Blockade of the renin???angiotensin system in heart failure in conscious dogs

Murakami, Marohito; Suzuki, Hiromichi; Naitoh, Motoko; Matsumoto, Akira; Kageyama, Yoh; Tsujimoto, Gozoh; Saruta, Takao

doi:10.1097/00004872-199512000-00006

Cited by 19 publications

(10 citation statements)

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“…It appeared that dogs with and without MMVD had equally low levels of myocardial Ang II receptors. In agreement with this, Murakami et al (1995) showed that the myocardial Ang II receptor density did not change with the development of heart failure in dogs. Furthermore, in humans, others have found a significant downregulation of myocardial Ang II receptors in end stage heart failure, but not in moderate heart failure (Regitz-Zagrosek et al, 1995;Asano et al, 1997).…”

Section: Discussionsupporting

confidence: 81%

No Expression of Angiotensin II Receptors and Angiotensin‐Converting Enzyme in Myxomatous Canine Mitral Valve Leaflets. An Autoradiographic Study

Mow

Pedersen²

1999

Journal of Veterinary Medicine Series A

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The renin-angiotensin system, including angiotensin (Ang) II and angiotensin-converting enzyme (ACE), plays an important role in cardiac fibrous tissue formation. Since changes in valvular collagen are a central part of myxomatous mitral valve disease in the dog, we speculated that Ang II and ACE might play a role in the pathogenesis of this disease.In 10 mitral valves, five with and five without clear myxomatous changes, the presence and distribution of Ang II receptors and ACE was examined autoradiographically, using 125 I-Ang II and 125 I-lisinopril, respectively. At postmortem examination, diseased valves were taken from old dogs, control valves from young adult dogs.No significant level of Ang II and lisinopril binding was found in normal as well as diseased valve leaflets. Equally low, insignificant levels of 125 I-Ang II binding were found in the myocardium of dogs with and without valvular disease. No significant level of myocardial 125 I-lisinopril binding was found.The lack of autoradiographic evidence of Ang II receptors and ACE in normal and diseased canine mitral valve leaflets suggests that the renin-angiotensin system does not play a major role in the pathogenesis of the valvular changes.

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Section: Discussionsupporting

confidence: 81%

No Expression of Angiotensin II Receptors and Angiotensin‐Converting Enzyme in Myxomatous Canine Mitral Valve Leaflets. An Autoradiographic Study

Mow

Pedersen²

1999

Journal of Veterinary Medicine Series A

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“…A Tygon tube was inserted into the abdominal aorta through the right femoral artery for measurement of mean arterial pressure and heart rate under the conscious condition (21). CKD was induced in dogs by heminephrectomy (1/2Nx group; n ϭ 8) or by the ligation of two or three branches of the left renal artery and the subsequent contralateral nephrectomy (five-sixths nephrectomy [5/6Nx] group; n ϭ 10).…”

Section: Animal Preparationmentioning

confidence: 99%

Role of Nitric Oxide–Producing and–Degrading Pathways in Coronary Endothelial Dysfunction in Chronic Kidney Disease

Tatematsu¹,

Wakino²,

Kanda³

et al. 2007

Journal of the American Society of Nephrology

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“…Data on systemic (MAP and HR) and renal (see below) haemodynamics were analysed with a Macintosh Laboratory system (Mac Lab ; Analog-Digital Instruments, Castle Hill, NSW, Australia) [23][24][25].…”

Section: Measurement Of Systemic and Renal Haemodynamicsmentioning

confidence: 99%

Divergent natriuretic action of calcium channel antagonists in mongrel dogs: renal haemodynamics as a determinant of natriuresis

Honda¹,

Hayashi²,

MATSUDA³

et al. 2001

Clinical Science

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This study examined the effects of different types of calcium channel antagonists on renal haemodynamics and natriuresis. The intravenous infusion of nifedipine (L-type blocker), efonidipine (L/T-type blocker) or mibefradil (predominant T-type blocker) into anaesthetized dogs elicited similar, albeit modest, reductions in blood pressure. Nifedipine (1 microgram.min(-1).kg(-1)) increased renal plasma flow (RPF) (23+/-6%; P<0.05) and glomerular filtration rate (GFR) (25+/-5%; P<0.05) (all values are means+/-S.E.M., n=7). Efonidipine (0.33 microgram .min(-1).kg(-1)) also elevated RPF (18+/-6%; P<0.05), and tended to increase GFR (17+/-8%; P=0.08). These antagonists exerted contrasting actions on the filtration fraction (FF), with an increase being elicited by nifedipine, whereas efonidipine had no effect. Furthermore, mibefradil (0.01-1 microgram.min(-1).kg(-1)) slightly elevated RPF (between 5+/-3% and 8+/-3%), but failed to alter GFR, resulting in a decrease in FF. Nifedipine slightly increased urinary sodium excretion (U(Na)V) (29+/-16% increase at 1 microgram .min(-1).kg(-1)) and fractional sodium excretion (FE(Na)) (18+/-14%), whereas efonidipine (0.33 microgram .min(-1).kg(-1)) elicited marked elevations in U(Na)V (110+/-38%; P<0.05) and FE(Na) (102+/-44%; P<0.05). Mibefradil (1 microgram .min(-1).kg(-1)) exerted a moderate natriuretic action [U(Na)V, +60+/-32% (P=0.1); FE(Na), +67+/-20% (P<0.05)]. Furthermore, although a positive correlation was observed between U(Na)V and urinary nitrate/nitrite excretion, no differences were noted between the various calcium channel antagonists. Collectively, this study demonstrates that the glomerular haemodynamic and natriuretic actions of these calcium channel antagonists, which possess diverse blocking activities on L/T-type channels, vary. Based on the divergent actions on FF (i.e. increase, no change and decrease by nifedipine, efonidipine and mibefradil respectively), the natriuretic action of calcium channel antagonists is possibly attributed to the inhibition of tubular sodium reabsorption associated with increased post-glomerular blood flow, rather than increased GFR.

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Blockade of the renin???angiotensin system in heart failure in conscious dogs

Cited by 19 publications

References 0 publications

No Expression of Angiotensin II Receptors and Angiotensin‐Converting Enzyme in Myxomatous Canine Mitral Valve Leaflets. An Autoradiographic Study

No Expression of Angiotensin II Receptors and Angiotensin‐Converting Enzyme in Myxomatous Canine Mitral Valve Leaflets. An Autoradiographic Study

Role of Nitric Oxide–Producing and–Degrading Pathways in Coronary Endothelial Dysfunction in Chronic Kidney Disease

Divergent natriuretic action of calcium channel antagonists in mongrel dogs: renal haemodynamics as a determinant of natriuresis

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