A Proposal of Ovarian ERAANPS (Endothelin-Renin-Angiotensin-Atrial Natriuretic Peptide System) and Effects of Tokishakuyakusan, Keishibukuryogan, Shakuyakukanzoto and Unkeito on the ERAANPS

We have previously shown the presence in a high concentration of endothelin-l (ET) in the corpus luteum and renin-angiotensin system (RAS) and binding sites for atrial natriuretic peptide (ANP) in the ovarian follicle. The present study was undertaken to identify the existence of ET, renin, angiotensin II and the binding site for ANP in the ovary at proestrus and examine in vivo the effects of herbal medicines [Tokishakuyakusan (TS), Keishibukuryogan (KB), Shakuyakukanzoto (SK) and Unkeito (UT)] on them. ET, all components of RAS and binding sites for ANP were found at high levels in the ovary. TS, KB, SK and UT decreased the ET levels in ovary, while components of RAS and binding sites for ANP have the propensity to increase. However, ET, renin, angiotensin II and ANP levels in plasma were not at all affected before and after treatment with TS, KB, SK or UT. Taken together with previous observations showing the existence of ET, RAS and the binding site for ANP in the ovary, we propose here the ERAANPS (endothelin-renin-angiotensin-ANP system) in the ovary as a functional regulator. Further, these results suggest that TS, KB, SK or UT may regulate the ovarian ERAANPS.

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Diurnal change in plasma atrial natriuretic peptide concentrations

Clinical Science ◽

10.1042/cs0730489 ◽

1987 ◽

Vol 73 (5) ◽

pp. 489-495 ◽

Cited By ~ 52

Author(s):

A. M. Richards ◽

G. Tonolo ◽

R. Fraser ◽

J. J. Morton ◽

B. J. Leckie ◽

...

Keyword(s):

Angiotensin Ii ◽

Atrial Natriuretic Peptide ◽

Antidiuretic Hormone ◽

Natriuretic Peptide ◽

Plasma Concentrations ◽

Dietary Sodium ◽

Sodium Balance ◽

Diurnal Changes ◽

Renin Angiotensin ◽

Atrial Natriuretic

1. Diurnal changes in plasma concentrations of atrial natriuretic peptide (ANP), renin, angiotensin II, aldosterone, Cortisol and antidiuretic hormone were investigated in seven normal volunteers studied under standardized conditions of dietary sodium, posture and physical activity. After completion of the diurnal study serial measurements of these variables were continued during, and on recovery from, a 2 day period of severe sodium depletion. 2. Clear diurnal variations in plasma concentrations of renin, angiotensin II, aldosterone, Cortisol and antidiuretic hormone were observed. 3. Plasma ANP concentrations also varied significantly over 24 h. Values peaked about mid-day and a distinct trough in peptide concentrations occurred in the early evening. However, variations in plasma ANP values were of relatively small amplitude and not clearly independent of modest parallel shifts in sodium balance. 4. Changes in plasma ANP concentrations both within the diurnal study period and during sodium deprivation were closely and positively correlated with concomitant changes in cumulative sodium balance. 5. No simple parallel or reciprocal relationships between plasma concentrations of ANP, on the one hand, and concurrent plasma concentrations of other hormones or in the rate of urinary sodium excretion, on the other, were observed during the 25 h of the diurnal study.

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Effect of Acute Hypercapnia on Alpha Atrial Natriuretic Peptide, Renin, Angiotensin II, Aldosterone, and Vasopressin Plasma Levels in Patients With COPD

CHEST Journal ◽

10.1378/chest.107.3.780 ◽

1995 ◽

Vol 107 (3) ◽

pp. 780-786 ◽

Cited By ~ 18

Author(s):

François Chabot ◽

Paul M. Mertes ◽

Nicolas Delorme ◽

Francine V. Schrijen ◽

Claude G. Saunier ◽

...

Keyword(s):

Angiotensin Ii ◽

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Plasma Levels ◽

Renin Angiotensin ◽

Atrial Natriuretic

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Effects of atrial natriuretic peptide, dopamine, and ouabain on aldosterone synthesis

Acta Endocrinologica ◽

10.1530/acta.0.1150057 ◽

1987 ◽

Vol 115 (1) ◽

pp. 57-62 ◽

Cited By ~ 7

Author(s):

Sadao Nakajima ◽

Hiromichi Suzuki ◽

Ikuo Saito ◽

Takao Saruta

Keyword(s):

Angiotensin Ii ◽

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

In Vivo Study ◽

Stimulatory Action ◽

Related Substances ◽

Natriuretic Factors ◽

Atrial Natriuretic

Abstract. This study was undertaken to examine the effects of atrial natriuretic peptide (ANP), dopamine, and ouabain, which each are considered to be a kind of natriuretic factor, on aldosterone synthesis in vivo and in vitro. In the in vivo experiments, during infusion of one of the natriuretic factors, ANP (64 pmol · min−1 · kg−1), dopamine (20 nmol · min−1 · kg−1) or ouabain (684 pmol · min−1 · kg−1), the stimulatory action of angiotensin II (20 pmol · min−1 · kg−1) or adrenocorticotropin (ACTH, 7 pmol · min−1 · kg−1) on aldosterone synthesis was investigated in 36 anaesthetized (pentobarbital, 40 mg/kg, iv) female rabbits. In the basal condition, aldosterone synthesis was suppressed slightly by each of the natriuretic factors. The stimulatory actions of angiotensin II and ACTH on aldosterone synthesis were significantly attenuated by pre-treatment with ANP and dopamine. However, ouabain infusion did not induce any changes in the synthesis of aldosterone, 18-hydroxycorticosterone (18-OHB), and corticosterone (B) in either the basal or the stimulated conditions. For the in vitro experiments, rabbit adrenal glomerulosa cells (105 cells/tube) were used. The effects of ANP and dopamine on the aldosterone synthesis revealed results identical to those from the in vivo study. However, in contrast to the in vivo study, ouabain completely inhibited the synthesis of aldosterone, 18-OHB and B. The above results obtained in vivo and in vitro suggest that ANP inhibits corticosterone methyloxidase II activity and dopamine inhibits corticosterone methyloxidase I activity. However, from the present study we were unable to specify the action of ouabain on the synthesis of aldosterone and its related substances.

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Endogenous angiotensin II modulates the effect of atrial natriuretic peptide on extracellular fluid partition

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1993.264.4.r676 ◽

1993 ◽

Vol 264 (4) ◽

pp. R676-R680

Author(s):

J. P. Valentin ◽

N. Nafrialdi ◽

J. Ribstein ◽

A. Mimran

Keyword(s):

Angiotensin Ii ◽

Arterial Pressure ◽

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Renin Angiotensin System ◽

Acute Administration ◽

Angiotensin System ◽

Renin Angiotensin ◽

Series Of Experiments ◽

Atrial Natriuretic

Atrial natriuretic peptide (ANP) has been shown to promote a fluid shift from the intravascular toward the interstitial compartment and to interact with the renin-angiotensin system at the renal as well as the extrarenal level. In the present studies, the interaction between the renin-angiotensin system and the effects of ANP infusion (100 ng.kg-1 x min-1 for 45 min) on arterial pressure and hematocrit were assessed in bilaterally nephrectomized, anesthetized rats. In a first series of experiments, suppression of angiotensin II generation was achieved by chronic (10 days) treatment by the angiotensin-converting-enzyme inhibitor (ACEI) captopril in rats maintained on a low-sodium diet. ACEI pretreatment prevented the rise in hematocrit associated with ANP infusion (+2.1 +/- 0.1 vs. +5.8 +/- 0.2%, P < 0.05), without influencing the effect of ANP on arterial pressure. In ACEI-pretreated rats, acute administration of angiotensin II at a subpressor dose (2.5 ng.kg-1 x min-1) restored the ANP-induced increase in hematocrit. In a second series of experiments, acute blockade of the renin-angiotensin system was obtained by the ACEI enalaprilat or the nonpeptide angiotensin II receptor antagonist losartan (both 1 mg/kg i.v. bolus). In the presence of either enalaprilat or losartan, the ANP-induced increase in hematocrit was similarly prevented. These results indicate that the effect of ANP on vascular permeability is modulated by endogenous angiotensin II, possibly due to distinct influences of the two peptides at the level of pre- and postcapillary resistances.

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Comparative Effects of Atrial Natriuretic Peptide and Brain Natriuretic Peptide on the Aldosterone and Pressor Responses to Angiotensin Ii in Man

Clinical Science ◽

10.1042/cs0880081 ◽

1995 ◽

Vol 88 (1) ◽

pp. 81-86 ◽

Cited By ~ 11

Author(s):

Robert I. Cargill ◽

Allan D. Struthers ◽

Brian J. Lipworth

Keyword(s):

Steady State ◽

Angiotensin Ii ◽

Atrial Natriuretic Peptide ◽

Brain Natriuretic Peptide ◽

Natriuretic Peptide ◽

Plasma Concentrations ◽

Plasma Aldosterone ◽

Renin Angiotensin Aldosterone System ◽

Renin Angiotensin ◽

Atrial Natriuretic

1. Atrial natriuretic peptide and brain natriuretic peptide have similar vasodilator and natriuretic properties, although little information is available regarding their relative effects as antagonists of the renin—angiotensin—aldosterone system. We have therefore compared how atrial natriuretic peptide and brain natriuretic peptide affect the systemic pressor and aldosterone responses to angiotensin II in eight male subjects. 2. Each subject was studied on three separate occasions, when they received a 60-min infusion of placebo, atrial natriuretic peptide (10 pmol min−1 kg−1) or brain natriuretic peptide (10 pmolmin−1 kg−1), with a concomitant infusion of angiotensin II (6 ng min−1 kg−1) given for the final 30 min of the infusion period. The change in haemodynamic parameters and plasma aldosterone induced by angiotensin II was measured. Plasma concentrations of atrial natriuretic peptide (182 ± 23 pmol/l) and brain natriuretic peptide (193 ± 25 pmol/l) achieved at steady-state during the infusion on each study day were not significantly different. 3. Increases in mean arterial pressure in response to angiotensin II were significantly lowered by concomitant infusion of atrial natriuretic peptide (21.0 ± 1.7 mmHg) and brain natriuretic peptide (20.1 ± 1.9 mmHg) compared with placebo (29.0 ± 4.1 mmHg). There were similar effects on systolic and diastolic blood pressure. Cardiac output was decreased on each study day to the same extent by angiotensin II infusion. Total systemic vascular resistance showed a non-significant trend towards an attenuated response to angiotensin II when atrial natriuretic peptide or brain natriuretic peptide was infused concomitantly in comparison with placebo. 4. Plasma aldosterone increased by 326 ± 49 pmol/l when angiotensin II was infused with placebo. Both atrial natriuretic peptide and brain natriuretic peptide significantly blunted this response, although the increase with atrial natriuretic peptide (19 ± 35 pmol/l) was significantly lower than the increase with brain natriuretic peptide (133 ± 19 pmol/l). 5. Atrial natriuretic peptide and brain natriuretic peptide were therefore equally effective in blunting the systemic pressor response to angiotensin II. It was apparent, however, in view of similar plasma concentrations at steady state, that on a molar basis atrial natriuretic peptide was a more potent inhibitor of angiotensin II-induced aldosterone secretion than brain natriuretic peptide. These results suggest a dissociation between the haemodynamic and hormonal effects of atrial natriuretic peptide and brain natriuretic peptide in terms of antagonism of the renin—angiotensin—aldosterone system.

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