Renin Secretion in Renal Hypertension

Warren, D J; Ferris, ThomasF.

doi:10.1016/s0140-6736(70)90404-6

Cited by 116 publications

(29 citation statements)

References 18 publications

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“…The hypothesis that increased renin release causes hypertension in these animals was therefore largely abandoned. It has since been recognized, however, that maintenance of "normal" values for circulating renin activity in the setting of increased blood pressure or sodium excretory load may reflect activation ofthe renin-angiotensin system (25,26). Thus failure of plasma renin levels to decrease despite a prominent increase in blood pressure in rats subjected to renal ablation could reflect an increase in the activity of the circulating renin angiotensin system in these animals ( 1,24).…”

Section: Resultsmentioning

confidence: 99%

Angiotensin II receptor blockade limits glomerular injury in rats with reduced renal mass.

Lafayette¹,

Mayer²,

Park³

et al. 1992

J. Clin. Invest.

340

178

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The effects of angiotensin II (All) blockade were compared with the effects of angiotensin converting enzyme inhibition in rats with reduced nephron number. Rats were subjected to fivesixths renal ablation and divided into four groups with similar values for blood pressure and serum creatinine after 2 wk. Group 1 then served as untreated controls, while group 2 received the All receptor antagonist MK954 (which has previously been designated DuP753), group 3 received the converting enzyme inhibitor enalapril, and group 4 received a combination of reserpine, hydralazine, and hydrochlorothiazide. Micropuncture and morphologic studies were performed 10 wk later. Converting enzyme inhibition, All receptor blockade, and the combination regimen were equally effective in reversing systemic hypertension (time-averaged systolic blood pressure: group 1, 185±5 mmHg; group 2, 125±2 mmHg; group 3, 127±2 mmHg; group 4, 117±4 mmHg). Micropuncture studies showed that glomerular transcapillary pressure was reduced significantly by converting enzyme inhibition and by AII blockade but not by the combination regimen (5P: group 1, 49±1 mmHg; group 2, 42±1 mmHg; group 3, 40±2 mmHg, group 4, 47±1 mmHg). Reduction of systemic blood pressure was associated with the development of markedly less proteinuria and segmental glomerular sclerosis in rats receiving enalapril and MK954 but not in rats receiving the combination regimen (prevalence of glomerular sclerotic lesions: group 1, 41±4%; group 2, 9±1%; group 3,9±1%; group 4, 33±6%). These results indicate that the effects of converting enzyme inhibition on remnant glomerular function and structure depend on reduction in All activity and are not attributable simply to normalization of systemic blood pressure. (J. Clin. Invest. 1992. 766-771.)

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Section: Resultsmentioning

confidence: 99%

Angiotensin II receptor blockade limits glomerular injury in rats with reduced renal mass.

Lafayette¹,

Mayer²,

Park³

et al. 1992

J. Clin. Invest.

340

178

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“…ge, ( Statham In-PRA was measured by a modification of the method of rded on a Sanborn Pickens, Bumpus, Lloyd, Smeby, and Page (7,8 A 0.25 ml solution of microspheres containing 0.01 ACi/ml was diluted with 10% dextran to a volume of 2.5 ml in a plastic syringe. Next, 2 ml was injected into the animal and the remaining 0.5 ml was diluted with 9.5 ml 10% dextran and counted in a Packard auto-gamma counter (Packard Instrument Co., Downers Grove, Ill.) The radioactivity remaining in the syringe following the injection was subtracted from the total.…”

Section: Methodsmentioning

confidence: 99%

Uterine blood flow and uterine renin secretion

Ferris¹,

Stein²,

Kauffman³

1972

J. Clin. Invest.

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“…Unfortunately, inappropriate activation of the RAS is also one of the characteristics of renal failure. 41 Besides the (dys)regulation of ECFV and vasoconstriction, one of the most deleterious actions of the RAS in the CRC is activation of NADPH-oxidase by Ang II, resulting in formation of ROS. 42 This has been documented in endothelial cells, vascular smooth muscle cells, 43 renal tubular cells, 44 and cardiomyocytes.…”

Section: The Rasmentioning

confidence: 99%

The severe cardiorenal syndrome: ‘Guyton revisited’

Bongartz

Cramer²,

Doevendans³

et al. 2004

European Heart Journal

415

287

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The incidence of cardiac failure and chronic renal failure is increasing and it has now become clear that the co-existence of the two problems has an extremely bad prognosis. We propose the severe cardiorenal syndrome (SCRS), a pathophysiological condition in which combined cardiac and renal dysfunction amplifies progression of failure of the individual organ, so that cardiovascular morbidity and mortality in this patient group is at least an order of magnitude higher than in the general population. Guyton has provided an excellent framework describing the physiological relationships between cardiac output, extracellular fluid volume control, and blood pressure. While this model is also sufficient to understand systemic haemodynamics in combined cardiac and renal failure, not all aspects of the observed accelerated atherosclerosis, structural myocardial changes, and further decline of renal function can be explained. Since increased activity of the renin-angiotensin system, oxidative stress, inflammation, and increased activity of the sympathetic nervous system seem to be cornerstones of the pathophysiology in combined chronic renal disease and heart failure, we have explored the potential interactions between these cardiorenal connectors. As such, the cardiorenal connection is an interactive network with positive feedback loops, which, in our view, forms the basis for the SCRS.

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Renin Secretion in Renal Hypertension

Cited by 116 publications

References 18 publications

Angiotensin II receptor blockade limits glomerular injury in rats with reduced renal mass.

Angiotensin II receptor blockade limits glomerular injury in rats with reduced renal mass.

Uterine blood flow and uterine renin secretion

The severe cardiorenal syndrome: ‘Guyton revisited’

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