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

Naruse, Mitsuhide; Zeng, Zheng-pei; Naruse, Kiyoko; Tanabe, Akiyo; Yoshimoto, Takanobu; Demura, Hiroshi

doi:10.1291/hypres.16.247

Cited by 1 publication

(1 citation statement)

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“…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 ET-1 [42]. This suggests that only the increase in plasma ET is not a factor eliciting chronic hypertension.…”

Section: Biological Actionsmentioning

confidence: 93%

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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Section: Biological Actionsmentioning

confidence: 93%