Effect of pinacidil on renal haemodynamics, tubular function and plasma levels of angiotensin II, aldosterone and atrial natriuretic peptide in healthy man

Abstract. In order to evaluate the role of calcium metabolism in blood pressure regulation, 15 patients with primary hyperparathyroidism and 9 healthy control subjects were studied before and during angiotensin II infusion. The patients were re-investigated 2–5 months after removal of the parathyroid adenoma. Blood pressure, plasma levels of angiotensin II, aldosterone, arginine vasopressin, and atrial natriuretic peptide, and creatinine clearance were determined. Blood pressure and the blood pressure response to angiotensin II infusion were both the same before and after the operation. Angiotensin II and arginine vasopressin during basal conditions were significantly higher before than after the operation (angiotensin II: 17 (median) to 10 pmol/l, P < 0.02; arginine vasopressin: 2.9 to 1.9 pmol/l, P < 0.01), whereas aldosterone, atrial natriuretic peptide, and creatinine clearance were unchanged. During angiotensin II infusion, aldosterone, arginine vasopressin, and atrial natriuretic peptide increased to approximately the same levels before and after the operation. Blood pressure was not correlated to any of the hormones measured. Thus, patients with primary hyperparathyroidism have elevated plasma levels of angiotensin II and arginine vasopressin which may be compensatory phenomena counteracting volume depletion owing to a decreased renal concentrating ability induced by hypercalcemia, and owing to PTH-induced inhibition of renal sodium reabsorption.

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Thirst and plasma levels of vasopressin, angiotensin II and atrial natriuretic peptide in patients with non-insulin-dependent diabetes mellitus

Diabetes Research and Clinical Practice ◽

10.1016/s0168-8227(05)80033-6 ◽

1991 ◽

Vol 11 (3) ◽

pp. 195-202 ◽

Cited By ~ 19

Author(s):

Kyuzi Kamoi ◽

Miyuki Ishibashi ◽

Tohru Yamaji

Keyword(s):

Diabetes Mellitus ◽

Angiotensin Ii ◽

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Plasma Levels ◽

Insulin Dependent Diabetes Mellitus ◽

Insulin Dependent Diabetes ◽

Dependent Diabetes Mellitus ◽

Insulin Dependent ◽

Atrial Natriuretic

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EFFECTS OF RAPAMYCIN ON RENAL HEMODYNAMICS, WATER AND SODIUM EXCRETION, AND PLASMA LEVELS OF ANGIOTENSIN II, ALDOSTERONE, ATRIAL NATRIURETIC PEPTIDE, AND VASOPRESSIN IN PIGS

Transplantation Journal ◽

10.1097/00007890-199412000-00002 ◽

1994 ◽

Vol 58 (12) ◽

pp. 1153-1157

Author(s):

K. GOLBAEKDAL ◽

C. B. NIELSEN ◽

J. C. DJURHUUS ◽

E. B. PEDERSEN

Keyword(s):

Angiotensin Ii ◽

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Plasma Levels ◽

Sodium Excretion ◽

Renal Hemodynamics ◽

Water And Sodium Excretion ◽

Atrial Natriuretic

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Renal and Hormonal Effects of Chronic Inhibition of Neutral Endopeptidase (EC 3.4.24.11) in Normal Man

Clinical Science ◽

10.1042/cs0850019 ◽

1993 ◽

Vol 85 (1) ◽

pp. 19-26 ◽

Cited By ~ 18

Author(s):

Janice E. O'Connell ◽

Alan G. Jardine ◽

David L. Davies ◽

James McQueen ◽

John M. C. Connell

Keyword(s):

Angiotensin Ii ◽

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Active Treatment ◽

Cyclic Gmp ◽

Plasma Levels ◽

Neutral Endopeptidase ◽

Active Therapy ◽

Days Of Therapy ◽

Atrial Natriuretic

1. Acute pharmacological inhibition of the enzyme neutral endopeptidase (EC 3.4.24.11), which cleaves the cardiac hormone atrial natriuretic peptide, raises endogenous levels of the hormone. Short-term administration of inhibitors causes natriuresis and diuresis in normal and hypertensive subjects; we report here the effects of an orally active neutral endopeptidase inhibitor (candoxatril, 200 mg) given twice daily for 10 days to normal salt-replete male subjects (n = 12) in a placebo-controlled cross-over study. 2. Candoxatril administration caused a transient natriuresis on day 1 of treatment, but this was not sustained, and cumulative sodium excretion at the end of the study was not altered by active therapy [1720 ± 40 versus 1734 ± 57 (placebo) mmol; means ± SEM]; exchangeable body sodium content was similarly unchanged. However, urinary cyclic GMP excretion was elevated throughout the active treatment phase when compared with placebo. 3. Although a change in plasma levels of atrial natriuretic peptide could not be demonstrated, platelet atrial natriuretic peptide binding sites were reduced by active treatment [23 ± 3 versus 39 ± 4 (placebo) fmol/109; P <0.001]. 4. Basal blood pressure and heart rate were not affected by candoxatril treatment. After 10 days of therapy subjects were given incremental infusions of angiotensin II (2, 4 and 8 ng min−1 kg−1) followed by phenylephrine. Although active therapy had not altered basal plasma concentrations of active renin and angiotensin II, levels of angiotensin II during infusion of the octapeptide were higher during the active phase. The diastolic pressor response to angiotensin II was increased during candoxatril treatment, although this is likely to reflect the higher plasma levels of angiotensin II during infusion of the octapeptide. In contrast, the systolic and diastolic pressor responses to phenylephrine were reduced by active treatment. 5. In conclusion, chronic candoxatril administration increases urinary cyclic GMP excretion without causing sustained natriuresis; evidence of atrial natriuretic peptide receptor down regulation was seen. There were no sustained hormonal or haemodynamic changes during therapy. The increased levels of angiotensin II during its infusion in the presence of candoxatril may reflect the role of neutral endopeptidase in clearing angiotensin II from the circulation.

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