The role of prostaglandins in the regulation of blood pressure with special reference to vascular reactivity.

Yoshimura, Manabu; Shikuma, Rieko; Takashina, Ryosaku; Yamazaki, Hideaki; Takeda, Kazuo; Takahashi, Hakuo; Sasaki, Susumu; Okajima, Hiroshi; Ijichi, Hamao

doi:10.1253/jcj.48.180

Cited by 3 publications

(1 citation statement)

References 12 publications

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“…The altered regulation of AQP channels in the medulla may thus be related with paracrine factors, including prostaglandins, produced by interstitial cells. Although prostaglandins have a role in the regulation of norepinephrine release [16], it is uncertain whether the sympathetic activity in turn plays a role in the regulation of prostaglandin synthesis in the kidney.…”

Section: Discussionmentioning

confidence: 99%

Decreased Expression of Aquaporin Water Channels in Denervated Rat Kidney

Lee¹,

Yoo²,

Kim

et al. 2006

Nephron Physiol

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Aims: A neural mechanism regulating aquaporin (AQP) water channels in the kidney was investigated. Methods: Male Sprague-Dawley rats were used. Renal denervation was induced by painting the renal vessels with 10% phenol. The expression of AQP1–4 proteins was determined in the denervated and contralateral kidneys. The expression was also examined in rats which were renally denervated and subjected to water restriction or deoxycorticosterone acetate (DOCA)-salt treatment. Results: Following the unilateral denervation, tissue contents of norepinephrine were significantly decreased in the denervated kidney, while increased in the contralateral kidney. Accordingly, the expression of AQP1–4 proteins was decreased by 15–40% in the denervated kidney, and increased by 30–50% in the contralateral kidney. Immunohistochemistry of AQP2 confirmed its decreases in the denervated kidney and increases in the contralateral kidney. In bilaterally denervated rats, the urine flow increased along with decreased osmolarity. The water restriction increased the expression of AQP channels, however, the magnitude of which was lower in the denervated than in the contralateral kidney. Renal denervation decreased the degree of DOCA-salt hypertension, along with lower expression of AQP channels. Conclusion: It is suggested that the sympathetic nerve should play a specific excitatory role in the regulation of AQP channels in the kidney.

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Section: Discussionmentioning

confidence: 99%

Decreased Expression of Aquaporin Water Channels in Denervated Rat Kidney

Lee¹,

Yoo²,

Kim

et al. 2006

Nephron Physiol

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Small dose of prostaglandin E1 increases cardiac output without altering blood volume

Fukuda

Kawamoto

Yuge

2001

Journal of Clinical Anesthesia

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Repeated sympathetic stimuli elicit the decline and disappearance of prostaglandin modulation and an increase of vascular resistance in humans.

Serneri

Castellani

Scarti

et al. 1990

Circulation Research

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To investigate the role of prostaglandins 12 and E2 in modulating the vasoconstrictor response to sympathetic stimulation, repeated and proximate cold pressor tests were performed in 23 healthy young volunteers. Limb vascular resistance (blood flow measured by venous occlusion plethysmography), prostaglandin 12 (as 6-ketoprostaglandin FJa) and prostaglandin E2 plasma levels (detected by radioimmunoassay), and plasma catecholamines (detected by highperformance liquid chromatography and electrochemical detection) were measured. A progressive increase in the duration of the vasoconstrictor response was observed with repetition of cold applications (p<0.001, by analysis of variance for trends). This increase was associated with a progressive decrease in cold-induced elevation of 6-ketoprostaglandin F,a and prostaglandin E2 plasma levels until, after five stimulations, neither prostaglandin was detectable.The maximum detected concentration of norepinephrine did not significantly change, but its area under the curve in time showed a trend toward an increase. Epinephrine levels did not significantly change. The increase of vascular resistance was significantly correlated with the decrease of both prostaglandins (r= 0.93, p<0.05 for prostaglandin E2 and r= 0.89,p<0.05 for 6-ketoprostaglandin F1j), whereas no significant correlations were found between variations of vascular resistance and catecholamines. Prostaglandin blockade induced by diclofenac sodium administration caused, from the first cold application, a pattern of the vasoconstrictor response and plasma prostaglandin and norepinephrine changes similar to that observed at the fifth cold application in untreated subjects, when prostaglandins are no longer detectable in plasma. We conclude that an increased vasoconstrictor response to sympathetic stimulation in humans may result from a diminished inhibitory influence of prostaglandins on adrenergic transmission. (Circulation Research 1990;67:580-588) In animal experiments, both exogenous catecholamines and nerve stimulation have been reported to induce prostaglandin release from different organs such as the spleen' and the kidneys2 as well as from isolated blood vessels.3-6 In tissue fragments and isolated perfused organs, prostaglandin 12 (PGI2) and prostaglandin E2 (PGE2) have been found to modulate the effects of sympathetic stim-

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The role of prostaglandins in the regulation of blood pressure with special reference to vascular reactivity.

Cited by 3 publications

References 12 publications

Decreased Expression of Aquaporin Water Channels in Denervated Rat Kidney

Decreased Expression of Aquaporin Water Channels in Denervated Rat Kidney

Small dose of prostaglandin E1 increases cardiac output without altering blood volume

Repeated sympathetic stimuli elicit the decline and disappearance of prostaglandin modulation and an increase of vascular resistance in humans.

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