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Biomedical subjects

H Schunkert

Publications and source records attributed to H Schunkert.

131 records · Page 8Linked to original sources
PubMed1988

Pharmacokinetics of ranitidine in patients undergoing haemofiltration.

The pharmacokinetics of ranitidine was investigated in 11 patients with acute or end stage renal failure during haemofiltration. Each patient received 50 mg ranitidine i.v. The mean distribution and elimination half lives were 0.13 and 2.57 h, respectively. The total body clearance (CL) and volume of distribution (Vz) were 298 ml.min-1 (5.19 ml.min-1.kg-1) and 1.08 l.kg-1, respectively. About 17.1% of the administered dose was removed by haemofiltration (in approximately 20 l filtrate). Five of the patients still had some urine output and they excreted 0.1 to 11.8% of the dose in urine in 24 h. The haemofiltration clearance was 66.9 ml.min-1 at a filtrate flow rate of 86 ml.min-1, corresponding to a mean sieving coefficient of 0.78 (n = 6). As plasma concentrations were still in an effective range after haemofiltration, dose supplementation is not recommended.

Acute Kidney Injury↗
PubMedDate not supplied

Polymorphism of the angiotensin-converting enzyme gene and cardiovascular disease.

The angiotensin-converting enzyme (ACE) is an integral part of two enzymatic cascades, one leading to the generation of angiotensin II and the other to the degradation of bradykinin. The great variety of cardiovascular effects mediated by these vasoactive peptides and the efficacy of ACE inhibitors in the treatment of hypertension and heart failure emphasize the prominent role of ACE in the cardiovascular system. Early in this decade convincing experimental evidence demonstrated the induction of this enzyme in several pathophysiological conditions, including myocardial infarction and left ventricular hypertrophy. In parallel, a deletion/insertion (D/I) polymorphism of the human ACE gene was characterized that is related to 14-50% of the interindividual variance in serum ACE activity. More recently this polymorphism has been implicated in the pathogenesis of a variety of cardiovascular disorders, including myocardial infarction, left ventricular hypertrophy, hypertension, diabetic and IgA nephropathy, carotid artery thickening, and lacunar cerebral stroke. However, the associations between the ACE D/I polymorphism and most of these conditions were found to be inconsistent when additional populations were investigated. This contribution reviews the current evidence on the relationship between the ACE D/I polymorphism and cardiovascular disease.

Animals↗
PubMedDate not supplied

Evolving concepts of the intrarenal renin-angiotensin system in health and disease: contributions of molecular biology.

Previous physiological and biochemical studies suggest the existence of an endogenous renin-angiotensin system (RAS) in the kidney. However, these data cannot exclude the contribution of the circulating RAS. Proof of the local synthesis of RAS components in the kidney has been obtained recently through the use of molecular biological techniques. Using Northern blot analysis, we have demonstrated the intrarenal expression of renin, angiotensinogen, and angiotensin-converting enzyme messenger RNAs. Employing in situ hybridization histochemistry, we have localized the intrarenal tissue sites of renin and angiotensinogen messenger RNA synthesis. Renin gene expression was found in cells of the juxtaglomerular apparatus. Angiotensinogen mRNA was primarily produced in the proximal convoluted tubule with lesser amounts in glomerular tufts and vasculature. These findings led us to hypothesize that the proximal tubule is a major site of renal Ang II synthesis and that locally synthesized Ang II might directly modulate tubular function. Both genes are subject to feedback regulation. Our studies showed that Ang II exerted a stimulatory effect on angiotensinogen but a negative feedback effect on renin gene expression. Dietary NaCl restriction stimulated the expression of both genes, although the onset of renin gene activation required more prolonged sodium chloride restriction. Furthermore, our data indicated that the sodium cation, irrespective of the anion, was primarily important in regulating renal angiotensinogen mRNA levels. Our studies also showed altered intrarenal renin or angiotensinogen expressions in pathophysiological states, e.g. in experimental heart failure and the spontaneously hypertensive rat. Taken together, these data support the existence of a intrarenal RAS and suggest its potential roles in the regulation of renal function in health and disease.

Animals↗