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Essential hypertension. Part I: definition and etiology.
TLDR
This review of current concepts regarding the definition, etiology, and treatment of essential hypertension is intended to aid the clinician in identifying those individuals at high risk who need to undergo evaluation and treatment, as well as in selecting optimal treatment strategies for hypertensive patients with comorbid conditions and/or target organ damage.
Effects of angiotensin-converting enzyme inhibitors and angiotensin II type 1 receptor antagonists in rats with heart failure. Role of kinins and angiotensin II type 2 receptors.
TLDR
In HF both ACEi and AT1-ant have a cardioprotective effect, which could be due to either a direct action on the heart or secondary to altered hemodynamics, or both.
Flow modulates myogenic responses in isolated microperfused rabbit afferent arterioles via endothelium-derived nitric oxide.
TLDR
It is suggested that intraluminal flow attenuates pressure-induced constriction in Af-Arts via endothelium-derived NO, and flow-stimulated NO release may be important in the fine control of glomerular hemodynamics.
Characterization of a mouse cortical collecting duct cell line.
TLDR
A cortical collecting duct cell line developed from a mouse transgenic for the early region of simian virus 40, Tg(SV40E)Bri/7, retained many characteristics of the CCD, including a typical epithelial appearance and CCD-specific antigens, and generated significant transepithelial solute gradients.
Echocardiographic assessment of cardiac function in conscious and anesthetized mice.
TLDR
This is the first study to demonstrate the feasibility of using echocardiography to assess cardiovascular function in the nonanesthetized mouse and clearly shows the adverse impact of anesthesia on basal cardiac function and the difficulty in interpreting data obtained from anesthetization mice.
N-acetyl-seryl-aspartyl-lysyl-proline prevents cardiac remodeling and dysfunction induced by galectin-3, a mammalian adhesion/growth-regulatory lectin.
TLDR
It is concluded that Ac-SDKP prevents Gal-3-induced cardiac inflammation, fibrosis, hypertrophy, and dysfunction, possibly via inhibition of the TGF-beta/Smad3 signaling pathway.
Upregulation of p67(phox) and gp91(phox) in aortas from angiotensin II-infused mice.
TLDR
The results suggest that ANG II-induced increases in O(2)(-) are due to increased adventitial NAD(P)H oxidase activity, brought about by the heightened expression and interaction of its components.
Angiotensin-Converting Enzyme Inhibitors: A New Mechanism of Action
TLDR
In Ang II–induced hypertension, the cardiac antifibrotic effect of ACE inhibitors is a result of the inhibition of Ac-SDKP hydrolysis, resulting in a decrease in cardiac cell proliferation, inflammatory cell infiltration, TGF-&bgr; expression, Smad2 activation, and collagen deposition.
Increased Systolic Performance With Diastolic Dysfunction in Adult Spontaneously Hypertensive Rats
TLDR
Heart performance in 10 to 11 months of age, before HF develops, SHR have increased systolic performance accompanied by delayed relaxation and increased diastolic stiffness, which is suggested to be a precursor to heart failure.
Superoxide enhances tubuloglomerular feedback by constricting the afferent arteriole.
TLDR
It is O(2) (-) rather than H (2)O(2)'s potentiation by acting directly on the afferent arteriole of the Af-Art and indirectly by scavenging NO in the MD that enhances TGF response.
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