By Raouf A. Khalil MD, PhD (auth.), Ichiro Wakabayashi, Klaus Groschner (eds.)
This booklet presents an advent to the foundations of either cardiovascular epidemiology and molecular pathophysiology; as a distinct point, it additionally outlines and discusses the molecular techniques underlying epidemiological observations. This moment quantity is targeted on all elements bearing on “secondary danger elements” when it comes to ailments linked to more desirable chance for cardiovascular occasions. The e-book promotes using interdisciplinary techniques within the box of preventive medication according to contemporary advances in molecular and mobile pathophysiology. The e-book deals a beneficial source for researchers in simple biomedical fields and scientific scientists alike, in addition to guidance for novel avenues of study in either easy pathophysiology and cardiovascular treatment and prevention.
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Additional info for Interdisciplinary Concepts in Cardiovascular Health: Volume II: Secondary Risk Factors
Kidney Int 55:252–260 Hilgers RH, Webb RC (2005) Molecular aspects of arterial smooth muscle contraction: focus on Rho. Exp Biol Med (Maywood) 230:829–835 Himpens B, Matthijs G, Somlyo AV, Butler TM, Somlyo AP (1988) Cytoplasmic free calcium, myosin light chain phosphorylation, and force in phasic and tonic smooth muscle. J Gen Physiol 92:713–729 Horowitz A, Menice CB, Laporte R, Morgan KG (1996) Mechanisms of smooth muscle contraction. Physiol Rev 76:967–1003 Huang PL, Huang Z, Mashimo H, Bloch KD, Moskowitz MA, Bevan JA, Fishman MC (1995) Hypertension in mice lacking the gene for endothelial nitric oxide synthase.
Hypertensive patients with baseline left ventricular hypertrophy exhibited lower free MMP-1 and CITP and higher free TIMP-1 than hypertensive patients without baseline left ventricular hypertrophy. Treated patients showed an increase in free MMP-1 and a decrease in free TIMP-1. In addition, serum levels of CITP were greater in treated hypertensive patients than normotensive subjects. It was concluded that systemic extracellular degradation of collagen type I is depressed in HTN and can be normalized by treatment with lisinopril.
Measurements of VSM [Ca2+]i have shown that both basal and maintained agonist-induced [Ca2+]i are greater in SHR than WKY (Sugiyama et al. 1986; Murphy and Khalil 2000). Agoniststimulated 45Ca2+ efflux and initial [Ca2+]i transient in Ca2+-free solution are not different in SHR and WKY, suggesting that the increased VSM [Ca2+]i in HTN is not due to increased Ca2+ release from the sarcoplasmic reticulum (Cauvin and van Breemen 1985; Murphy and Khalil 2000). In contrast, the agonist-induced 45Ca2+ influx and maintained [Ca2+]i are greater in SHR than WKY, suggesting an increase in the permeability of plasmalemmal Ca2+ channels in SHR (Crews et al.