion pressure (CPP) compared to wildtype (WT) littermates in response to the vasodilators bradykinin (ΔCPP: WT=31.7±2.7%, KO=21.1±2.9%, n=8, p<0.05) and acetylcholine (ΔCPP: WT=36.4±4.4%, KO=18.5±3.8%, n=6, p<0.05). Shear-stress induced coronary dilatation (i.e. reactive hyperaemia) was also blunted in ecCNP KO hearts (AUC: WT=2804±280 [a.u.], KO=1493±280 [a.u.], n=8, p<0.05). Under basal conditions the heart rate (BPM: WT=605±5, KO 579±4, n=5, p<0.001) and contractility (QA interval; WT=13.7±0.1ms, KO=14.8±0.1ms, n=5, p<0.001) were significantly reduced in cardiomyocyte-specific CNP (cmCNP) KO mice compared to WT. Myocardial infarct size was larger in cmCNP KO following I/R injury ex vivo (Infarct size: WT=14.1±6.3%, KO=21.8±1.8 %, n=6, p<0.05). Furthermore, cmCNP KO mice exhibited greater cardiac dysfunction following pressure-overload (e.g. fractional shortening: WT=34.4±0.9%, KO=30.5±1.4%, n=8, p<0.05). Conclusion: These data suggest that CNP of endothelial and cardiomyocyte origin preserves cardiac function and morphology via the regulation of coronary vascular tone, heart rate, and myocardial contractility/hypertrophy.

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