Relationship between angiotensinogen, leptin and blood pressure levels in young normotensive men
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Although the relationship between an increase in adipose tissue and a rise in blood pressure has long been recognized, the mechanism linking these two phenomena has yet to be fully understood. Recently, it has become evident that adipose tissue is a rich source of metabolically active molecules, including free fatty acids, leptin and angiotensinogen, the precursor of angiotensin II. The latter finding has prompted speculation on the possible role of adipocyte-derived angiotensinogen in the relationship between body weight and blood pressure. Therefore we examined the relationship between blood pressure, angiotensinogen, body mass index (BMI) and leptin levels in healthy normotensive subjects who are genetically predisposed to the development of hypertension.We studied 40 subjects with a positive family history of hypertension and 51 subjects with a negative family history. After the blood pressure measurements, blood samples were collected for the assessment of angiotensinogen, leptin, glucose, insulin, renin activity and electrolytes. Oral glucose tolerance was studied by an oral glucose tolerance test (75 g glucose).Plasma angiotensinogen was significantly correlated with both BMI (r=0.29, P < 0.01) and plasma leptin (r=0.40, P < 0.001). While plasma angiotensinogen and blood pressure were positively correlated only in subjects with a positive family history of hypertension (r=0.33, P< 0.05), plasma leptin was related to blood pressure in both groups (r=0.26, P=0.01). Furthermore, the insulin response to an oral glucose load was significantly related to both plasma angiotensinogen (r=0.22, P< 0.05) and plasma leptin (r=0.47, P< 0.001).These findings support the hypothesis that circulating angiotensinogen levels are related to adipose mass in young, normotensive, nonobese men. Further studies on the relationship between adipose tissue and systemic or local renin-angiotensin systems appear warranted.Keywords:
Plasma renin activity
Plasma renin activity
Essential hypertension
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Plasma renin reactivity (PRR) is the rate of angiotensin generation in vitro after addition of exogenous renin to plasma. To evaluate the hypothesis that suppressed plasma renin activity (PRA) in patients with low renin essential hypertension may be related to an alteration of the kinetics of the in vitro renin reaction, PRR was compared in plasma of patients with low renin and normal renin essential hypertension. Prostaglandin A (PGA) inhibits renin, and PGA was also measured to determine if suppressed PRA may be related to increased PGA. Low renin and normal renin hypertension were defined by comparing PRA responses of 30 hypertensive patients and 16 matched control subjects to upright posture and furosemide (80 mg p.o.). Nine of 30 patients had low PRA. Compared to that in plasma of patients with normal renin hypertension, PRR was suppressed (P < 0.005) during 30, 60, and 180 min incubations in the low renin patients. Overall, in the hypertensive patients, there was a significant positive correlation (r = +0.58; P < 0.01) between PRR and the PRA response to furosemide. PGA in patients with low renin hypertension (0.86 ng/ml ± 0.06 SE) was less (P < 0.05) than that in patients with normal renin hypertension (1.10 ng/ml ± 0.07 SE) and control subjects (1.18 ng/ml ± 0.10 SE); PGA of normal renin patients and control subjects did not differ (P > 0.1). These results suggest that an alteration of the kinetics of the renin reaction may contribute to the apparent renin suppression in patients with low renin hypertension. Hypertensive patients with suppressed PRA also have low PGA.
Plasma renin activity
Essential hypertension
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Components of the renin-angiotensin system (plasma renin activity, total and inactive renin, angiotensinogen and angiotensin II) were examined in 90 patients with labile and stable essential hypertension before and after functional and pharmacologic tests. New data have been obtained on intrasystemic regulatory mechanisms of the pressor renin-angiotensin systems. Different patterns of plasma active and inactive renin variations in response to salt loading are demonstrated in patients with different "renin" variants of essential hypertension. Angiotensin II is shown to have a stimulating effect on angiotensinogen synthesis.
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Renin activity, concentration, substrate and reactivity were determined in normal subjects as well as in hypertensive subjects with suppressed and normal plasma renin activity. Renin substrate measurements were similar in all groups. Renin reactivity, a measure of circulating modifiers of the renin reaction, was significantly increased in both hypertensive groups. Reactivity was significantly greater in the normal renin hypertensive group than the low renin hypertensive group. Renin concentration was significantly suppressed in both hypertensive groups, but to a greater degree in the low renin hypertensives. These findings suggest that plasma renin concentration may be suppressed in most hypertensive subjects. Furthermore, plasma renin activity may be "normalized" in most hypertensive subjects by the effect of circulating modifiers of the renin reaction. While renin reactivity in the plasma of low-renin hypertensive subjects is accelerated to a lesser degree than that of the normal-renin hypertensives, this finding alone does not explain the low plasma renin activity.
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Plasma renin activity
Essential hypertension
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AbstractHomogenates of rat aortic wall can generate angiotensin I when incubated with nephrectomised rat plasma. This renin-like activity is due to a mixture of proteolytic enzymes. Thus the capacity to generate angiotensin I is greater at pH 5.3 than pH 6.5, although the latter is the pH optimum for rat renal renin. The present work addresses itself to two questions. Is this activity derived from plasma renin? Secondly, does vascular renin-like activity play a role in blood pressure control? Plasma and aortic renin were altered by bilateral nephrectomy and modulation of salt intake. In addition four models of hypertension were studied (early and chronic Goldblatt 2-kidney 1-clip, DOC-salt and spontaneous hypertension). The results indicated that in steady state conditions, aortic and plasma renin-like activity (measured with an incubation pH of 6.5) changed in parallel. When plasma renin was altered acutely however by intravenous injection of renin into nephrectomised rats the half-life of plasma renin was much shorter than the half life of aortic renin. Under these circumstances the pressor response to renin correlated much better with aortic than with plasma renin-like activity. Whilst these studies suggest therefore that renin taken up by the arterial wall is an important determinant of blood pressure, they provide no evidence that accumulation of renin locally produces hypertension in the presence of normal or low plasma renin activity.Key Words: arterial reninrenin-like activityblood pressureGoldblatt hypertensionspontaneously hypertensive ratsdeoxycorticosterone-salt hypertension
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Plasma renin activity
Saralasin
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