Bradykinin and kallidin levels in the trapezius muscle in patients with work-related trapezius myalgia, in patients with whiplash associated pain, and in healthy controls - A microdialysis study of women.

The origins of chronic muscle pain development and maintenance are debated regarding the relative contributions of peripheral nociception and central pain processing. Bradykinin (BKN) and kallidin (KAL) have been suggested to be algesic kinins involved in muscle pain. This in vivo study investigates whether there were significant differences in interstitial muscle concentrations of BKN and KAL between chronic work-related trapezius myalgia (TM), chronic whiplash associated disorders (WAD), and healthy controls (CON).

Ca2+ signalling of kinins in cells expressing rat, mouse and human B1/B2-receptor.

With respect to functional aspects, the kallikrein-kinin-system can be divided into a plasma kallikrein-kinin-system and a tissue kallikrein-kinin-system. At least four functional kinin peptides act via two different G-protein-coupled receptors, an inducible B1-receptor and a constitutively expressed B2-receptor. B1R and B2R couple to G(q/11) and lead via phospholipase C to Ca2+ mobilization.

Kallidin-like peptide mediates the cardioprotective effect of the ACE inhibitor captopril against ischaemic reperfusion injury of rat heart.

1. The potential cardioprotective effect of ACE inhibitors has been attributed to the inhibition of bradykinin degradation. Recent data in rats documented a kallidin-like peptide, which mimics the cardioprotective effect of ischaemic preconditioning.

A kallidin-like peptide is a protective cardiac kinin, released by ischaemic preconditioning of rat heart.

Bradykinin is thought to play a major role among the endogenous cardioprotective candidates of ischaemic preconditioning (IPC). Little attention has been paid to the fact that in the tissue kallidin (KAL), rather than bradykinin might be the physiological mediator of the kallikrein-kinin system. In order to evaluate the importance of one or the other peptide the release and effect of both kinins has been investigated in isolated rat hearts following IPC.

Rat tissue kallikrein releases a kallidin-like peptide from rat low-molecular-weight kininogen.

The kallikrein-kinin system is subdivided into the plasma and tissue-kallikrein-kinin system, with bradykinin (BK) and kallidin (KAL) (Lys(0)-bradykinin) as functional peptides. This occurs in both humans and other mammals. Both peptides are released by plasma and tissue-kallikrein.

Kinins are involved in the antiproteinuric effect of angiotensin-converting enzyme inhibition in experimental diabetic nephropathy.

The present study examined non-insulin-treated streptozotocin (STZ)-induced diabetic rats to determine the role of kinins in diabetic nephropathy. Their involvement in the renoprotective effect of the angiotensin-converting enzyme inhibitor (ACEI) ramipril was investigated using the bradykinin (BK) B(2)-receptor antagonist, icatibant (HOE 140), or a combination of the two drugs.Although, none of the treatments prevented the decline of the glomerular filtration rate (GFR) in diabetic rats, ramipril (3 mg/kg/day), but not icatibant (HOE 140; 500 microg/kg/day), prevented proteinuria in these animals.

Regulatory effects of salt diet on renal renin-angiotensin-aldosterone, and kallikrein-kinin systems.

The interaction of the renin-angiotensin-aldosterone system (RAAS) and the kallikrein-kinin system (KKS) was investigated in rats fed on a low, normal, and high-salt diet for 2 weeks. At the beginning of the second week, either a B2-receptor antagonist (icatibant), or an AT1-receptor antagonist (losartan), or an aldosterone receptor antagonist (spironolactone) was applied via osmotic pump delivering a constant amount of drug for 7 days. The urinary bradykinin (BK) levels corresponded with increasing NaCl diet and the activity of urinary kallikrein.

Increased activity of the renal kallikrein-kinin system in autosomal dominant polycystic kidney disease in rats, but not in humans.

The kallikrein-kinin system (KKS) was investigated in autosomal dominant polycystic kidney disease (ADPKD)-affected rats (PKD) and compared to unaffected controls (SD) and 5/6 nephrectomized rats (5/6 Nx). In addition, patients with ADPKD compared to patients with nonpolycystic kidney disease and healthy controls have been investigated. Plasma and urine samples for determination of creatinine, protein, kallikrein (KAL) and bradykinin (BK) were taken in male 3- and 9-month-old PKD, SD and 9-month-old 5/6 Nx.

Contraction-related factors affect the concentration of a kallidin-like peptide in rat muscle tissue.

In order to study the effects of the manipulation of various factors related to muscular activity on the concentration of kinins in muscular tissue, a microdialysis probe was implanted in the adductor muscle of the hindlimb in anaesthetized rats. After collection of baseline samples, the perfusion fluid was changed to a Ringer solution containing sodium lactate (10 or 20 mM), adenosine (50 or 100 microM) or a lower pH (7.0 or 6.

Activation of the tissue kallikrein-kinin system in stroke.

Edema formation is a major problem in large ischemic infarcts, and the underlying breakdown of the blood-brain barrier is only incompletely understood. Here, we report that the tissue kallikrein-kinin system, which influences the permeability of the blood-brain barrier, is activated in stroke. In 22 patients with large infarcts in the territory of the middle cerebral artery, we found elevated plasma concentrations of the tissue kinin kallidin.

Activity and functional significance of the renal kallikrein-kinin-system in polycystic kidney disease of the rat.

Unlabelled: Activity and functional significance of the renal kallikrein-kinin-system in polycystic kidney disease of the rat.

Background: The kallikrein-kinin-system is a complex multienzymatic system that has been implicated in the control of systemic blood pressure, glomerular filtration rate, and proteinuria. The present study investigated its functional role in rat polycystic kidney disease (PKD), which is characterized by progressive renal failure and proteinuria in the absence of systemic hypertension and stimulated renin-angiotensin-system.