Plasma Renin and Prorenin (Inactive Renin) in Diabetes Mellitus: Effects of Intravenous Furosemide*

Bryer‐Ash, Michael; Fraze, E.; Luetscher, John A.

doi:10.1210/jcem-66-2-454

Cited by 26 publications

(12 citation statements)

References 13 publications

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“…Other studies have found reciprocal changes in active and inactive renin in normal subjects during acute stimulation of the renin-angiotensin system, which suggests that active renin is derived from inactive renin. 25 BryerAsh et al 26 have recently reported that in some diabetic patients renal conversion of inactive renin to active renin may be impaired, which results in elevated inactive renin levels with reduced PRA levels. We actually found a direct relation between inactive renin and PRA levels in both the control and diabetic groups in response to dietary sodium and posture.…”

Section: Discussionmentioning

confidence: 99%

Renin regulation in type II diabetes mellitus: influence of dietary sodium.

et al. 1989

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Numerous abnormalities in the renin-angiotensin system have been described in diabetes mellitus. Plasma renin activity (PRA) has been noted to be low, normal, and high La diabetic patients; these variable results may be explained by differences in patient selection and standardization of study conditions. We evaluated PRA and inactive renin responses in Type II normotensive (n=7) and hypertensive (n=12) diabetic patients specifically selected for no or minimal evidence (background retinopathy) for microvascular complications. Patients were studied in a metabolic ward after 7 days on a constant low sodium (20 meq/day) and 7 days on a high sodium (250 meq/day) diet. Nondiabetic control subjects (n=7) were evaluated under similar conditions. On low sodium intake, mean PRA levels were significantly reduced in the hypertensive diabetic group, but were not different between the control and normotensive diabetic groups. Hypertensive diabetic patients on high sodium intake also had greater reductions in PRA responses compared with the other study groups. In general, diabetic subjects on high sodium intake excreted less sodium and had more cumulative sodium retention than control subjects. Levels of inactive renin were not significantly different between the normotensive and hypertensive diabetic patients and were comparable with the levels in control subjects. Inactive renin levels changed in a similar direction and magnitude as PRA in response to sodium intake and posture in the three study groups. Infusion of angiotensin II led to comparable reductions in PRA in both diabetic groups and in the control group, suggesting an intact short feedback loop control. We conclude that Type II hypertensive diabetic patients with no or minimal complications have abnormalities of renin secretion that are best brought out under conditions of dietary sodium balance. The reduced PRA responses in these patients cannot be explained by defective activation of renin or by abnormalities of the angiotensin II short feedback loop of PRA control. Advanced age and abnormabties in renal sodium excretion in diabetic patients in combination with elevated blood pressure may account for the abnormal PRA responses in Type II diabetic hypertensive subjects. (Hypertension 1989; 13:200-205)

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Section: Discussionmentioning

confidence: 99%

Renin regulation in type II diabetes mellitus: influence of dietary sodium.

et al. 1989

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“…Angiotensin II also increases Animal models suggest that both ACE and chymase/ chymase-like pathways contribute to angiotensin II synthe cellular expression of fibronectin [59]. However, in 415 Renin-Angiotensin-Aldosterone-Kinin System and CVD in DM tissue angiotensin II levels has previously been reported, [63][64][65][66] both in types I and II diabetes mellitus [68,69].…”

Section: Anatomicmentioning

confidence: 99%

“…Some diabetics manifest attenuated renin release in Plasma renin activity response to furosemide-induced volume depletion [64]. 12 months of diabetes [72].…”

Section: Anatomicmentioning

confidence: 99%

“…Diabetics have higher circulating prorenin levels than nondiabetics [63][64][65]. Moreover, in diabetics compared thesis after balloon-induced injury in dog carotid arteries [61].…”

Section: Anatomicmentioning

confidence: 99%

“…Vascular smooth muscle cells manifest a hyper-to nondiabetic controls, there is an exaggerated rise in circulating prorenin levels and a lesser rise in total renin trophic response in the presence of TGF-1 or a hypoplastic response in its absence [62]. In the human aorta, only in response to furosemide-induced volume depletion [64].…”

Section: Anatomicmentioning

confidence: 99%

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Renin-Angiotensin-Aldosterone-Kinin System Influences on Diabetic Vascular Disease and Cardiomyopathy

Flack

Hamaty

Staffileno

1998

Mineral Electrolyte Metab

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Diabetes mellitus is associated with an inordinately high risk of virtually all manifestations of cardiovascular-renal disease including atherosclerotic coronary and peripheral vascular disease, congestive heart failure, stroke, nephropathy, and cardiomyopathy unassociated with coronary heart disease. Abnormalities in the renin-angiotensin-aldosterone-kinin (RAAK) cascade have been implicated in the pathogenesis and clinical expression of these cardiovascular-renal sequelae. Thus, pharmacological modulation of the RAAK system is an attractive therapeutic target in diabetes mellitus. Indeed, emerging data from human clinical studies appear to confirm this thesis.

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Active and inactive renin after exercise

Ikeda

Matsusaki

Kinoshita

et al. 1992

Europ. J. Appl. Physiol.

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The effects of graded exercise on plasma concentrations of active and inactive renin were studied in seven healthy men. Exercise was performed on a cycle ergometer at four different exercise intensities (corresponding to 30%, 50%, 80% and 87% of VO2max) for 10 min each. Concentrations of active renin and total renin after activation by trypsin were measured by direct immunoradiometric assay. Non-trypsin-activated renin concentration (inactive) was obtained by subtraction. Active renin concentrations at 30%, 50%, 80% and 87% of VO2max were 1.2, 1.9, 3.1 and 4.6 times higher than the control concentration, respectively. Similar increases in plasma renin concentration, determined by conventional enzymatic assay, were observed at every stage. In contrast, changes in inactive renin concentration were not significant at any stage. Significant increases in noradrenaline concentration were found at every exercise stage, but adrenaline, aldosterone and lactate concentrations were significantly elevated only after exercise at 50%, 80% and 87% of VO2max. The similarity between the changes in concentration of active renin and noradrenaline would suggest that sympathetic nerve activity may have been responsible either for the release of active renin or for the conversion of inactive renin to its active form in the kidney.

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Plasma Renin and Prorenin (Inactive Renin) in Diabetes Mellitus: Effects of Intravenous Furosemide*

Cited by 26 publications

References 13 publications

Renin regulation in type II diabetes mellitus: influence of dietary sodium.

Renin regulation in type II diabetes mellitus: influence of dietary sodium.

Renin-Angiotensin-Aldosterone-Kinin System Influences on Diabetic Vascular Disease and Cardiomyopathy

Active and inactive renin after exercise

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