Possible role of the endogenous kallikrein-kinin system in suppression of doca-salt-induced hypertension in rats

Murakami, Masataka; Hanazuka, Mitsuo; Mizogami, Susumu; Katori, Makoto; Oh-ishi, S; Nakano, Takesi

doi:10.1016/0014-2999(90)94422-t

Cited by 2 publications

(5 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Both systems operate independently in vitro and in vivo (Uchida & Katori, 1985;Katori et al, 1988;1989;Majima et al, 1990). The plasma kallikrein-HMW kininogen system is activated via the activation of factor XII (Hageman factor) and activated plasma prekallikrein (plasma kallikrein) can release bradykinin from its substrate, HMW-kininogen.…”

Section: Discussionmentioning

confidence: 99%

Increased secretion of glandular‐kallikrein in the bronchial washings induced by intravenous injection of leukotriene C₄ in guinea‐pigs

Jin

Katori

Murakami

et al. 1992

British J Pharmacology

View full text Add to dashboard Cite

1 Intravenous administration of leukotriene C4 (LTC4) and LTD4 (1-10nmolkg-1) caused a dosedependent increase in secretion of glandular-kallikrein in the bronchial washings of guinea-pigs, as measured by cleavage of a synthetic substrate and the formation of kinin. LTC4 was more potent than LTD4 and pilocarpine was much less potent than peptide leukotrienes on a molecular basis. 2 The increases in levels of glandular-kallikrein in the bronchial washings that were induced by LTC4 (3 nmol kg-1, i.v.) were almost completely inhibited by pretreatment with an antagonist of leukotrienes (ONO-1078), with an antagonist of thromboxane (S-1452), with an inhibitor of thromboxane synthetase (OKY-046), with indomethacin, with atropine or with scopolamine. These results indicate that the LTC4-induced increase in levels of glandular-kallikrein may have been mediated by the formation of thromboxane and the release of acetylcholine. 3 The increases in levels of glandular-kallikrein in the bronchial washings induced by STA2 (20 pmol kg-1, i.v.), a stable analogue of thromboxane A2, were completely blocked by pretreatment with atropine, whereas increases induced by pilocarpine (41 pmol kg-1, i.v.) were not blocked by pretreatment with indomethacin, although such increases were inhibited by atropine. This result indicates that secretion of kallikrein stimulated by LTC4 may have been mediated by the successive formation of thromboxane A2 and release of acetylcholine. 4 Intravenous administration of bradykinin (3-30 nmol kg-1) caused a dose-dependent increase in levels of glandular-kallikrein in the bronchial washings. This increase was completely inhibited by pretreatment with atropine, with indomethacin or with an antagonist of thromboxane. 5 The increases in levels of glandular-kallikrein in the bronchial washings induced by LTC4 (3 nmol kg'-, i.v.) and pilocarpine (41 flmol kg-1, i.v.) were significantly inhibited by pretreatment with an antagonist of bradykinin. These results suggest that intravenous LTC4 may increase secretion of glandular-kallikrein via formation of thromboxane A2 and release of acetylcholine in that order, and kinin released by kallikrein may enhance the rate of secretion of glandular-kallikrein.

show abstract

Section: Discussionmentioning

confidence: 99%

Increased secretion of glandular‐kallikrein in the bronchial washings induced by intravenous injection of leukotriene C₄ in guinea‐pigs

Jin

Katori

Murakami

et al. 1992

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…Deficient BN-Ka rats that cannot generate kinin in urine excreted less sodium and water in urine under a mild dietary NaCI loading or subcutaneous infusion of a nonpressor dose of angiotensin II. Hence, sodium was accumulated in the cerebrospinal fluid and erythrocytes, causing an elevation in blood pressure (1)(2)(3)(4)(5)(6). During the treatment of rats with sodium loading or angiotensin II infusion, supplementation of LMW kininogen to deficient BN-Ka rats reduced the systemic blood pressure with increased excretion of urinary kinin, urinary sodium and urine volume, whereas subcutaneous infusion of a bradykinin B2 receptor antagonist, Hoe 140, increased the blood pressure with reduced excretion of urinary sodium and urine volume, indicating direct linkage between kinin release, sodium excretion and high blood pressure.…”

Section: Discussionmentioning

confidence: 99%

“…Deficient BN-Ka rats (Rattus norvegicus, BN/fMai) were initially obtained from the Katholiek Universiteit of Leuven, Belgium, and they were fed in our animal facilities (1)(2)(3)(4)(5). Normal rats from the same strain were already being kept in Kitasato University (BN-Ki rats).…”

Section: Animalsmentioning

confidence: 99%

“…In kininogen-deficient Brown Norway Katholiek (deficient BN-Ka) rats, which do not generate kinin in their urine, hypertension was induced easily in comparison with normal rats from the same strain, that is BN-Kitasato (normal BN-Ki) rats (1)(2)(3)(4)(5)(6).…”

mentioning

confidence: 99%

“…Subcutaneous infusion of the deficient BN-Ka rats with a non-pressor dose (20 pg/day/rat) of angiotensin II caused an increase in the systemic blood pressure and accumulation of sodium in the cerebrospinal fluid and the erythrocytes through aldosterone release (5). In deoxycorticosterone acetate (DOCA)-salt hypertension models, the systemic blood pressure was increased gradually up to 180 mmHg 10 weeks after the start of treatment in normal BN-Ki rats, whereas deficient BN-Ka rats, with their lower sodium and water excretion, exhibited systemic blood pressure rises to the maximum values within two weeks after DOCA-salt treatment was initiated (1)(2)(3).…”

mentioning

confidence: 99%

See 2 more Smart Citations

Increase in Vascular Sensitivity to Angiotensin II and Norepinephrine after Four-Day Infusion of 0.3 M Sodium Chloride in Conscious Kininogen-Deficient Brown Norway Katholiek Rats

Murakami

Adachi

Kuribayashi

et al. 1995

Japanese Journal of Pharmacology

View full text Add to dashboard Cite

Kininogen-deficient Brown Norway Katholiek (deficient BN-Ka) rats excreted a small amount of kinin in their urine, compared with normal BN Kitasato (normal BN-Ki) rats from the same strain. Intraarterial (i.a.) infusion (6 ml/kg/hr) of conscious deficient BN-Ka rats with 0.15 M NaCI did not increase mean arterial blood pressure (MBP) [from 103±2 (pre) to 93±6 mmHg (day 4)] and did not cause sodium accumulation in the serum, cerebrospinal fluid or erythrocytes, but 0.3 M NaCI infusion significantly increased MBP from 104 ± 3 (pre) to 130 ± 5 mmHg (day 4) with increased sodium levels in the serum, cerebrospinal fluid and erythrocytes. Infusion of 0.3 M NaCI in normal BN-Ki rats neither increased MBP nor accumulated sodium. The dose-response curve of the increase in MBP for angiotensin II injection (i.a., bolus, 1-1000 pmol/kg) in 0.3 M NaCI-infused deficient BN-Ka rats shifted to the left by a factor of 10 compared with that in 0.15 M NaCI-infused deficient BN-Ka rats, and that for norepinephrine injection shifted to the left by a factor of 30. Normal BN-Ki rats did not show any enhancement in MBP elevation with 0.3 M NaCI. These results suggest that the sodium accumulation attributable to a lack of kinin generation may be related to increased vascular reactivity to angiotensin II and norepinephrine.

show abstract

Possible role of the endogenous kallikrein-kinin system in suppression of doca-salt-induced hypertension in rats

Cited by 2 publications

References 0 publications

Increased secretion of glandular‐kallikrein in the bronchial washings induced by intravenous injection of leukotriene C₄ in guinea‐pigs

Increased secretion of glandular‐kallikrein in the bronchial washings induced by intravenous injection of leukotriene C₄ in guinea‐pigs

Increase in Vascular Sensitivity to Angiotensin II and Norepinephrine after Four-Day Infusion of 0.3 M Sodium Chloride in Conscious Kininogen-Deficient Brown Norway Katholiek Rats

Contact Info

Product

Resources

About

Possible role of the endogenous kallikrein-kinin system in suppression of doca-salt-induced hypertension in rats

Cited by 2 publications

References 0 publications

Increased secretion of glandular‐kallikrein in the bronchial washings induced by intravenous injection of leukotriene C4 in guinea‐pigs

Increased secretion of glandular‐kallikrein in the bronchial washings induced by intravenous injection of leukotriene C4 in guinea‐pigs

Increase in Vascular Sensitivity to Angiotensin II and Norepinephrine after Four-Day Infusion of 0.3 M Sodium Chloride in Conscious Kininogen-Deficient Brown Norway Katholiek Rats

Contact Info

Product

Resources

About

Increased secretion of glandular‐kallikrein in the bronchial washings induced by intravenous injection of leukotriene C₄ in guinea‐pigs

Increased secretion of glandular‐kallikrein in the bronchial washings induced by intravenous injection of leukotriene C₄ in guinea‐pigs