Plasma kinin concentration in deoxycorticosterone-salt hypertension.

Nakagawa, M.; Nasjletti, Alberto

doi:10.1161/01.hyp.11.5.411

Cited by 26 publications

(18 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The urine volumes for BN-Ka rats were slightly increased (2.5-fold) and dispersed (7,8,17,12, and 67 ml/24 hr during the treatment versus 6, 8, 8, 9, 10, 13, and 14 ml/24 hr without the treatment). The creatinine amounts were decreased in both strains during the treatment (Table 2), and the reduction was significant in normal BN-Ki rats (/?<0.05).…”

Section: Resultsmentioning

confidence: 91%

See 1 more Smart Citation

Suppression of rat deoxycorticosterone-salt hypertension by kallikrein-kinin system.

et al. 1991

View full text Add to dashboard Cite

Brown Norway kininogen-deficient rats had very low levels of plasma kininogens and lower levels of plasma prekallikrein, compared with those of normal rats of the same strain. Systolic blood pressure, determined by the tail-cuff method, of 5-week-old kininogen-deficient rats (106±0.4 mm Hg, n=l) and the rate of systolic blood pressure increase with age were not different from those in normal rats. Weekly injections of deoxycorticosterone acetate (5 mg/kg s.c) with 1% sodium chloride solution in drinking water after uninephrectomy at 7 weeks of age caused a gradual increase in the blood pressure of normal rats, reaching a plateau at 18 weeks of age, whereas that of deficient rats rose rapidly to 158 ±6 mm Hg 2 weeks after the start of treatment and continued to increase slightly, becoming significantly higher than normal rats at 8, 9,10,11, and 12 weeks of age (p<0.05 or 0.01). The levels of urinary prokallikrein and active kallikrein were slightly higher in deficient rats before deoxycorticosterone acetate-salt treatment but were not significantly increased after this treatment, whereas these levels in normal rats were increased 3.6-and 4.7-fold by this treatment Urinary free kinin, collected from the ureter in untreated deficient rats, was below the detection limit The plasma level of low molecular weight kininogen, the substrate of glandular kallikrein, was decreased in normal rats during the treatment Continuous subcutaneous injection of aprotinin by an osmotic pump to normal rats induced significant increase in blood pressure. These results indicate that glandular kallikrein may play a suppressive role in deoxycorticosterone acetate-salt hypertension. {Hypertension 1991;17:806-813) I t was pointed out early on that kallikrein may be related to hypertensive diseases. 1 Recently, urinary kallikrein levels were reported to be lower in patients with essential hypertension than in normotensive controls 2 " 5 but were normal in renal artery stenosis and raised in pheochromocytoma and primary aldosteronism.2 Spontaneously hypertensive rats and rats with deoxycorticosterone acetate (DOCA)-salt hypertension showed greater increases in urinary kallikrein excretion than normotensive Wistar control rats from the National Institutes of Health.3 However, the role of the endogenous kallikrein-kinin system in development of hypertension remains unclear. The kallikrein-kinin system is a system for generating vasodilating peptides, bradykinin, or kallidin, by means of proteolytic enzymes, plasma, or glandular kallikrein, from its own precursor protein, high molecular weight (HMW) or low molecular weight (LMW) kininogen. Brown Norway Katholiek (BNKa) rats have been reported to have a congenitally abnormal kallikrein-kinin system 6 -8 and have been extensively studied and compared with normal rats of the same strain (BN-Kitasato [BN-Ki]). 9- 19 In a previous study, it was reported that not only HMW but also LMW kininogens were lacking in plasma from mutant BN-Ka rats, and only T-kininogen was present. -12 Because of the lack of...

show abstract

Section: Resultsmentioning

confidence: 91%

“…was injected subcutaneously at the back of the neck once a week, according to an already reported method. 17 …”

Section: Deoxycorticosterone Acetate-salt Hypertensionmentioning

confidence: 99%

Suppression of rat deoxycorticosterone-salt hypertension by kallikrein-kinin system.

et al. 1991

View full text Add to dashboard Cite

show abstract

“…The experiments were conducted in rats made hypertensive by complete ligation of the aorta between the renal arteries, a model of hypertension that is angiotensin-dependent in the initial stage and angiotensin-independent in the late stage, 9 and in rats with deoxycorticosterone (DOC)-salt-induced hypertension, a model of angiotensin-independent hypertension. 10 We contrasted the hypertensive rats and their normotensive controls in terms of plasma renin activity, production of TXB2, and 6-keto-PGF la by vascular tissue ex vivo, renal excretion of TXB2 and 6-keto-PGF la , and effects on blood pressure of treatment with either a blocker of TXA2/PG endoperoxide receptors, an inhibitor of thromboxane synthase, or an inhibitor of cyclooxygenase.…”

mentioning

confidence: 99%

Role of prostanoids in renin-dependent and renin-independent hypertension.

et al. 1991

Self Cite

View full text Add to dashboard Cite

We investigated the role of prostanoid-mediated pressor mechanisms in setting the level of blood pressure in renin-dependent and renin-independent models of hypertension in unanesthetized rats. Intravenous administration of a blocker of thromboxane A^prostaglandin endoperoxide receptors, SQ29548 (2 mg/kg bolus injection plus 2 mg/kg/hr for 3 hours), reduced from 162±4 to 144±5 mm Hg (/?<0.05) the blood pressure of rats with aortic coarctation-induced hypertension at 7-14 days after coarctation when plasma renin activity is greatly increased. In contrast, treatment with SQ29548 was without effect on the blood pressure of either normotensive or hypertensive rats (i.e., aortic coarctation-induced hypertension at 90-113 days after coarctation, deoxycorticosterone-salt-induced hypertension) having normal or depressed values of plasma renin activity. The blood pressure-lowering effect of SQ29548 in the early phase of aortic coarctation-induced hypertension was positively correlated with the prevailing plasma renin activity and could not be demonstrated in hypertensive rats pretreated with indomethacin. We attribute the hypotensive effect of SQ29548 to interference with pressor mechanisms that depend on activation of thromboxane Aj/prostaglandin endoperoxide receptors and suggest that such prostanoid-mediated mechanisms are operational and contribute to an increase in blood pressure in angiotensin-dependent forms of hypertension. Also prostanoid-mediated vasodepressor mechanisms are operational in the early phase of aortic coarctation-induced hypertension since the blood pressure of rats pretreated with SQ29548 was increased by the subsequent administration of indomethacin. Accordingly, the blood pressure of rats with aortic coarctationinduced hypertension is influenced by the interplay of prostanoid-mediated pressor and vasodepressor mechanisms. (Hypertension 1991;17:517-525) I nhibitors of cyclooxygenase were reported to lower the blood pressure of human subjects and rats with renin-dependent hypertension. '-4 Inasmuch as the cyclooxygenase inhibitors also caused reduction of plasma renin activity, the accompanying hypotensive effect was attributed to diminished expression of prostanoid-mediated mechanisms of renin secretion. "4 However, the blood pressurelowering effect of inhibitors of cyclooxygenase in renin-dependent models of hypertension also may be the consequence of decreased synthesis of thromboxane (Tx)A 2 and prostaglandin (PG) endoperoxides, which are known to stimulate contraction of vascular smooth muscle via activation of common receptors. 5The demonstration that inhibitors of cyclooxygenase cause blood pressure to fall in forms of renindependent hypertension suggests contribution of prostanoid-mediated pressor mechanisms to the hypertension. 6 Recent studies have linked TxA 2 or the PG endoperoxides to the mechanisms of angiotensin-induced hypertension. For example, a blocker of TXA2/PG endoperoxide receptors was reported to lower the blood pressure of rats made hypertensive by chronic angiotensin II...

show abstract

“…Induction of hypertension DOCA-salt induced hypertension Hypertension was induced experimentally in female rats (150 -200 g) by unilateral nephrectomy (Nakagawa and Nasjletti, 1988). Rats were anaesthetized with diethyl ether and a lateral incision was made in the area overlapping the kidney.…”

Section: Drugs and Chemicalsmentioning

confidence: 99%

Effect of an herbal formulation on DOCA-salt and fructose induced models of hypertension in rats

Athare¹,

Mohan²,

Kasture³

2008

Oriental Pharmacy and Experimental Medicine

View full text Add to dashboard Cite

SUMMARYThe present study was carried out to investigate the antihypertensive effect of a folklore herbal formulation (HF) (300mg/kg/day; p.o.) in deoxycorticosterone acetate (DOCA)-salt induced and fructose induced hypertensive rats. In DOCA model, DOCA (15 mg/kg, s.c., twice a week) was administered to unilateral nephrectomized rats for 4 weeks. In fructose model, drinking water was replaced with 10% fructose solution for 6 weeks to induce hypertension. Systolic blood pressure (BP) was measured once every week during the treatment schedule. After completion of treatment schedule, BP and vascular reactivity to various agonists like Noradrenaline, Adrenaline, Phenylephrine and Serotonin (5-hydroxytrptamine; 5-HT) were recorded in rats of both models. A cumulative concentration response curve of 5-HT was carried out in isolated rat fundus strip of the DOCA-salt induced and fructose induced hypertensive rats. The results tend to suggest that HF possesses antihypertensive activity.

show abstract

Plasma kinin concentration in deoxycorticosterone-salt hypertension.

Cited by 26 publications

References 19 publications

Suppression of rat deoxycorticosterone-salt hypertension by kallikrein-kinin system.

Suppression of rat deoxycorticosterone-salt hypertension by kallikrein-kinin system.

Role of prostanoids in renin-dependent and renin-independent hypertension.

Effect of an herbal formulation on DOCA-salt and fructose induced models of hypertension in rats

Contact Info

Product

Resources

About