Effects of Endothelin on Systemic and Renal Haemodynamics and Neuroendocrine Hormones in Conscious Dogs

Nakamoto, Hidetomo; Suzuki, Hiromichi; Murakami, Marohito; Kageyama, Yoichi; Ohishi, Akira; Fukuda, Keiichi; Hori, Shingo; Saruta, Takao

doi:10.1042/cs0770567

Cited by 38 publications

(15 citation statements)

References 21 publications

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“…While it has previously been shown that ET-1 is able to cause the acute stimulation of ACTH release in the dog [10], in the present studies no stimulation of the release of the major ACTH-releasing hormone CRH was seen. In the peripheral vascular system, ET-1 may lead to the stim ulation of NO synthesis, which in turn may counteract at least in part some of the effects of ET-1 on the vascula ture; this effect is thought to occur mainly via the E T b receptor subtype [19], As NO has been shown to inhibit the stimulated release of CRH [27], we were concerned that the lack of effect of ET-1 might be due to the cosyn thesis of NO; however, even in the presence of the potent NO synthesis inhibitor, T-NO-Arg, no stimulation of CRH release was seen, suggesting that NO production was not masking any stimulatory effect of ET-1.…”

Section: Discussioncontrasting

confidence: 51%

“…However, all three endothelins and their receptors have also been identified in the central ner vous system [3] with the highest levels of endothelin mRNA in hypothalamic neurons [4], suggesting that they may function as central neuromodulators [1,5,6]. Yoshizawa et al [7] originally demonstrated the pres ence of ET-1 in the endocrine hypothalamus, particularly the paraventricular and supra-optic nuclei and the poste rior pituitary; furthermore, ET-1 immunoreactivity was depleted in parallel with vasopressin in response to an osmotic stimulus, suggesting that it may be concerned in the regulation of vasopressin release [7], More direct evi dence for this control was provided by the observation that ET-1 stimulated vasopressin release from the perifused rat hypothalamus [8] or posterior pituitary [9] in vitro, while in vivo peripheral infusion of ET-1 led to a parallel increase in both vasopressin and adrenocorticotropin (ACTH) in the dog [10]. In addition, circulating levels of ET-1 and vasopressin appear to correlate in the human under different pathophysiological states [11], Specific endothelin-binding sites have been demonstrated in the central nervous system, particularly the cortex and cerebellum but also the hypothalamus [12], thus further confirming the suggested role of endothelins in the regula tion of neuro-endocrine function.…”

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confidence: 99%

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Endothelin-1 Stimulates the in vitro Release of Neurohypophyseal Hormones, but Not Corticotropin-Releasing Hormone, via ET<sub>A</sub> Receptors

et al. 1994

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The endothelins consist of a family of vasoconstrictor peptides originally isolated from endothelial tissue which are now known to be involved in neuroendocrine regulation. However, while there are data indicating the involvement of endothelins in the modulation of the hypothalamo-pituitary-adrenal (HPA) axis, the precise mechanisms involved have been unclear. We have therefore used a previously validated rat hypothalamic explant system in order to investigate the possible modulation of the neurohypophyseal hormones vasopressin and oxytocin, and corticotropin-releasing hormone (CRH), by endothelin-1 (ET-1) and endothelin-3 (ET-3). Following a period of stabilisation, the release of vasopressin, oxytocin and CRH remained approximately constant in successive 20-min incubations. Addition of ET-1 stimulated the release of vasopressin at a dose of 0.1 nmol/l (p < 0.05), and both vasopressin and oxytocin at 10 nmol/l (p < 0.01 and 0.05, respectively). The release of vasopressin and oxytocin induced by 10 nmol/l ET-1 were both totally blocked by co-incubation with either 1 or 10 µmol/l of the specific ET_A receptor subtype antagonist cyclo (D-Trp-D-Asp-Pro-D-Val-Leu) (BQ-123). ET-1 had no effect on CRH release in the dose range of 0.1-1,000 nmol/l. In case any possible stimulation of CRH might be masked by simultaneous generation of nitric oxide (NO), an inhibitor of CRH secretion, addition of ET-1 was also carried out in the presence of the NO synthase inhibitor, L-NO-Arg: ET-1 was again without effect in this dose range. ET-3 had no effect on any hormone at any concentration. It is concluded that ET-1 may be involved in the control of both vasopressin and oxytocin secretion, most probably at receptors relatively unresponsive to ET-3, the ET_A recpetor. Any direct effect of the endothelins on the HPA axis is likely to be exerted via hypothalamic vasopressin rather than CRH.

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Section: Discussioncontrasting

confidence: 51%

mentioning

confidence: 99%

Endothelin-1 Stimulates the in vitro Release of Neurohypophyseal Hormones, but Not Corticotropin-Releasing Hormone, via ET<sub>A</sub> Receptors

et al. 1994

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“…Intravenous injection of ET decreases renal blood flow and glomerular filtration rate and increases PRA and the level of plasma AVP, ALD, and ANP in animals (27)(28)(29)(30), whereas a low dose of ET produces diuretic and natriuretic effects (31). Because the level of plasma ET did not change during PEEP in our study, ET, at least in the systemic circulation, probably does not play a role in the renal effect of PEEP.…”

Section: Anesth Analgmentioning

confidence: 99%

Positive End-Expiratory Pressure Ventilation Decreases Plasma Atrial and Brain Natriuretic Peptide Levels in Humans

Shirakami

Magaribuchi²,

Shingu³

et al. 1993

Anesthesia & Analgesia

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To investigate the possible role of atrial and brain natriuretic peptides (ANP and BNP) in the renal effects of mechanical ventilation with positive end-expiratory pressure (PEEP), we measured changes in plasma ANP and BNP levels during PEEP in patients undergoing subtotal esophagectomy. Application of 15 cm of H2O PEEP for 1 h decreased the levels of plasma ANP and BNP from 24.4 +/- 5.5 (mean +/- SEM) and 19.0 +/- 3.5 fmol/mL to 14.4 +/- 2.1 and 15.3 +/- 3.0 fmol/mL, respectively (P < 0.05). The level of plasma cyclic guanosine monophosphate, an intracellular second messenger of ANP and BNP, also decreased from 8.4 +/- 1.5 to 5.7 +/- 0.8 pmol/mL (P < 0.05). PEEP increased the levels of plasma arginine vasopressin from 2.0 +/- 0.5 to 4.2 +/- 1.2 pg/mL, aldosterone from 36.1 +/- 4.9 to 65.3 +/- 12.7 pg/mL, and plasma renin activity from 1.4 +/- 0.5 to 2.7 +/- 0.7 ng.mL-1.h-1. During PEEP ventilation, urine output, urinary sodium and potassium excretion, osmolar clearance, and cardiac index all decreased. PEEP increased free water clearance, right atrial pressure, pulmonary arterial pressure, and pulmonary capillary wedge pressure. The level of plasma endothelin, mean blood pressure, and heart rate did not change significantly. These results suggest that not only hemodynamics and the vasopressin and renin-angiotensin-aldosterone system, but also the natriuretic peptide system (ANP and BNP), are involved in the renal effects of PEEP.

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“…Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan Material and Methods Surgery and animal preparation Fourteen male mongrel dogs weighing between 12 and 18 kg were used in these experiments. Under pentobarbital anesthesia, catheters (Tygon, Akron, OH) were placed in the right iliac artery and vein as previously described (18,19). The catheters were inserted sc, externalized through the back between the scapula and secured.…”

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confidence: 99%

Calcitonin gene-related peptide modulates adrenal hormones in conscious dogs

Murakami

Suzuki²,

Nakamoto³

et al. 1991

Acta Endocrinologica

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The effects of a small dose (2 pmol/kg) of human calcitonin gene-related peptide I on plasma renin activity and hormones, including, aldosterone, ACTH, cortisol, AVP and ANH, were investigated in 14 conscious dogs. In addition, we studied the effects of calcitonin gene-related peptide on aldosterone secretion when it is stimulated by angiotensin II and ACTH. An intravenous bolus injection of 2 pmol/kg of calcitonin gene-related peptide raised plasma renin activity (by 216%, p<0.05), ACTH (by 85%, p<0.05), AVP (by 89%, p<0.05), and ANH (by 36%, p<0.05). Despite the elevation of plasma renin activity, aldosterone was decreased (by 52%, p<0.05). Cortisol did not change significantly. Infusion of 1 pmol \m=.\kg\m=-\1 \m=.\min\m=-\1of angiotensin II produced an elevation of aldosterone (by 186%, p<0.01), which was completely inhibited by pretreatment with an injection of 2 pmol/kg of calcitonin gene-related peptide. On the other hand, aldosterone secretion stimulated by ACTH was not altered significantly by pretreatment with an injection of 2 pmol/kg of calcitonin gene-related peptide. These results suggest that calcitonin gene-related peptide inhibits aldosterone secretion, especially when aldosterone is stimulated by angiotensin II. In addition, calcitonin gene-related peptide may be involved as an endocrine modulator in the physiological control of other several hormones closely related to the hemodynamics.Calcitonin gene-related peptide (CGRP) is a 37-amino acid polypeptide that results from the tissuespecific processing of the primary RNA transcript of the calcitonin gene (1). CGRP is detected in the systemic circulation (2,3), and the plasma level of CGRP increases during normal human pregnancy (4), in endotoxemia (5) or after sensory nerve injury (6).CGRP has been reported to have a potent vasodilatory action on various isolated vascular tissue preparations (7-9). Intravenous administration of CGRP induced potent dose-related hypotensive and tachycardiac responses in rats and human sub¬ jects (10,11).In addition to its potent vasoactive property, CGRP has an effect on hormonal regulation. CGRP immunoreactivity and specific binding sites for the peptide have been detected in the heart, the adre¬ nal gland, the hypothalamus and the pituitary gland as well as in other organs (12,13). CGRP was shown to stimulate renin secretion both in normal human subjects and in rat renal juxtaglomerular cells (14). More recently CGRP has been found to exhibit stimulatory effects on ANH secretion in vitro in the isolated rat atria (15,16). More recently, we reported that CGRP had an inhibitory action on aldosterone secretion in isolated glomerulosa cells (17). However, possible interaction of CGRP with angiotensin II and ACTH on the adrenal gland in vivo received little attention. Therefore, this study was designed to examine the endocrine responses to intravenous administration of a small dose of CGRP with a specific focus on adrenal hormones, especially aldosterone, in conscious dogs.

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Effects of Endothelin on Systemic and Renal Haemodynamics and Neuroendocrine Hormones in Conscious Dogs

Cited by 38 publications

References 21 publications

Endothelin-1 Stimulates the in vitro Release of Neurohypophyseal Hormones, but Not Corticotropin-Releasing Hormone, via ET<sub>A</sub> Receptors

Endothelin-1 Stimulates the in vitro Release of Neurohypophyseal Hormones, but Not Corticotropin-Releasing Hormone, via ET<sub>A</sub> Receptors

Positive End-Expiratory Pressure Ventilation Decreases Plasma Atrial and Brain Natriuretic Peptide Levels in Humans

Calcitonin gene-related peptide modulates adrenal hormones in conscious dogs

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