Studies on kallikrein-kinin system in normotensive and hypertensive rats with and without diabetes
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Date
1995
Authors
Kesavarao, Uma
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Abstract
This research investigated the role of kallikrein-kinin system in
normotensive and hypertensive rats with and without diabetes.
<·.Furthermore, the influence of kallikrein-kinin system on the effects of
angiotensin converting enzyme inhibitor, captopril on diapetes and
hypertension were evaluated.
Diabetes was induced in Wistar kyoto and spontaneously hypertensive
rats by a single intraperitoneal injection of streptozocin 50mg/kg,
followed up for five weeks and compared with respective nondiabetic
controls. Blood pressure was significantly elevated (**p < 0.001) in the
diabetic groups of both Wistar lcy_oto and spontaneously hypertensive rats
compared wit their respective nondiabetic controls .. Active urinary
kallikrein was. significantly depressed in the diabetic Wistar kyoto and
diabetic spontaneously hypertensive rats (**p < 0.001). For the first time,
to our knowledge, this research has revealed a lo\Vering of cardiac
tissue kallikrein, both total and active, in diabetic Wistar kyoto,
spontaneously hypertensive rats and diabetic spontaneously hypertensive
rats when compared to control Wistar kyoto rats. However, the plasma
prekallikrein and high molecular weight kininogen were raised
significantly in the diabetic groups when compared to respective
nondiabetic controls of both Wistar kyoto and spontaneously hypertensive
rats. Morphological estimation of heart revealed an increase in left
ventricular wall thickness including the interventHcular septum thus
indicating hypertrophic changes in the diabetic Wistar kyoto,
spontaneously hypertensive rats and diabetic spontaneously hypertensive
rats when compared to control Wistar kyoto rats.
Influence of kallikrein-kinin system on angiotensin converting
enzyme inhibitor, captopril, administered in two different doses,
40mg/kg and 80mg/kg body weight for five weeks in diabetic rats both
Wistar kyoto and spontaneously hypertensive groups was compared with
nondiabetic control Wistar kyoto and control spontaneously hypertensive',.
rats treated with captopril. A significant decrease (**p < 0.001) in blood
pressure and blood sugar was observed in the· diabetic Wistar kyoto and
diabetic spontaneously hypertensive rats treated with captopril. The
urinary. kallikrein, both active and total were increased in the diabetic
Wistar kyoto and· spontaneously hypertensive rats treated with captopril.
Total and active cardiac tissue kallikrein were significantly
decreased(p<0.001)in ··the diabetic groups .when compared to their
respec~ive nondiabetic controls. Plasma prekallikrein and high molecular
weight kininogen were depressed in both diabetic Wistar kyoto and
diabetic spontaneously hypertensive rats when compared to" their
respective control.Measurement of left ventricular wall thickness showed
no hypertrophic changes in diabetic Wistar kyoto, control spontaneously
hypertensive rats and diabetic spontaneously hypertensive ~ats treated
with captopril. It is of interest to note thae captopril at a dose of 40mglkg
which prevented left ventricular hypertrophy failed to produce
normalization of blood pressure in the diabetic spontaneously
hypertensive rats.
Our study confirms the abnormal regulation of kallikrein-kinin system
in diabetes and hypertension and a definite influence of this system on the
antihypertensive, hypoglycemic and cardioprotective effects of
angiotensin converting enzyme inhibitor, captopril. The possible
mechanisms of action of kinin components in these pathological
conditions and their treatment have been discussed.
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Keywords
Hypertensive rats , Kallikrein-kinin system