Differing actions of endothelin-1 on canine systemic resistance and capacitance vessels.

Takai, Kuniyuki; Ito, Hiroyasu; Sahashi, Teruchika; Wada, Hisayasu; Segawa, Tomonori; Hirakawa, Senri

doi:10.1253/jcj.56.847

Cited by 5 publications

(2 citation statements)

References 13 publications

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“…Methylene blue also did not alter blood pressure in dogs (Archer et al, 1986) or cats (Hyman et al, 1989). However, methylene blue lowered blood pressure in rats (Loeb & Longnecker, 1992) and dogs (Takai et al, 1992) and raised blood pressure in lambs (Fineman et al, 1991). In the latter study, methylene blue also caused tachycardia and pulmonary edema (Fineman et al, 1991).…”

Section: Discussionmentioning

confidence: 80%

Vascular pharmacology of methylene blue in vitro and in vivo: a comparison with N^G‐nitro‐l‐arginine and diphenyleneiodonium

Wang

Cheng

Pang

1995

British J Pharmacology

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1 The vascular effects of the soluble guanylyl cyclase inhibitor, methylene blue as well as the nitric oxide (NO) synthase inhibitors, NG-nitro-L-arginine (L-NOARG) and diphenyleneiodonium (DPI) were studied in rat isolated aortic rings and conscious, unrestrained rats. 2 Acetylcholine (ACh) and sodium nitroprusside (SNP) caused concentration-dependent relaxation of preconstricted aortic rings. Both methylene blue (1 x 10-5 M) and L-NOARG (3 x 10-5 M) abolished ACh-induced relaxation; however, methylene blue but not L-NOARG shifted the concentration-response curve of SNP to the right.3 In conscious rats, i.v. infusion of methylene blue (1.1 x 10-'mol kg-'min-1), at a concentration which reduced the aortic tissue level of cyclic GMP by 50%, did not significantly alter mean arterial pressure (MAP) and heart rate (HR). In contrast, i.v. bolus injection of L-NOARG (1.5 x 10-mol kg-') markedly increased MAP and decreased HR. 4 Both ACh and SNP dose-dependently decreased MAP in conscious rats. Methylene blue did not alter the magnitude or duration of ACh-or SNP-induced depressor responses. L-NOARG, on the other hand, significantly though incompletely, reduced the magnitude and duration of the depressor response to ACh but not SNP. The depressor response to ACh or SNP was not altered by pretreatment with indomethacin (1.4 x 10-mol kg-') or capsaicin (3.3 x 10-mol kg-'). 5 NG-nitro-L-arginine methyl ester (L-NAME) also caused dose-dependent increases in MAP in conscious rats. Both methylene blue and DPI (1 x 105mol kg-') selectively shifted the dose-pressor response curve of L-NAME to the right. 6 These results suggest that: (1) the inhibition of endogenous NO biosynthesis does not necessarily lead to pressor response in vivo, (2) L-NOARG may not produce pressor response solely via the inhibition of endogenous endothelial NO biosynthesis, and (3) the depressor responses to ACh and SNP may not involve the release of NO or prostanoids or afferent nerve transmitters.

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Section: Discussionmentioning

confidence: 80%

Vascular pharmacology of methylene blue in vitro and in vivo: a comparison with N^G‐nitro‐l‐arginine and diphenyleneiodonium

Wang

Cheng

Pang

1995

British J Pharmacology

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“…Studies in healthy humans have shown that decreased venous pressure, hypovolemia, and postural changes elicit increased ET-1 secretion (32,33,50). Furthermore, infusion of ET-1 in dogs and rats has been shown to increase mean circulatory filling pressure, a measure of capacitance vessel tone (52,61). Kiowski et al (18) found that ET-receptor antagonist treatment in CHF patients significantly reduced right atrial pressure and PCWP, which are indirect measures of capacitance vascular tone (36).…”

Section: Discussionmentioning

confidence: 99%

Regulation of ET: pulmonary release of ET contributes to increased plasma ET levels and vasoconstriction in CHF

Kjekshus¹,

Smiseth²,

Klinge³

et al. 2000

American Journal of Physiology-Heart and Circulatory Physiology

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Endothelin (ET) contributes to the increased systemic vascular resistance and elevated cardiac filling pressures seen in congestive heart failure (CHF). We investigated to what extent ET-mediated vasoconstriction in CHF occurs through an endocrine action of elevated plasma ET or by an autocrine/paracrine mechanism related to induction of vascular ET gene expression. Three weeks of pacing (225 beats/min) induced a marked release of ET-1 from the pulmonary circulation with a sixfold elevation of arterial plasma ET in CHF pigs compared with sham-operated pigs. Arterial plasma ET was the strongest and only independent predictor of systemic vascular resistance. In contrast, vascular preproET-1 and ET-receptor mRNA expression were unaltered or decreased in CHF pigs and did not correlate with indexes of vascular tone. However, myocardial preproET-1 mRNA expression increased twofold in CHF pigs. PreproET-2 and preproET-3 mRNAs were not detectable in cardiovascular tissues. In conclusion, plasma ET was markedly increased because of an augmented release from the pulmonary circulation during CHF, and arterial plasma ET correlated with systemic vascular resistance. The absence of ET induction in the peripheral vasculature suggests that ET increases vascular tone during CHF by an endocrine, not an autocrine/paracrine, mechanism.

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Vascular effects of endothelin-1 in stage 21 chick embryos

Kajio

Nakazawa

1997

Heart Vessels

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Endothelin-1 is a very potent vasoconstrictor, but its function has not yet been investigated in the early stage of cardiovascular development. The purpose of the present study was to clarify whether endothelin-1 exerts a hemodynamic effect in stage 21 chick embryos. We measured vitelline artery blood pressure with a servo-null micropressure system and blood flow velocity at the dorsal aorta with a 20 MHz pulsed Doppler velocity meter. The vitelline vessels were directly measured with a microscope video system. While monitoring these parameters, endothelin-1 was infused into a vein by a microinjector and data were collected. Endothelin-1 increased the blood pressure and heart rate, but decreased the dorsal aortic blood flow. Only the vitelline veins with a diameter of between 100 and 200 microm constricted after endothelin infusion, but smaller or larger veins and the arteries did not show any significant change in size, although the resistant arteries could not be measured by this method. In conclusion, endothelin-1 has apparent constrictive effects in the selected vessel in the early stages of cardiovascular development when the endocrine and autonomic nervous systems have not yet developed.

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Differing actions of endothelin-1 on canine systemic resistance and capacitance vessels.

Cited by 5 publications

References 13 publications

Vascular pharmacology of methylene blue in vitro and in vivo: a comparison with N^G‐nitro‐l‐arginine and diphenyleneiodonium

Vascular pharmacology of methylene blue in vitro and in vivo: a comparison with N^G‐nitro‐l‐arginine and diphenyleneiodonium

Regulation of ET: pulmonary release of ET contributes to increased plasma ET levels and vasoconstriction in CHF

Vascular effects of endothelin-1 in stage 21 chick embryos

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Differing actions of endothelin-1 on canine systemic resistance and capacitance vessels.

Cited by 5 publications

References 13 publications

Vascular pharmacology of methylene blue in vitro and in vivo: a comparison with NG‐nitro‐l‐arginine and diphenyleneiodonium

Vascular pharmacology of methylene blue in vitro and in vivo: a comparison with NG‐nitro‐l‐arginine and diphenyleneiodonium

Regulation of ET: pulmonary release of ET contributes to increased plasma ET levels and vasoconstriction in CHF

Vascular effects of endothelin-1 in stage 21 chick embryos

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Vascular pharmacology of methylene blue in vitro and in vivo: a comparison with N^G‐nitro‐l‐arginine and diphenyleneiodonium

Vascular pharmacology of methylene blue in vitro and in vivo: a comparison with N^G‐nitro‐l‐arginine and diphenyleneiodonium