The Actions of Bradykinin and Eledoisin in the Canine Isolated Kidney: Relationships to Prostaglandins

McGiff, John C.; Itskovitz, Harold D.; Terragno, Norberto A.

doi:10.1042/cs0490125

Cited by 67 publications

(59 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Bradykinin stimulates prostaglandin synthesis in blood vessels and in the kidney, probably by activating enzymes which make substrate available for prostaglandin synthetase (8)(9)(10)(11). The response of plasma bradykinin to postural change, sodium depletion, and saline infusion parallels temporally the response of PRA and of angiotensin II (12).…”

Section: Introductionmentioning

confidence: 99%

The Kallikrein-Kinin System in Bartter's Syndrome and Its Response to Prostaglandin Synthetase Inhibition

Vinci¹,

Gill²,

Bowden³

et al. 1978

J. Clin. Invest.

120

View full text Add to dashboard Cite

A B S T R A C T The kallikrein-kinin system was characterized in seven patients with Bartter's syndrome on constant metabolic regimens before, during, and after treatment with prostaglandin synthetase inhibitors. Patients with Bartter's syndrome had high values for plasma bradykinin, plasma renin activity (PRA), urinary kallikrein, urinary immunoreactive prostaglandin E excretion, and urinary aldosterone; urinary kinins were subnormal and plasma prekallikrein was normal. Treatment with indomethacin or ibuprofen which decreased urinary immunoreactive prostaglandin E excretion by 67%, decreased mean PRA (patients recumbent) from 17.3+5.3 (S.E.M.) ng/ml per h to 3.3±1.1 ng/ml per h, mean plasma bradykinini (patients recumbent) from 15.4±4.4 ng/ml to 3.9±0.9 ng/ml, mean urinary kallikrein excretion from 24.8±3.2 tosyl-arginine-methyl ester units (TU)/ day to 12.4±2.0 TU/day, but increased mean urinary kinin excretion from 3.8±1.3 ,ug/day to 8.5±2.5 ,ug/day. Plasma prekallikrein remained unchanged at 1.4 TU/ml. Thus, with prostaglandin synthetase inhibition, values for uriniary kallikrein and kinin and plasma bradykinin returned to normal pari passu with changes in PRA, in aldosterone, and in prostaglandin E. The

show abstract

Section: Introductionmentioning

confidence: 99%

The Kallikrein-Kinin System in Bartter's Syndrome and Its Response to Prostaglandin Synthetase Inhibition

Vinci¹,

Gill²,

Bowden³

et al. 1978

J. Clin. Invest.

120

View full text Add to dashboard Cite

show abstract

“…When BK is injected into the renal artery, it causes diuresis and natriuresis by increasing renal blood flow (12). These actions of BK have been attributed to prostaglandin release in the renal circulation (13). In 1934, Elliot and Nuzum had already noticed that hypertensive patients without clinically apparent renal disease have significantly low levels of urinary kallikrein than normotensive subjects (14).…”

Section: Pathophysiological Roles Of Bradykinin System In Hypertensiomentioning

confidence: 99%

Activation of the Bradykinin System by Angiotensin-Converting Enzyme Inhibitors

Sharma

2010

Eur J Inflamm

View full text Add to dashboard Cite

The Bradykinin (BK) system has a very significant role in the regulation of blood pressure (BP). Hence, reduced activity of BK receptors mediated via decreased circulating endogenous kinin might explain the cause of high BP. This system also governs the activation of the angiotensin system at various axes in control of the physiological BP. The BK receptor antagonists can block the hypotensive action of angiotensin-converting enzyme inhibitors (ACEls) in hypertensive and normotensive animals. The hypotensive action of BK is highly increased with ACEIs or kininase II inhibitor treatment. The development of specific BK agonists may provide a new direction to explore the experimental approach for examining the role of BK in hypertension.

show abstract

“…Bu veriler ışığında, renalbradikinin sistemin hipertansiyonun oluşumunda önemli bir role sahip olduğu hipotezi kurulabilir (3). BK'nin renal arterlere geçişi, prostaglandinlerin ve nitrik oksitin (NO) salı-nımına neden olarak, böbreklere kan akışını arttırır ve diürez ve natriürez oluşturur (23,24). BK'nın üretim oranı ya da metabolizması hipertansiyonun patofizyolojisini değiştire-bilir.…”

Section: Introductionunclassified

Relationship of Bradykinin B2 Receptor Gene C-58T Variation with Total-Cholesterol and Glucose in Essential Hypertension

Susleyici¹,

Gündüz²,

Zengin³

et al. 2016

Bezmialem Science

View full text Add to dashboard Cite

ÖZAmaç: Hipetansiyon, dünya nüfusunun %25'inde etkili olan ve patogenezinde %30 oranında genlerin rol aldığı bir hastalıktır. Bu çalışmada amacımız, Bradikinin B 2 R geni C-58T genotiplerinin hipertansiyonlu ve hipertansiyonlu olmayan bireylerdeki sıklıklarının tespit edilmesi, C-58T genotiplerinin antropometrik, şişmanlık ve hipertansiyon ilişkili göstergeler üzerine etkisini belirlemektir. Yöntemler: Bradikinin B 2 reseptör geni C-58T genotipleri 63 hipertansiyonlu ve 56 hipertansiyonlu olmayan bireylerde PZR-RFLP yöntemi ile belirlenmiştir. Bulgular: Bradikinin B 2 reseptör geni C-58T genotip sıklıkları hipertansiyonlu ve hipertansiyonlu olmayan bireylerde sırasıyla homozigot yabanıl tip (T/T) %25,4, %28,6; heterozigot (T/C) %49,2, %58.9 ve homozigot polimorfik tip (C/C) %25,4, %12,5 dir. Çalışma gruplarının genotip sıklıkları arasında istatistiksel anlamlı bir farklılık görülmemiştir. Hipertansiyonlu çalışma grubunda C/C genotipinin açlık kan şekerini (p=0,05) yükseltici, total kolesterolü (p=0,008) düşürücü etkisi tespit edilmiştir. Hipertansiyonlu olmayan çalışma grubunda ise C/C genotipinin bel çevre ölçümünü arttırıcı etkisi saptanmıştır (p=0,041). Hipertansiyonlu çalışma grubunda C/C genotipine sahip bireylerde sulfanülüre (p=0,021) kullanımın sıklığının fazla olduğu ve T/T genotipine sahip bireylerde ise diüretik (p=0,007) kullanım sıklığının fazla olduğu belirlenmiştir. Hipertansiyonu olmayan grupta C/C genotipine sahip bireylerde asetilsalisilik asit (p=0,003) kullanım sıklığının diğer genotiplere kıyasla daha yüksek olduğu tespit edilmiştir. Sonuç: Bradikinin B 2 reseptör geni C-58T polimorfizminin açlık kan şekeri, total kolesterol ve bel çevre ölçümleri üzerine etkili olduğu, ancak sistolik ve diastolik kan basıncı üzerine etkili olmadığı görülmüştür. Anahtar Kelimeler: Bradikinin, hipertansiyon, kolesterol, bel çevresi, kan şekeri ABSTRACT Objective: Hypertension, which affects 25% of the world's population, is a complex disease, with 30% genes affecting its pathogenesis. In this study, we aimed to examine the frequency of the bradykinin B 2 receptor gene C-58T genotypes in patients with essential hypertension and non-hypertensive controls. In addition, we evaluated the effects of C-58T genotypes on demographic characteristics, phenotypes related to obesity, and hypertension. Methods: Genotyping was performed in 63 hypertensive patients and 56 non-hypertensive subjects by PCR-RFLP. Results: The frequency of bradykinin B 2 receptor gene C-58T genotypes in hypertensive patients and control subjects was 25.4% and 28.6% for homozygous wild-type (T/T), 49.2% and 58.9% for heterozygous (T/C), and 25.4% and 12.5% for homozygous polymorphic (C/C) genotypes, respectively. Genotype frequencies did not differ significantly among study groups. The C allele was found to have an increasing effect on blood glucose levels (p=0.05) and decreasing effect on total cholesterol levels (p=0.008) in hypertensive patients, whereas it was found to have an increasing effect on waist circumference (p=0.041) in control subj...

show abstract

The Actions of Bradykinin and Eledoisin in the Canine Isolated Kidney: Relationships to Prostaglandins

Cited by 67 publications

References 16 publications

The Kallikrein-Kinin System in Bartter's Syndrome and Its Response to Prostaglandin Synthetase Inhibition

The Kallikrein-Kinin System in Bartter's Syndrome and Its Response to Prostaglandin Synthetase Inhibition

Activation of the Bradykinin System by Angiotensin-Converting Enzyme Inhibitors

Relationship of Bradykinin B2 Receptor Gene C-58T Variation with Total-Cholesterol and Glucose in Essential Hypertension

Contact Info

Product

Resources

About