Renal and femoral vascular responses to endothelin in anesthetized dogs: role of prostaglandins

Miura, K; Yukimura, Tokihito; Yamashita, Yasuko; Shimmen, Tomoji; Okumura, Michiaki; Yamanaka, Shinya; Imanishi, Masaki; Yamamoto, Kohji

doi:10.1016/0014-2999(90)93587-g

Cited by 10 publications

(11 citation statements)

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“…Klabunde et al 11 have reported that the pressor response of anesthetized dogs to a NO synthase inhibitor, N Gmonomethyl L-arginine, is abolished by treatment with indomethacin. However, in the present study, treatment with aspirin in a dose sufficient to abolish the release of prostaglandins 23 did not significantly alter the hypertensive effect of L-NA, suggesting that the involvement of cyclooxygenase products is excluded.…”

Section: Discussioncontrasting

confidence: 79%

Neural mechanism of hypertension by nitric oxide synthase inhibitor in dogs.

1993

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This study aimed to determine the mechanism of hypertension associated with nitric oxide synthase inhibition. Intravenous injections of JV G -nitro-L-arginine, a nitric oxide synthase inhibitor, produced a sustained increase in systemic blood pressure and a decrease in heart rate in anesthetized dogs, whereas iV G -nitro-D-arginine had no effect. L-Arginine reversed the pressor response. yV G -Nitro-L-arginine-induced hypertension was markedly attenuated or abolished by treatment with hexamethonium; this inhibition was still observed when the blood pressure fall caused by the ganglionic blocking agent was compensated by continuous infusion of angiotensin II. In dogs treated with phentolamine in a dose sufficient to lower blood pressure to the level similar to that elicited by hexamethonium and to suppress the pressor response to norepinephrine, the hypertensive effect of JV G -nitro-L-arginine was not attenuated. We conclude that hypertension caused by the nitric oxide synthase inhibitor is associated with an elimination of nitroxidergic neural function rather than an impairment of the basal release of nitric oxide from the endothelium. 4 -6 Intravenous injections of NO synthase inhibitors raise systemic blood pressure in anesthetized and conscious rats and anesthetized guinea pigs, rabbits, and dogs, 7 -11 and intra-arterial injections decrease blood flow and increase vascular resistance. 1213 The pressor and vasoconstrictor effects of NO synthase inhibitors are prevented by L-arginine but not by D-arginine. The hypertensive effects of NO synthase inhibitors are considered to be due to the suppression of the basal release of NO from the endothelium of resistance vessels. However, whether the NO involved originates solely from the endothelium has not been fully determined.NO transmits information from nonadrenergic, noncholinergic vasodilator nerve to smooth muscle in dog and monkey cerebral arteries.14 - 16 In addition, the presence of NO synthase in perivascular nerve has been demonstrated histochemically.17 Therefore, NO is thought to act as a transmitter, 18 In a recent study, we observed that intraluminally applied L-NA potentiates the neurally induced vasoconstriction, as does extraluminal L-NA (Zhang et al, unpublished data).We undertook the present study to elucidate whether elimination of neurogenic vasodilator control is involved in the hypertension induced by L-NA administered to anesthetized dogs. Methods Thirty-two mongrel dogs of both sexes (9-16 kg) were used for study. All animals were fed standard chow and water ad libitum and were housed according to institutional guidelines at the Shiga University of Medical Sciences. These studies were approved by the Animal Rights Committee, Shiga University of Medical Sciences. Dogs were anesthetized with sodium pentobarbital (25 mg/kg i.p.) and were intubated. Supplemental doses of the anesthetic were applied via the femoral vein when necessary. The animals were permitted to breathe spontaneously. Arterial systolic and diastolic blood pressures were moni...

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Section: Discussioncontrasting

confidence: 79%

Neural mechanism of hypertension by nitric oxide synthase inhibitor in dogs.

1993

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“…In vitro studies have shown that ET-1 release is stimulated by hemodynamic shear stress, hypoxia, inflammatory cytokines (tumor necrosis factor, interleukin-1, and transforming growth factor-p), vasoac tive hormones (angiotensin II. vasopressin, bradykinin, and epinephrine), and thrombin [5,[11][12][13][14], There is evi dence that ETs function as a local hormone synthesized The renal vasculature is much more sensitive to the vasoconstricting effects of ET-1 than any other vascular bed [12], The hemodynamic actions of ET-1 in the kidney have been extensively examined by exogenous adminis tration and are characterized by initial transient vasodila tion, followed by intense, prolonged vasoconstriction [18][19][20], The vasodilatory response involves the ET-1 stimula tion of renal release of endothelium-derived NO and pros tacyclin [18,19,21], Inhibiting the production of either of these vasodilatory substances modifies or abolishes the vasodilatory responses and markedly intensifies vasocon striction [18,19,21], In the glomerular microcirculation, ET-1 causes vasoconstriction of afferent and efferent arte rioles, as well as mesangial contraction, leading to a reduc tion in GFR [22][23][24][25][26][27], In general, the decrease in GFR noted in animal studies is less severe than the reduction in renal blood flow [ 18. 22, 23], a finding also observed in a human study in which a small dose of ET-1 was infused intravenously raising only diastolic but not systolic blood pressure [28],…”

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confidence: 99%

Endothelins and Kidney Diseases

Brown¹,

Chou²,

Porush³

1996

Nephron

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“…Levin and colleagues described the endothelins, a 21 amino acid peptide family, of which isoforms endothelin- Fig. Endothelin-1 can activate PA 2 stimulating AA metabolism and eicosanoid production, while PGI 2 will inhibit platelet aggregation and permit transient vasodilatation [8,9]. Eicosanoid biosynthesis.…”

Section: Physiology Of Eicosanoid Production and Endothelial Dysfunctionmentioning

confidence: 99%

Recent Insights into the Role of Prostanoids in Atherosclerotic Vascular Disease

Reiss

Edelman²

2006

CVP

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Atherosclerosis is characterized by chronic inflammation and enrichment of inflammatory cells in the vessel wall. Acute inflammation can lead to damaged endothelium triggering the coagulation cascade and thrombus formation. Likewise, the clotting cascade may elicit an inflammatory response. The vascular endothelium regulates vascular tone, permeability, inflammation, thrombosis, and coagulation. Dysfunction of the vascular endothelium can promote atherosclerotic disease processes. Prostanoids (prostaglandins, thromboxane, and prostacyclin) have been established as inflammatory mediators in vascular endothelial function and there continues to be growing insights into their role in atherosclerotic disease. This review examines the role of prostanoids as paracrine inflammatory mediators of atherosclerotic vascular disease, highlighting the relevant physiology of eicosanoid production and endothelial dysfunction. We consider the role of prostanoids in systemic diseases associated with high cardiovascular morbidity and mortality, including diabetes mellitus, coronary artery disease, peripheral arterial disease, rheumatologic disorders, and dyslipidemia. We present emerging evidence that cardio-protective and lipid lowering medications, such as irbesartan and simvastatin may exert their effects via prostanoid mediated pathways. Both serum and urinary prostanoids may be utilized as diagnostic predictors of disease; for example 8-iso-PGF(2alpha) in the serum has recently been reported as an independent predictor of symptomatic peripheral arterial disease. In addition, we discuss current recommendations on established therapeutic uses of prostanoids for atherosclerotic diseases, such as the use of PGE(1) for the treatment of peripheral arterial disease. Finally, we investigate original therapeutic modalities of various prostanoids involved in the aforementioned diseases.

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Renal and femoral vascular responses to endothelin in anesthetized dogs: role of prostaglandins

Cited by 10 publications

References 1 publication

Neural mechanism of hypertension by nitric oxide synthase inhibitor in dogs.

Neural mechanism of hypertension by nitric oxide synthase inhibitor in dogs.

Endothelins and Kidney Diseases

Recent Insights into the Role of Prostanoids in Atherosclerotic Vascular Disease

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