Calcium channel blockers reverse the sustained elevation of blood pressure induced by chronic infusion of endothelin in conscious rats.

Yasujima, Minoru; Abe, Keishi; Kanazawa, Masayuki; Yoshida, Kazunori; Sato, Makito; Takeuchi, Kazuhisa; Tsunoda, Kazuo; Kudo, Kohsuke; Kohzuki, Masahiro; Omata, Ken; Yabe, Tamami; Hiwatari, Masao; Sato, Tokutaro; Yoshinaga, Kaoru

doi:10.1620/tjem.160.157

Cited by 6 publications

(5 citation statements)

References 19 publications

(23 reference statements)

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“…Both plasma ET-1 levels and systolic blood pressure showed significant increases after 1 week of ET-1 infusion. The increase in systolic blood pressure agrees with the results of previous studies in which synthetic ET-1 was infused for a similar period (2,3). However, in these two prior investigations, plasma ET levels after infusion were not determined.…”

Section: Discussionsupporting

confidence: 89%

“…Intravenous, bolus administration of the peptide into both anesthetized and conscious rats has been shown to produce a sustained pressor response (1). Infusion of ET-1 for periods of up to a week has also been reported to elevate blood pressure (2,3). ET-1 shows diverse actions on renal (4-6) and endocrine functions, including secretion of renin (5,7), aldosterone (5,8), catecholamines (5,9), and vasopressin (10), as well as on cardiac functions (5,11).…”

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confidence: 99%

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Is Chronic Elevation of Plasma Endothelin Levels a Cause of Hypertension?

Naruse¹,

Zeng

Naruse³

et al. 1993

Hypertens Res

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LevelsEndothelin (ET) has been postulated to be hypertensinogenic through its potent and long-lasting vasoconstriction.Whether sustained increase in plasma ET levels causes hypertension remains to be clarified. We investigated the effects of chronic infusion of ET-1 on blood pressure, relevant to the plasma levels in normal Wistar rats. Synthetic ET-1 was administered intravenously using osmotic minipumps at a rate of 16,cig/kg/day for 4 weeks. Systolic blood pressure, heart rate, and plasma ET-1 levels were determined before and after the infusion. After one-week infusion, both plasma ET-1 levels and systolic blood pressure were significantly higher than those in the control group. The systolic blood pressure showed a sustained elevation over a period of 2 weeks and then started to decrease gradually to the control levels, while plasma ET-1 levels remained elevated. There were no significant differences in heart rate and body weight between the ET-infusion and control groups. These results suggest that even a mild increase in plasma ET-1 levels could cause elevation of blood pressure. However, normalization of systolic blood pressure despite the sustained increase in plasma ET-1 levels after chronic infusion suggests that an increase in plasma ET-1 levels alone is not sufficient to cause chronic elevation of blood pressure in normal rats. (Hypertens Res 1993; 16: 247-251)

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Section: Discussionsupporting

confidence: 89%

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confidence: 99%

Is Chronic Elevation of Plasma Endothelin Levels a Cause of Hypertension?

Naruse¹,

Zeng

Naruse³

et al. 1993

Hypertens Res

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“…Even an increase in blood pressure in rats with the ET-1 gene knocked out by gene targeting techniques is in agreement with this concept [37]. This is quite in contrast to the case of nitric oxide which plays an important role in the maintenance of basal vascular tone [38,39].The chronic infusion of ET-1 for one week resulted in a sustained increase in blood pressure [40,41]. Interestingly, however, the administration of ET-1 over a period of 4 weeks in normal rats was associated with normalization of the once elevated blood pressure despite the sustained increase in plasma .…”

mentioning

confidence: 64%

“…The chronic infusion of ET-1 for one week resulted in a sustained increase in blood pressure [40,41]. Interestingly, however, the administration of ET-1 over a period of 4 weeks in normal rats was associated with normalization of the once elevated blood pressure despite the sustained increase in plasma .…”

Section: Biological Actionsmentioning

confidence: 95%

Recent Advances in Endothelin Research on Cardiovascular and Endocrine Systems.

Naruse¹,

Naruse²,

Demura³

1994

Endocr J

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IntroductionSince the quite exciting discovery in 1988 of endothelin (ET) in the culture medium of aortic endothelial cells by Yanagisawa and coworkers [1], evidence has accumulated to support its important roles in the regulation of blood pressure and body fluid homeostasis and its pathophysiological significance in various cardiovascular diseases. The discovery of ET and the opponent substances including nitric oxide [2] and natriuretic peptides [3] during the last decade was epoch-making in the field of "Cardiovascular Endocrinology". Because of its impressive potency and the long duration of its pressor action [1], the roles of ET in the regulation of cardiovascular homeostasis have been extensively studied.However, the co-expression or close localization of ET and its receptors in various tissues other than the vascular vessels suggest non-vascular roles of ET [4][5][6]. In the present review, we firstly integrate the information relevant to its physiological role in blood pressure regulation and possible pathogenic role in hypertension.We secondarily focus on the possible roles of ET in the endocrine system, especially in the pituitary and adrenal.Substantial review articles on ET in the kidney [7,8], ET and the heart [9], the growth regulating properties of ET [10], and ET in bronchial diseases [11, 12] have been published. Structure of ET and ET ReceptorThe molecular and biochemical aspects of ET family peptides and ET receptors have been reviewed by Masaki and Yanagisawa [13] and others [14][15][16]. We here describe the fundamentals. ET PeptidesThe ET molecule consists of 21 amino acid residues with two intramolecular disulfide bonds between cystein residues at 1 and 15 and 3 and 11, respectively. The ring structure and the hydrophobic amino acid residues at the C-terminus are indispensable to its full biological activities. There are three distinct isof orms of ET: ET-1, . The difference in the amino acid sequence is seen in the ring structure, while they share the same sequence in the linear C-terminal portion. Interspecies differences are minimal [13][14][15][16]. Interestingly, the amino acid sequence of a family of rare snake venoms, the sarafotoxins, is very similar to the sequence of ET [16], composing the ET-sarafotoxin family and suggesting the importance of the peptide in evolution.PreproET-1, the precursor of the peptide, is synthesized through the gene transcription and translation. Expression of the preproET-1 mRNA in the endothelial cells is stimulated by various humoral and physical factors: thrombin, TGF-f3, interleukin-1, TNF-a, angiotensin II (Ang II), vasopressin, and shear stress (for review see [13][14][15] produced.In addition, the existence of ET was also shown by immunoassay in a variety of tissues other than the vascular endothelium [22]. The ET-1 content is the highest in the posterior pituitary and the lung followed by the anterior pituitary, brain, and adrenal gland. The ET-3 content is highest in the posterior and anterior pituitaries.The ET-1 content is significantly hi...

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“…The vasopressor response, induced by synthetic endothelin was dependent on extracellular calcium ion and was inhibited by voltagedependent calcium channel blockers (Hirata et al 1988 ; Yanagisawa et al 1988), whereas other possible mechanism has been postulated to be involved in the vasopressor response induced by endothelin (Hirata 1990). We have previously reported that benidipine (Kubo et al 1985;Fujii et al 1988) and nilvadipine (Ohtsuka et al 1983), newly developed blockers of calcium channel, reversed the elevation of blood pressure induced by chronic infusion of endothelin in conscious rats (Yasujima et al 1990a). However, it remains to be elucidated whether the antihypertensive effect of calcium channel blockers in endothelin-infused rats is specific to blockade of calcium channels.…”

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confidence: 99%

Antihypertensive effect of captopril and enalapril in endothelin-infused rats.

Yasujima

Abe²,

Kanazawa

et al. 1991

Tohoku J. Exp. Med.

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Comparative effects of angiotensin converting enzyme inhibitors and calcium channel blockers were assessed in rats infused chronically with synthetic endothelin. When 50 mg/kg/ day of captopril orally or 6 mg/kg/day of enalapril intraperitoneally was administered simultaneously with 60pg/kg/day of endothelin, the systolic blood pressure was on Day 1 142.7±5.9 mmHg (p <0.05) or 128.7±6.7 mmHg (p <0.05), respectively, compared to the rise to 163.8±4.7 mmHg when endothelin alone was infused. The antihypertensive effect of captopril or enalapril was sustained for the entire experimental period and was not associated with a significant change in urinary sodium excretion, whereas both drugs induced a significant increase in urine volume. Chronic infusion of angiotensin II intraperitoneally at a subpressor dose (400 pg/kg/day) reversed the antihypertensive effect of captopril in endothelin-infused rats. When 6 mg/kg/day of benidipine or 10 mg/kg/day of nilvadipine orally was administered simultaneously with 60 p g/kg/day of endothelin, the systolic blood pressure was on Day 1 137.0±2.4 mmHg (p <0.05) or 119.7±5.9 mmHg (p <0.05), respectively, compared to the rise when endothelin alone was infused. The antihypertensive effect of benidipine or nilvadipine was sustained for the entire experimental period and was not associated with any significant changes in urine volume and urinary sodium excretion. These results indicate that the reduced sensitivity of the peripheral arteries to endothelin may be involved in the mechanism of the hypotensive action of angiotensin converting enzyme inhibitors, dependent on the suppressed angiotensin II formation.

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Calcium channel blockers reverse the sustained elevation of blood pressure induced by chronic infusion of endothelin in conscious rats.

Cited by 6 publications

References 19 publications

Is Chronic Elevation of Plasma Endothelin Levels a Cause of Hypertension?

Is Chronic Elevation of Plasma Endothelin Levels a Cause of Hypertension?

Recent Advances in Endothelin Research on Cardiovascular and Endocrine Systems.

Antihypertensive effect of captopril and enalapril in endothelin-infused rats.

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