Urinary Kallikrein Excretion and Plasma Renin Activity in Patients with Essential Hypertension and Primary Aldosteronism

1978 ◽  
Vol 55 (1) ◽  
pp. 51-55 ◽  
Author(s):  
A. Lechi ◽  
G. Covi ◽  
C. Lechi ◽  
A. Corgnati ◽  
E. Arosio ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Plasma Renin Activity ◽  
Primary Aldosteronism ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Renin Activity ◽  
Urinary Kallikrein ◽  
Hypertensive Patients ◽  
Urinary Kallikrein Excretion ◽  
Low Renin Hypertension

1. The 24 h urinary excretion of kallikrein has been studied in 40 normotensive control subjects and in 74 age-matched patients with essential hypertension under similar conditions. By use of the renin-sodium index, hypertensive patients were divided into two subgroups: low-renin hypertension and normal-renin hypertension patients. Urinary kallikrein determinations were also obtained from six hypertensive patients with primary aldosteronism. 2. Urinary kallikrein was significantly lower both in patients with normal-renin and low-renin essential hypertension. Urinary kallikrein excretion was very high in the patients with primary aldosteronism. 3. In nine hypertensive patients β-adrenoreceptor-blocking therapy caused a significant decrease of plasma renin activity, but had no significant effect on urinary kallikrein excretion. 4. The results support the concept that low urinary kallikrein is likely to be a marker of essential hypertension. Under certain conditions its excretion is positively related to mineralocorticoid hormone concentrations but it is not primarily related to the renin-angiotensin system.

Renin—angiotensin and Kallikrein—kinin Systems in Sodium Homeostasis and Hypertension in Rats

1976 ◽  
Vol 51 (s3) ◽  
pp. 283s-286s
Author(s):  
C. I. Johnston ◽  
P. G. Matthews ◽  
E. Dax
Keyword(s):  
Plasma Renin Activity ◽  
Kinetic Method ◽  
Plasma Renin ◽  
Significant Rise ◽  
Renin Activity ◽  
Urinary Kallikrein ◽  
Urinary Kallikrein Excretion ◽  
Sodium Load ◽  
Renal Hypertensive Rats ◽  
Goldblatt Hypertension

1. Urinary kallikrein excretion was measured in rats by an enzyme kinetic method employing radioimmunoassay of generated bradykinin. 2. Rats given a sodium load (NaCl solution, 20 g/l, to drink) for 28 days showed acute and prolonged significant falls in urinary kallikrein excretion associated with suppression of plasma renin and angiotensin. 3. Conversely sodium-depleted rats showed increases in urinary kallikrein excretion, associated with rises in plasma renin and angiotensin. 4. A close and significant direct relation between plasma renin activity and urinary kallikrein excretion was demonstrated. 5. The diuresis and natriuresis induced by frusemide in rats was associated with increased urinary kallikrein excretion and acute rises in plasma renin. 6. In chronic renal hypertensive rats urinary kallikrein excretion was increased only in the animals with two-kidney Goldblatt hypertension. This group was also the only group that demonstrated a significant rise in plasma renin activity.

Plasma Renin in Long-Term Diuretic Treatment of Hypertension: Effect of Discontinuation and Restarting Therapy

1982 ◽  
Vol 63 (2) ◽  
pp. 121-125 ◽  
Author(s):  
S. Swart ◽  
R. F. Bing ◽  
J. D. Swales ◽  
H. Thurston
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Juxtaglomerular Apparatus ◽  
Significant Rise ◽  
Renin Activity ◽  
Hypertensive Patients ◽  
Diuretic Treatment ◽  
Low Renin Hypertension ◽  
Before And After

1. Plasma renin activity, body weight and blood pressure were measured before and after 7 days' treatment with bendrofluazide in ten hypertensive subjects. They were then treated with bendrofluazide alone (5 mg daily) for a minimum of 3 years. The diuretic was then discontinued and the measurements were repeated before and again after 7 days with bendrofluazide. The results were compared with those obtained before chronic treatment with the diuretic. 2. Chronic diuretic treatment was associated with a persistent and progressive rise in plasma renin activity, that fell promptly to pretreatment levels when diuretics were discontinued. This was associated with significant weight gain but no immediate significant rise in blood pressure. 3. When acutely challenged with bendrofluazide the patients showed a greater increase in plasma renin activity on the second occasion than on the first. Three out of five patients with an initially subnormal response had normal responses after chronic diuretic treatment. 4. Chronic diuretic treatment increased the responsiveness of the juxtaglomerular apparatus in some hypertensive patients. 5. Classification of hypertensive patients into renin subgroups may be influenced by previous therapy, even when that therapy has been discontinued for 4 weeks. In particular ‘low renin hypertension’ may be masked by recent use of diuretics, as shown by three of the five patients in this subgroup in the present study.

Role of Prostaglandin in the Antihypertensive Mechanism of Captopril in Low Renin Hypertension

1980 ◽  
Vol 59 (s6) ◽  
pp. 141s-144s ◽  
Author(s):  
Keishi Abe ◽  
Toru Ito ◽  
Makito Sato ◽  
Toshiaki Haruyama ◽  
KO Sato ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Prostaglandin E ◽  
Hypertensive Patients ◽  
Endogenous Prostaglandin ◽  
Low Renin Hypertension ◽  
Prostaglandin System

1. The role of endogenous prostaglandins in the antihypertensive mechanism of the angiotensin converting enzyme inhibitor, captopril, was investigated. 2. An unequivocal reduction in blood pressure and significant increase in plasma renin activity and urinary prostaglandin E excretion were found after the captopril administration. 3. The changes in blood pressure, plasma renin activity and urinary prostaglandin E excretion induced by captopril were reversed after the inhibition of endogenous prostaglandin synthesis by indomethacin. However, the responses in low renin hypertension were different from those in normal renin hypertension. 4. In low renin hypertensive patients who responded to captopril, the hypotensive effect was abolished after the addition of indomethacin, whereas no marked change in blood pressure was induced by indomethacin in normal renin hypertensive patients. In contrast, plasma renin activity was markedly increased after captopril administration in normal renin hypertension, and no significant change was found in low renin hypertension. 5. Potentiation of the prostaglandin system seems to be a principal factor in the antihypertensive mechanism of captopril in low renin hypertension, and inhibition of the renin-angiotensin system is important in normal renin hypertensives. 6. The increase in renin release after the administration of captopril was inhibited by indomethacin, suggesting that an endogenous prostaglandin system may contribute to the short feedback mechanism of renin release.

Reduced Plasma Renin Activity in Essential Hypertension: Effects of Blood Pressure, Age and Sodium

1976 ◽  
Vol 51 (s3) ◽  
pp. 185s-188s ◽  
Author(s):  
G. W. Thomas ◽  
J. G. G. Ledingham ◽  
L. J. Beilin ◽  
A. N. Stott
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Plasma Renin Activity ◽  
Inverse Relationship ◽  
Plasma Renin ◽  
Renin Activity ◽  
Hypertensive Patients ◽  
Significant Inverse Relationship ◽  
Control Subjects ◽  
And Control

1. Supine plasma renin activity and its responsiveness to erect posture and frusemide were reduced in fifty-one patients with essential hypertension, compared with fifty-one age- and sex-matched control subjects. 2. Twenty-four hour urinary sodium excretion was similar in hypertensive patients and control subjects, but after intravenous frusemide hypertensive patients excreted significantly less sodium. 3. A significant inverse relationship between plasma renin activity and diastolic blood pressure was demonstrated in hypertensive patients and in normotensive control subjects. 4. A significant inverse relationship between plasma renin activity and age, independent of blood pressure, was shown in hypertensive patients and control subjects. 5. It is concluded that the reduced renin values found in essential hypertension are, in part, the result of the elevated blood pressure acting on the kidney.

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