Control of renin release.

Vander, Arthur J.

doi:10.1152/physrev.1967.47.3.359

Cited by 508 publications

(180 citation statements)

References 33 publications

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“…Despite evidence for significant ACE inhibition by captopril, PRA was not significantly increased on the day that drug was given by itself. This finding suggests that the short loop feedback of angiotensin II on renin release is not the same in CHF as in normal individuals [21].…”

Section: Resultsmentioning

confidence: 91%

The renin angiotensin aldosterone system and frusemide response in congestive heart failure.

Reed

Greene

Ryan

et al. 1995

Brit J Clinical Pharma

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1. To test the hypothesis that basal renin angiotensin aldosterone system (RAAS) activity impairs the acute natriuretic response to frusemide in patients with mild or moderate congestive heart failure (CHF), we studied eight adult volunteers with preserved renal function, stable New York Heart Association Class II or III CHF, and echocardiographic evidence of left ventricular dysfunction due to myocardial infarction, hypertension, or both causes. 2. All patients received three dosing regimens administered in random order: (a) intravenous frusemide: 40 mg bolus then 40 mg h‐1 for 3 h, (b) captopril: two 12.5 mg oral doses separated by 2 h, (c) combined dosing: the first captopril dose preceded the frusemide bolus by 30 min. Sodium balance on an 80 mmol day‐1 sodium diet was documented prior to each dosing regimen. Sodium excretion was quantitated in urine collected at intervals until 3.5 h after initiating drug administration. During this time, urine output was replaced intravenously with an equivalent volume of 0.45% saline. 3. Captopril significantly lowered plasma angiotensin converting enzyme (ACE) activity and plasma aldosterone concentration, and raised inulin clearance. The drug had essentially no effect on the time course of magnitude of frusemide's natriuretic effect. Maximal fractional sodium excretion during frusemide infused by itself and in combination with captopril was 24.7 +/‐ 1.9% vs 28.2 +/‐ 3.8%, respectively (difference 3.5%; 95% CI, ‐4.0 to 11.0%; P > 0.05). Cumulative sodium excretion ending at 3.5 h was 429 +/‐ 53 mmol when frusemide was given alone and 455 +/‐ 69 mmol when captopril was added (difference, 26 mmol; CI, ‐121 to 174 mmol; P > 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Resultsmentioning

confidence: 91%

The renin angiotensin aldosterone system and frusemide response in congestive heart failure.

Reed

Greene

Ryan

et al. 1995

Brit J Clinical Pharma

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“…There is increasing evidence that acute and chronic hypoperfusion of one kidney causes characteristic changes not only of the renin content (for review [22]), but also of the levels of renin mRNA, in such a way that renin mRNA levels increase ipsilaterally and decrease contralaterally [13,15,19]. Since the regulation of the renin gene at the cellular level is in general only poorly understood, the mechanisms responsible for this differential regulation of renin gene expression in the kidneys in beings with unilateral renal artery stenosis have not yet been elucidated.…”

Section: Introductionmentioning

confidence: 99%

Role of the macula densa in the control of renal renin gene expression in two-kidney/one-clip rats

et al. 1994

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Abstract. This study was designed to examine whether macula densa function is involved in the changes of renal renin gene expression upon acute hypoperfusion of one kidney. To block macula densa function, rats with free access to salt and water were subcutaneously infused with furosemide (12 mg/day) for 6 days. Then, 4 days after the start of the infusion, the left renal arteries were clipped with 0.2-ram silver clips and renin mRNA levels in ipsilateral and contralateral kidneys, as well as plasma renin activities (PRA), were determined 48 h after clipping. In non-clipped animals furosemide increased PRA from 10 to 47 ng angiotensin I 9 h -1 9 ml 1 and raised renin mRNA levels in both kidneys 2.5-fold. In vehicle-infused animals, clipping of the left renal artery increased PRA to 37 ng angiotensin I. h -l. m1-1 and led to a 5-fold rise of renin mRNA levels in the ipsilateral kidneys and to a suppression to 20% of the control values in the contralateral kidneys. PRA values in clipped and furosemide-infused animals were 45 ng angiotensin I. h 1. ml-'. In these animals renin mRNA levels increased in the ipsilateral kidneys to similar absolute values as in vehicle-infused rats, whilst contralateral renin mRNA levels fell to about 25% of the respective controls. These findings indicate that the stimulations of renin gene expression by inhibition of macula densa salt transport and by renal artery clipping are not additive, suggesting that the macula densa mechanism may participate in the stimulation of renin gene expression upon hypoperfusion. The macula densa mechanism, however, appears to be not essentially involved in the suppression of renin gene expression in the contralaterals to stenosed kidneys.

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“…This suggests that the pooling of blood into the lower extremities in UP might also play a role in the retention of body fluid. Indeed, it has been shown that a reduction in the effective circulating blood volume brings about an increased release of angiotensin, aldostesone, and ADH (Vander, 1967, Kimura et al, 1976. On the other hand, administration of hydrocortisone did not significantly improve the impaired water diuresis in UP, suggesting that neither increased capillary permeability of an inflammatory or allergic nature nor impaired water diuresis due to glucocorticoid deficiency might exist in this edema.…”

Section: Discussionmentioning

confidence: 99%

The effects of postural changes on ADH release and the renal handling of sodium and water in patients with idiopathic edema.

et al. 1984

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In order to investigate the role of ADH and the renal handling of sodium and water in patients with idiopathic edema, 21 patients were subjected to acute oral water load tests. Although a normal water diuresis was observed in all patients in supine posture, it was markedly impaired in upright posture with significant decreases in sodium, free water, and osmolar clearances. In particular, two patients exihibited the continuous production of concentrated urine after the water load in upright posture. The fractional reabsorption of sodium at the proximal tubules was significantly increased in upright posture, while the glomerular filtration rate did not change significantly. The constricting of both legs with elastic bandages tended to improve the water diuresis in upright posture, suggesting that the pooling of blood into the lower legs might be contributing to the formation of idiopathic edema. The patients showed normal osmoregulation of ADH release in supine, but not in upright posture: the suppression of ADH release in upright posture was only transient or incomplete despite a sufficient fall in plasma osmolality following the water load. Thus, both an increase in renal sodium reabsorption and the insufficient suppression of ADH release in upright posture might contribute to the retention of body fluid in patients with idiopathic edema.

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Control of renin release.

Cited by 508 publications

References 33 publications

The renin angiotensin aldosterone system and frusemide response in congestive heart failure.

The renin angiotensin aldosterone system and frusemide response in congestive heart failure.

Role of the macula densa in the control of renal renin gene expression in two-kidney/one-clip rats

The effects of postural changes on ADH release and the renal handling of sodium and water in patients with idiopathic edema.

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