Investigation of different blood pressure regulating systems in kininogen-deficient BNK rats
type: CreativeWork
description: The kininogen-deficient BNK rats were shown to progressively develop salt-sensitive hypertension by accumulation of Na+. It was believed that the kininogen-deficiency is responsible for the defective NaCl excretion leading to a cardiovascular damage. In addition to the kallikrein-kinin system (KKS), endothelin (ET) and aldosterone have important implications in the regulation of salt homeostasis. To precisely characterize the relations between the KKS, ET and aldosterone male BN and BNK rats were given standard or high salt diet in presence or absence of spironolactone for 10 days. Besides for experiments with metabolic cages the rats were characterized by tail-cuff measurements of blood pressure. Kininogens, bradykinin (BK), kallidin-like peptide (KLP), ET-1, deoxycorticosterone (DOC), corticosterone and aldosterone were measured by specific RIAs in plasma and 24h urine. Corticoids were additionally determined in brain tissue. Activity of plasma and urinary kallikrein was measured with chromogenic substrates. Expression analysis of adrenal steroidogenic enzymes 11ß-hydroxylase and aldosterone synthase was performed by real-time RT-PCR in LightCycler. Functional cardiac parameters were assessed in isolated hearts perfused according to Langendorff technique. Acute effects of 30min global ischaemia with or without previous ischaemic preconditioning (IPC) were investigated. Myocardial damage was judged by the creatine kinase activity in the coronary effluent measured with a specific kit. BNK rats are characterized by plasma kininogen deficiency that is reflected in lower levels of plasma kallikrein activity and consequently in lower plasma BK and KLP levels. The renal KKS of BNK rats was almost identical to that of wild type BN rats. Plasma and urinary KLP was found to be the major kinin responsible for most physiological effects mediated by the B2 receptor in both rat strains. We found that the deleterious effects of salt diet in BNK rats are in fact attributable to e…
abstract: The kininogen-deficient BNK rats were shown to progressively develop salt-sensitive hypertension by accumulation of Na+. It was believed that the kininogen-deficiency is responsible for the defective NaCl excretion leading to a cardiovascular damage. In addition to the kallikrein-kinin system (KKS), endothelin (ET) and aldosterone have important implications in the regulation of salt homeostasis. To precisely characterize the relations between the KKS, ET and aldosterone male BN and BNK rats were given standard or high salt diet in presence or absence of spironolactone for 10 days. Besides for experiments with metabolic cages the rats were characterized by tail-cuff measurements of blood pressure. Kininogens, bradykinin (BK), kallidin-like peptide (KLP), ET-1, deoxycorticosterone (DOC), corticosterone and aldosterone were measured by specific RIAs in plasma and 24h urine. Corticoids were additionally determined in brain tissue. Activity of plasma and urinary kallikrein was measured with chromogenic substrates. Expression analysis of adrenal steroidogenic enzymes 11ß-hydroxylase and aldosterone synthase was performed by real-time RT-PCR in LightCycler. Functional cardiac parameters were assessed in isolated hearts perfused according to Langendorff technique. Acute effects of 30min global ischaemia with or without previous ischaemic preconditioning (IPC) were investigated. Myocardial damage was judged by the creatine kinase activity in the coronary effluent measured with a specific kit. BNK rats are characterized by plasma kininogen deficiency that is reflected in lower levels of plasma kallikrein activity and consequently in lower plasma BK and KLP levels. The renal KKS of BNK rats was almost identical to that of wild type BN rats. Plasma and urinary KLP was found to be the major kinin responsible for most physiological effects mediated by the B2 receptor in both rat strains. We found that the deleterious effects of salt diet in BNK rats are in fact attributable to e…
author: Lukasova, Martina
date published: 2006-02-22
date modified: 2026-07-24T02:30:19Z
provider: Universität Heidelberg
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: Universität Heidelberg