Oxytocin, Norepinephrine And Olfactory Bulb Mediated Recognition
acetylcholine; acid; male-rats; maternal experience; memory; release; responses; sheep; social recognition; vasopressin
Dluzen D E; Shang Y; Landgraf R
2001
2001
Book/Monograph
n/a
Kallistatin is a potent new vasodilator
Research & Experimental Medicine; expression; purification; endothelium; vasopressin; inhibitor; bradykinin; blood pressure; human tissue kallikrein; hypertensive rats; kallikrein; kallikrein-binding protein; kallistatin; kinins; renal pressure; vasorelaxation
Kallistatin is a serine proteinase inhibitor which binds to tissue kallikrein and inhibits its activity, The aim of this study is to evaluate if kallistatin has a direct effect on the vasculature and on blood pressure homeostasis. We found that an intravenous bolus injection of human kallistatin caused a rapid, potent, and transient reduction of mean arterial blood pressure in anesthetized rats. Infusion of purified kallistatin (0.07-1.42 nmoVkg) into cannulated rat jugular vein produced a 20-85 mmHg reduction of blood pressure in a dose-dependent manner. Hoe 140, a bradykinin B-2-receptor antagonist, had no effect on the hypotensive effect of kallistatin yet it abolished the blood pressure-lowering effect of kinin and kallikrein. Relaxation of isolated aortic rings by kallistatin was observed in the presence (ED50 of 3.4 x 10(-9) M) and in the absence of endothelium (ED50 of 10(-9) M). Rat kallikrein-binding protein, but not kinin or kallikrein, induced vascular relaxation of aortic rings. Neither Hoe 140 nor N-omega-nitro-L-arginine methyl ester, a nitric oxide synthase inhibitor, affected vasorelaxation induced by kallistatin. Kallistatin also caused dose-dependent vasodilation of the renal vasculature in the isolated, perfused rat kidney, Specific kallistatin-binding sites were identified in rat aorta by Scatchard plot analysis with a K-d of 0.25+/-0.07 nM and maximal binding capacity of 47.9+/-10.4 fmol/mg protein (mean+/-SEM, n = 3). These results indicate that kallistatin is a potent vasodilator which may function directly through a vascular smooth muscle mechanism independent of an endothelial bradykinin receptor. This study introduces the potential significance of kallistatin in directly regulating blood pressure to reduce hypertension.
Chao J L; Stallone J N; Liang Y M; Chen L M; Wang D Z; Chao L
Journal of Clinical Investigation
1997
1997-07
Journal Article or Conference Abstract Publication
<a href="http://doi.org/10.1172/jci119502" target="_blank" rel="noreferrer noopener">10.1172/jci119502</a>
An Update on the Pathophysiology and Treatment of Cardiorenal Syndrome.
cardiac resynchronization therapy; Cardiorenal syndrome; cardiovascular events; Chronic kidney disease; Chronic kidney disease; decompensated heart-failure; Heart failure; impact; left-ventricular dysfunction; preserved ejection fraction; risk; vasopressin; worsening renal-function
Cardiorenal syndrome (CRS) encompasses various disorders of the heart and kidneys; dysfunction of one organ leads to acute or chronic dysfunction of the other. It incorporates the intersection of heart-kidney interactions across several mediums, hemodynamically, through the alterations in neurohormonal markers, and increased venous and renal pressure, all of which are hallmarks of its clinical phenotypes. This article explores the epidemiology, pathology, classification and treatment of each type of CRS.
Raina Rupesh; Nair Nikhil; Chakraborty Ronith; Nemer Lena; Dasgupta Rahul; Varian Kenneth
Cardiology research
2020
2020-04
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
journalArticle
<a href="http://doi.org/10.14740/cr955" target="_blank" rel="noreferrer noopener">10.14740/cr955</a>