Hepatic Inactivation of Renin

Heacox, Robert; Harvey, Alice M.; Vander, Arthur J.

doi:10.1161/01.res.21.2.149

Cited by 74 publications

(28 citation statements)

References 9 publications

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“…All deter minations were made in duplicate, thus each CRF test yielded 4 ACTH determinations. Two standards were used: (I) synthetic arginine-vasopressin (Sigma), and (2) crude hypothalamic median eminence acidic extracts (HME) [14]. Typical dose-response curves are shown in figure 3.…”

Section: Discussionmentioning

confidence: 99%

Pharmacological Evidence that Stimulation of Central Serotonergic Pathways Increases Renin Secretion

Zimmermann

Ganong²

1980

Neuroendocrinology

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To determine if serotonin plays a role in the regulation of renin secretion, pentobarbital-anesthetized dogs were injected intravenously with drugs which modify serotonin metabolism. Renal perfusion pressure was kept constant by a clamp on the aorta proximal to the renal arteries. 5-Hydroxytryptophan (5-HTP) caused a significant increase (p < 0.05) in arterial plasma renin activity (PRA) that was abolished when peripheral and central aromatic amino acid decarboxylase activities were inhibited by administration of benserazide, but not reduced when only the peripheral decarboxylase activities were inhibited by administration of carbidopa. The serotonin receptor blocking drug metergoline also abolished the renin response to 5-HTP. L-Tryptophan in two different doses increased PRA. This increase was not reduced by carbidopa but was reduced or abolished by benserazide, metergoline, and renal denervation. The increase in PRA produced by 5-HTP and L-Tryptophan occurred without any change in blood pressure. 5-HTP had no effect on heart rate but L-Tryptophan reduced heart rate. These data indicate that 5-HTP and L-Tryptophan act on the central nervous system to produce an increase in renin secretion that is mediated via the renal nerves and occurs without a concomitant increase in sympathetic output to the heart or blood vessels. The increase appears to be due to the release of serotonin within the central nervous system.

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Section: Discussionmentioning

confidence: 99%

Pharmacological Evidence that Stimulation of Central Serotonergic Pathways Increases Renin Secretion

Zimmermann

Ganong²

1980

Neuroendocrinology

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“…Renin has a half-life in the circulation of the dog of more than 15 min (Hodge, Lowe & Vane, 1966a). It will therefore recirculate many times, the gradual decrease in concentration probably being a result of inactivation in the liver (Heacox, Harvey & Vander, 1967). By its action on angiotensinogen in the blood, renin generates angiotensin I throughout the circulation.…”

Section: Peptides (A) Br-advkininimentioning

confidence: 99%

The release and fate of vaso‐active hormones in the circulation

Vane

1969

British J Pharmacology

641

248

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“…How ever, PRA is only 7% of the normal value in anephric men [21]; this information indicates that circulating renin must derive primarily from the kidney. It should also be recognized that a decreased renal function does not change the half-life of renin as demonstrated by kinetic studies after nephrectomy [22], Since the liver is the major organ that removes renin from the circulation [23], the absence of clinical and laboratory features of hepatic dysfunction in our patients with CRD makes diminished inactivation by the liver an unlikely explanation for the observed high PRA. Consequently, the increased PRA in patients with CRD is most likely due to augmented renin production rather than diminished degradation of this substrate.…”

Section: Discussionmentioning

confidence: 68%

Inappropriately High Plasma Renin Activity Accompanies Chronic Loss of Renal Function

Yeyati¹,

Adrogué²

1996

Am J Nephrol

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Stimulation of both the systemic and local renin-angiotensin systems participates in the pathogenesis of tissue injury observed in experimental renal disease. However, substantial information demonstrating excessive activation of the renin-angiotensin system in patients with chronic renal disease is not available in spite of the well-established role of this system in the progression of renal damage. This investigation examined the plasma renin activity (PRA) and the ratio of this parameter to the simultaneously measured glomerular filtration rate (PRA/GFR) in normal volunteers (mean values 3.2 ng/ml/h and 3.0 ng/ml/h/100 ml GFR, respectively) and in patients with chronic renal disease (1.6 ng/ml/h and 28.5 ng/ml/h/100 ml GFR, respectively). A mean tenfold increase in the PRA/GFR ratio was observed in patients with chronic renal disease as compared to normal volunteers. The observed augmentation in PRA was not caused by physiologic mechanisms aimed at conserving urinary sodium since a positive correlation was found between PRA/GFR and the fractional excretion of sodium (y = 2.75+ 2.23x; r = 0.781, p < 0.01), as opposed to that of normal controls (y = 5.3- 1.46x; r = -0.640, p < 0.01). Consequently, our results support the existence of inappropriate activation of the renin-angiotensin system in humans with chronic renal disease. Such stimulation might play a critical role in the pathophysiology of advanced renal injury.

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Hepatic Inactivation of Renin

Cited by 74 publications

References 9 publications

Pharmacological Evidence that Stimulation of Central Serotonergic Pathways Increases Renin Secretion

Pharmacological Evidence that Stimulation of Central Serotonergic Pathways Increases Renin Secretion

The release and fate of vaso‐active hormones in the circulation

Inappropriately High Plasma Renin Activity Accompanies Chronic Loss of Renal Function

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