Behaviour of Adrenomedullin during Acute and Chronic Salt Loading in Normotensive and Hypertensive Subjects

1996 ◽  
Vol 91 (3) ◽  
pp. 293-298 ◽  
Author(s):  
Toshihiko Ishimitsu ◽  
Toshio Nishikimi ◽  
Hiroaki Matsuoka ◽  
Kenji Kangawa ◽  
Kazuo Kitamura ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Salt Intake ◽  
Isotonic Saline ◽  
Salt Loading ◽  
Salt Load ◽  
High Salt Intake ◽  
Normotensive Subjects ◽  
Atrial Natriuretic

1. Responses of adrenomedullin to acute and chronic salt loading were examined in normotensive and hypertensive subjects. 2. In the acute salt load study, isotonic saline (50 ml/kg for 1 h) was intravenously infused into nine normotensive subjects and 11 patients with essential hypertension. Plasma adrenomedullin was higher in hypertensive than in normotensive subjects but was unchanged by saline infusion in either the normotensive (before infusion, 2.4 ± 0.2 fmol/ml; after infusion, 2.4±0.1 fmol/ml) or hypertensive (before infusion, 3.0±0.1 fmol/ml; after infusion, 2.9 ± 0.2 fmol/ml) group, while renin was suppressed and atrial natriuretic peptide was markedly increased. Plasma endothelin was not affected either. 3. In the chronic salt load study, seven normotensive subjects and 23 patients with essential hypertension underwent two 7-day periods of 30 and 260 mmol/day sodium intake. Depending on the blood pressure change, 13 hypertensive subjects were classified as salt-resistant and 10 as salt-sensitive. Salt-sensitive hypertensive subjects had suppressed plasma renin activity even during low salt intake. Plasma adrenomedullin or endothelin were not affected by the salt intake changes in any group; however, the high salt intake increased atrial natriuretic peptide in all groups. 4. These data indicate that the circulating level of adrenomedullin is not changed by either acute or chronic salt loading in normotensive subjects and patients with essential hypertension.

Fluid, Ionic and Hormonal Changes Induced by High Salt Intake in Salt-Sensitive and Salt-Resistant Hypertensive Patients

1996 ◽  
Vol 91 (2) ◽  
pp. 155-161 ◽  
Author(s):  
Alejandro De La Sierra ◽  
María Del Mar Lluch ◽  
Antonio Coca ◽  
María Teresa Aguilera ◽  
Vicente Giner ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Salt Intake ◽  
Plasma Aldosterone ◽  
High Salt ◽  
Plasma Noradrenaline ◽  
Hypertensive Patients ◽  
High Salt Intake ◽  
Atrial Natriuretic

1. The aim of the study was to detect differences between salt-sensitive and salt-resistant hypertensive patients in the response of the renin—aldosterone axis, plasma noradrenaline and atrial natriuretic peptide to high salt intake. 2. Fifty essential hypertensive patients followed 2 weeks of a standard diet with 20 mmol of NaCl daily, supplemented by placebo tablets for the first 7 days and by NaCl tablets for the last 7 days, in a single-blind fashion. Salt sensitivity was defined as a significant rise (P < 0.05) in 24 h mean blood pressure obtained by ambulatory blood pressure monitoring from the low- to the high-salt period. Biochemical and hormonal measurements were performed on the last day of both periods. 3. Twenty-two (44%) patients fulfilled criteria of salt-sensitive hypertension, whereas the remaining 28 (56%) were considered salt-resistant. High salt intake promoted a significant decrease (P < 0.05) in plasma creatinine, potassium, glucose, cholesterol, low-density lipoprotein-cholesterol, triacylglycerols, uric acid and plasma renin activity, and a significant increase in plasma atrial natriuretic peptide and 24 h urinary calcium excretion. The direction of these changes did not differ between salt-sensitive and salt-resistant patients. Salt-resistant hypertensive patients exhibited a significant decrease in plasma aldosterone induced by high salt intake (from 446 ∓ 35 to 226 ± 35 pmol/l; P < 0.001), whereas this parameter was not significantly modified in salt-sensitive patients (from 485 ± 76 to 364 ± 83 pmol/l; P not significant). Salt-sensitive patients showed an increase in plasma noradrenaline after high salt intake (from 1.15 ± 0.11 to 1.56 ± 0.14 nmol/l; P < 0.05), whereas salt-resistant patients presented a decrease in this parameter (from 1.48 ± 0.08 to 1.12 ± 0.08 nmol/l; P < 0.05). The change in plasma noradrenaline was directly correlated with the change in mean blood pressure induced by high salt intake (r = 0.479; P = 0.003). 4. We conclude that the increase in blood pressure induced by high salt intake in salt-sensitive patients is associated with a stimulation of the sympathetic nervous system and a blunted decrease in plasma aldosterone. Conversely, changes in renal function, electrolyte excretion and plasma concentrations of atrial natriuretic peptide induced by high salt intake seem to be similar in both salt-sensitive and salt-resistant patients.

Response of atrial natriuretic peptide to acute saline loading in essential hypertension

1988 ◽  
Vol 255 (6) ◽  
pp. F1085-F1090 ◽  
Author(s):  
A. Mimran ◽  
J. Nussberger ◽  
J. Ribstein ◽  
B. Waeber ◽  
H. R. Brunner
Keyword(s):  
Essential Hypertension ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Volume Expansion ◽  
Isotonic Saline ◽  
Fractional Excretion ◽  
Normal Subjects ◽  
Saline Loading ◽  
Fractional Excretion Of Sodium ◽  
Atrial Natriuretic

To further investigate the mechanism(s) of the exaggerated natriuretic response of hypertensives to volume expansion (VE; 1,800 ml iv isotonic saline over 3 h), the plasma levels of immunoreactive atrial natriuretic peptide (ANP) were measured in 11 normal subjects (NT) and 12 patients with mild essential hypertension (HT). NT and HT groups were similar with respect to age and basal levels of renin, aldosterone and ANP (34.5 +/- 5.5 in NT and 32.5 +/- 6.3 pg/ml in HT, mean +/- SE). In response to VE, ANP increased to the same extent in both groups (a change of 19.3 +/- 5.2 in NT and of 22.2 +/- 7.1 pg/ml in HT) despite the finding of an exaggerated natriuretic response to VE in essential hypertension (36 +/- 3.5 in NT and 54.9 +/- 6.3 nmol/3 h in HT, P less than 0.02). In addition, the fall in hematocrit and serum protein associated with saline infusion was less marked in HT than NT. The change in ANP induced by VE was inversely correlated with the percent fall in hematocrit and the increment in the fractional excretion of sodium in both groups. These observations suggest that ANPs may participate in the control of the renal response to isotonic VE; however they do not support an unequivocal influence of ANP in the exaggerated natriuretic response to VE of patients with essential hypertension.

Isotonic Saline Infusion Stimulates Plasma Release of Atrial Natriuretic Peptide (ANP) in Man

1986 ◽  
Vol 70 (s13) ◽  
pp. 74P-74P ◽  
Author(s):  
JV Anderson ◽  
J Donckier ◽  
W McKenna ◽  
ACR Burns ◽  
SR Bloom
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Isotonic Saline ◽  
Saline Infusion ◽  
Atrial Natriuretic

Atrial Natriuretic Peptide: Regulator of Chronic Arterial Blood Pressure

Physiology ◽  
2000 ◽  
Vol 15 (3) ◽  
pp. 143-149 ◽  
Author(s):  
Luis Gabriel Melo ◽  
Stephen C. Pang ◽  
Uwe Ackermann
Keyword(s):  
Blood Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Salt Intake ◽  
Gene Knockout ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Arterial Blood ◽  
Gene Knockout Mouse ◽  
Atrial Natriuretic

Recent findings in atrial natriuretic peptide (ANP) transgenic and gene knockout mouse models uncovered a tonic vasodilatory effect of this hormone that contributes to chronic blood pressure homeostasis. With elevated salt intake, ANP-mediated antagonism of the renin-angiotensin system is essential for blood pressure constancy, suggesting that a deficiency in ANP activity may underlie the etiology of sodium-retaining disorders.

Different Responses of Atrial Natriuretic Peptide Secretion and Its Receptor Density to Salt Intake in Rats

2004 ◽  
Vol 229 (1) ◽  
pp. 65-71 ◽  
Author(s):  
Kyung Sun Lee ◽  
So Young Kim ◽  
Jeong Hee Han ◽  
Yun Ah Kim ◽  
Chunhua Cao ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Salt Intake ◽  
Receptor Density ◽  
Peptide Secretion ◽  
Atrial Natriuretic
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